Monsanto’s Roundup Found in Animals with Birth Defects

I never said I was an expert nor according to your attempted insult, a know it all.
Thanks, tho! Appreciate it.

I post things that people may have an interest in.
If you don't like it, don't read it and why do you care how much or how little I post?

Everything, including pesticides, that goes onto plants, soil, etc., especially in our islands, ends up eventually in our water tables and our oceans, here and worldwide.

You can see for yourselves our surrounding waters after heavy rains brown with run-off from the land and the following advisories from DPNR relating to water quality and advising people to stay out of the water. Actually, it doesn't even have to be a heavy rain event for the advisory to be posted.

Why use any harmful pesticide when there are natural alternatives?
We, as the dominant species, are pretty much screwing up the planet.
Glad you're proud of that.

https://yourlogicalfallacyis.com/appeal-to-nature

Top 10 Reasons to Stop Using Pesticides
Honey Colony
Jan 31, 2015

Whether it’s the proven harmful effects on our health and ecosystems or the lack of regulatory oversight, there are just too many reasons to not stop using pesticides.

Top 10 Reasons

1) Pesticides don’t solve pest problems.

If they did, we wouldn’t repeatedly use them, now would we? Americans use more than a billion pounds of pesticides each year to combat pests on farm crops, in homes, places of business, schools, parks, hospitals, and other public places. YUCK! Instead, it would be wise to change the conditions that make pests thrive.

2) Pesticides are hazardous to our health.

Imagine, some people don’t believe this! According to the Environmental Protection Agency (who regularly sleeps with all of the pharmaceutical companies), adverse effects of pesticide exposure range from mild symptoms of dizziness and nausea to serious, long-term neurological, developmental, and reproductive disorders.

For instance, Glyphosate, better known as Roundup, damages genes and causes birth defects. And it’s the most widely used herbicide in the United States; we use almost 200 million pounds a year.

3) Pesticides cause special problems for children.

Let’s remember that for their size, children drink more water and eat more food and than adults, and both of these can be (and often are) contaminated with pesticides. Their play increases their potential exposure. Imagine, for instance, your child playing on turf or on a grassy lawn or park treated with pesticides.

As Dr. Lynn Goldman wrote while she was an assistant administrator at EPA, “As a pediatrician, I know that children can be more vulnerable to environmental contaminants.”

4) Pesticides contaminate our food.

Even after peeling and washing fruits and veggies, about 60 percent of our produce still contains more than one pesticide, says the USDA.

5) Pesticides are particularly hazardous for farmers, farm workers, and people who live near them.

There are no comprehensive systems for keeping track of the number and type of pesticide illnesses in the U.S., but research shows that farmers and farmworkers face risks of acute poisoning and long-term illness.

Because agricultural pesticides account for over 75 percent of total U.S. pesticide use, farmers and farmworkers are often exposed to large amounts of pesticides. The EPA has estimated that between 10 and 20 thousand pesticide-related illnesses occur among farmers and farmworkers every year, but the agency believes that these large numbers are actually serious underestimates.

Mothers, meanwhile, who live near farms and are exposed to insecticides are more likely to have children with ADHD.

6) Pesticides are dangerous to pets.

Pesticide poisoning of pets is common. For example, in 1990 the American Association of Poison Control Centers received over 11,000 calls regarding pesticide-poisoned pets. Only antifreeze causes more pet poisoning deaths than rodent control pesticides and organophosphate insecticides.

Exposure to herbicide-treated lawns and gardens increases the risk of bladder cancer by four to seven times in Scottish Terriers, according to a study by Purdue University veterinary researchers.

7) Pesticides contaminate our water.

According to a national study, 90 percent of our nation’s urban streams are contaminated with pesticides.

8) Pesticides are not good for fish and birds.

When pesticides contaminate water they can be particularly toxic to fish. In addition to fish, other marine or freshwater animals are endangered by pesticide contamination. A pesticide’s capacity to harm fish and aquatic animals is largely a function of its (1) toxicity, (2) exposure time, (3) dose rate, and (4) persistence in the environment.

It is clear that some chemicals have the potential to affect entire food chains. Routine environmental use of neonicotinoids, for instance, perpetuates the propensity for runoff, groundwater infiltration, and the cumulative and largely irreversible damage to invertebrates, all of which raise significant environmental concerns.

9) Pesticide “Health & Safety Testing” is conducted by chemical companies.

As we mention in Vanishing of the Bees, this is a bad case of the fox guarding the hen house. The Environmental Protection Agency does not conduct independent studies. They rely on the chemical companies to do due diligence. And my oh my, what a surprise that they find all the poisons relatively safe. Well, be certain that doesn’t mean a thang!

10) Pesticides just have too many secrets.

Where are pesticides used? When? How much? What’s in them? We almost never have good answers to these questions. But we do know many persist in the environment and that they synergize when combined. And inactive ingredients are really not inactive at all.

by Maryam Heinen, from Honey Colony http://www.care2.com/greenliving/top-10-reasons-to-stop-using-pesticides.html?onswipe_redirect=no&oswrr=4#comments

LAWN CHEMICALS INCREASE CANCER RISK IN DOGS

Exposure to herbicide-treated lawns and gardens increases the risk of bladder cancer by four to seven times in Scottish Terriers, according to a study by Purdue University veterinary researchers published in the April 15, 2004 issue of the Journal of the American Veterinary Medicine Association (J Am Vet Med Assoc 2004; 24:1290-1297). The study adds to earlier research conducted by the National Institutes of Health that found elevated rates of canine lymphoma in dogs exposed to lawn pesticides (1991). (See Beyond Pesticides factsheet) Meanwhile the American Veterinary Medical Association issued a release, "Herbicide Exposure May Increase Cancer Risk in Dogs," with the study authors' recommendations that owners of Scottish Terriers "should decrease their dogs' exposure to lawns or gardens treated with common herbicides, particularly phenoxy herbicides and possibly nonphenoxy herbicides" and "veterinarians should perform routine (every six months) cytologic urine exams in Scottish Terriers and other 'genetically high risk' breeds over six years old."

As these warnings about lawn pesticides are hitting the news wires, EPA and the chemical industry, hoping for support from the environmental community, are planning to issue guidelines and/or tips that urge people to "use pesticides safely" or "read the pesticide label." The group putting the documents together has refused to (i) disclose the Purdue study and other studies alerting the public to the link between lawn pesticides and adverse health and environmental effects, and (ii) support the public's right-to-know when pesticides are going to be used through neighborhood notification, so that people can take precautionary action by vacating the area and staying off treated lawns and landscapes. Local environmental and public health advocates have been successful in recent years in moving schools, parks, and town and city governments to adopt alternative practices that do not use toxic lawn pesticides. (See Daily News, February 19, 2004) [Join the Pesticide-Free Zone Campaign and national network]

A team of veterinary researchers including Lawrence T. Glickman, VMD, Dr.PH, has found an association between risk of transitional cell carcinoma of the urinary bladder in Scottish terriers and the dogs' exposure to chemicals found in lawn treatments. The study, based on a survey of dog owners whose pets had recently contracted the disease, may be useful not only for its revelation of potentially carcinogenic substances in our environment, but also because studying the breed may help physicians pinpoint genes in humans that signal susceptibility to bladder cancer.

"The risk of transitional cell carcinoma (TCC) was found to be between four and seven times more likely in exposed animals," said Dr. Glickman, a professor of epidemiology and environmental medicine in Purdue's School of Veterinary Medicine. "While we hope to determine which of the many chemicals in lawn treatments are responsible, we also hope the similarity between human and dog genomes will allow us to find the genetic predisposition toward this form of cancer found in both Scotties and certain people."

The research, which Dr. Glickman conducted the research with Malathi Raghavan, Deborah W. Knapp, Patty L. Bonney and Marcia H. Dawson, all of Purdue's School of Veterinary Medicine, and Indianapolis veterinarian Marcia Dawson.

According to the National Cancer Institute, about 38,000 men and 15,000 women are diagnosed with bladder cancer each year. Only about 30 percent of human bladder cancers develop from known causes. As Scottish terriers - often called Scotties - have a history of developing bladder cancer far more frequently than other breeds, Dr. Glickman and his team decided to examine the dogs' diet, lifestyle and environmental exposures for a possible link to bladder cancer.

In an earlier study, Dr. Glickman and his colleagues found Scotties are already about 20 times more likely to develop bladder cancer as other breeds. "These dogs are more sensitive to some factors in their environment," Dr. Glickman said. "As pets tend to spend a fair amount of time in contact with plants treated with herbicides and insecticides, we decided to find out whether lawn chemicals were having any effect on cancer frequency."

Dr. Glickman's group obtained their results by surveying the owners of 83 Scottish terriers. All of the animals had bladder cancer and were of approximately the same age. Based on an 18-page questionnaire, owners documented their dogs' housing, duration of exposure to the lawn or garden and information on the particular lawn treatment used (dog owners provided either the label from the treatment bottle or, if a company sprayed the lawns directly from a truck, the name of the lawn service). The results were then compared with a control group of 83 unexposed Scottish terriers of similar age that were undergoing treatment for unrelated ailments.

"We found that the occurrence of bladder cancer was between four and seven times higher in the group exposed to herbicides," Dr. Glickman said. "The level of risk corresponded directly with exposure to these chemicals: The greater the exposure, the higher the risk."

Dr. Glickman said it is possible the active ingredient in most lawn and garden sprays - a compound known by its chemical name of 2,4-D - was to blame, although EPA has not classified it as a carcinogen despite other epidemiological studies linking it to cancer in dogs and people. However, he said, it also is possible that one of the so-called inert ingredients in the mixture - ingredients which often make up nearly two-thirds of a treatment's volume - could be responsible for the increased risk.

"These other ingredients are thought to be inert and, therefore, are not tested or even listed on the product label," Dr. Glickman said. "But 4 billion pounds of these other untested chemicals reach our lawns and gardens every year, and we theorize they are triggering cancer in these animals, which are already at risk because of a peculiarity in their genome."

Scottish terriers' genetic predisposition toward developing bladder cancer makes them ideal as "sentinel animals" for researchers like Dr. Glickman because they require far less exposure to a carcinogen than other breeds before contracting the disease.

"You might compare them to the canaries used in coal mines a century ago," he said. "The difference is that we don't deliberately place our research animals in harm's way. We study animals that have already contracted diseases, bring them to the hospital and then try to find out what combination of genetic predisposition and environmental influence added up to make them ill." Dr. Glickman said the similarity between dog and human genomes could lead researchers to find the gene in humans that makes them susceptible to developing bladder cancer.

While environmental and public health advocates have pointed to studies like these and called for the banning of aesthetic lawn pesticides, especially in view of documented off-target drift of the chemicals and widespread and uncontrolled involuntary exposure in the outdoor and indoor environment, Dr. Glickman said that, "Finding the dog gene could save years in the search for it in humans and could also help us determine which kids need to stay away from lawn chemicals." "If such a gene exists in dogs, it's likely that it exists in a similar location in the human genome," Dr. Glickman said. But Dr. Glickman emphasized that because the effect was a combination of chemical and genetic predisposition, the results do not suggest that everyone should avoid treated lawns.

With an implied departure from environmental and public health policy to protect the most vulnerable, which in this case could be millions of people, Dr. Glickman said, "We don't want to indicate that every person is susceptible." "Because this study shows that exposure to the chemicals exacerbates a genetic predisposition in Scotties towards developing TCC, it's likely that only a segment of the human population would be in similar danger. "But we still need to find out who those individuals with the same predisposition are. Until we do, we won't know who's safe and who isn't."

As a next step, Dr. Glickman will survey children, as well as dogs, in households that have treated lawns and compare the chemicals in their urine samples with those from households where lawns have not been treated.

"It's important to find out which lawn chemicals are being taken up by both children and animals," he said. "We hope to start this spring."

Funding for this research was provided in part by the Scottish Terrier Club of America and the American Kennel Club's Canine Health Foundation.

Source: Lawrence T. (Larry) Glickman, (765) 494-6301, ltg@purdue.edu
Purdue News Service: (765) 494-2096; purduenews@purdue.edu

ABSTRACT
Herbicide Exposure and the Risk of Transitional Cell Carcinoma of the Urinary Bladder
in Scottish Terrier Dogs
Lawrence T. Glickman, Malathi Raghavan,
Deborah W. Knapp, Patty L. Bonney
and Marcia H. Dawson

Objective: To determine whether exposure to lawn or garden chemicals was associated with an increased risk of transitional cell carcinoma (TCC) of the urinary bladder in Scottish terriers. Design: Case-control study. Animals: 83 Scottish terriers with TCC (cases) and 83 Scottish terriers with other health-related conditions (controls). Procedure: Owners of study dogs completed a written questionnaire pertaining to exposure to lawn or garden chemicals during the year prior to diagnosis of TCC for case dogs and during a comparable period for control dogs. Results: The risk of TCC was significantly increased among dogs exposed to lawns or gardens treated with both herbicides and insecticides (odds ratio [OR], 7.19) or with herbicides alone (OR, 3.62), but not among dogs exposed to lawns or gardens treated with insecticides alone (OR, 1.62), compared with dogs exposed to untreated lawns. Exposure to lawns or gardens treated with phenoxy herbicides (OR, 4.42) was associated with an increased risk of TCC, compared with exposure to untreated lawns or gardens, but exposure to lawns or gardens treated with nonphenoxy herbicides (OR, 3.49) was not significantly associated with risk of TCC. Conclusions and Clinical Relevance: Results suggest that exposure to lawns or gardens treated with herbicides was associated with an increased risk of TCC in Scottish terriers. Until additional studies are performed to prove or disprove a cause-and-effect relationship, owners of Scottish terriers should minimize their dogs' access to lawns or gardens treated with phenoxy herbicides. (J Am Vet Med Assoc 2004;24:1290-1297
http://ecochem.com/ENN_herbicide_dogs.html

Publications and Educational Resources
Pesticides and Aquatic Animals: A Guide to Reducing Impacts on Aquatic Systems
420-013

Louis A. Helfrich, Extension Specialist, Fisheries and Wildlife Sciences, Virginia Tech; Diana L. Weigmann, Director, Office of Science, Engineering, and Technology, Carson City, Nevada; Patricia Hipkins, Virginia Pesticide Programs, Department of Entomology, Virginia Tech; and Elizabeth R. Stinson, Virginia Department of Game and Inland Fisheries, Blacksburg, Virginia

Introduction

Fisheries and aquatic resources (ponds, lakes, rivers, streams, and oceans) are exceptionally valuable natural assets enjoyed by millions of Americans. They provide citizens with generous long-term benefits in return for minimal care and protection. These benefits can be direct financial ones that provide employment, profit, and dollar savings. For example, the seafood industry provides jobs for commercial fishers, wholesalers, and retailers. More indirect, but equally valuable, benefits of fish and aquatic ecosystems include recreational boating, sport fishing, swimming, relaxation, and natural beauty.

Appreciation of fisheries and aquatic systems has been accompanied by increasing concern about the effects of growing human populations and human activity on aquatic life and water quality. Pesticides are one group of toxic compounds linked to human use that have a profound effect on aquatic life and water quality.

Pesticides are substances used to control pests, including insects, water weeds, and plant diseases. Naturally-occurring pesticides have been used for centuries, but widespread production and use of modern synthetic pesticides did not begin until the 1940s. Today, pesticides are big business. Over a billion pounds of pesticides are used in the United States at a value of $8 billion per year.

Pesticides are beneficial chemicals. They can protect against forest and farm crop losses and can aid in more efficient food production. They are used to slow the spread of destructive forest insects like the gypsy moth. They are used to establish and maintain lawns and recreational areas. They are used to help reduce malnutrition and starvation of humans and animals. Pesticides also have been instrumental in controlling many insect-borne human diseases such as malaria, encephalitis, and bubonic plague. They promote public safety on roads, railroads, powerlines, and rights-of-ways.

Pesticides are (1) relatively easy to apply, (2) generally cost-effective and, (3) the only practical method of control in some situations. However, the benefits of pesticides are not derived without consequences. Pesticides must be used with great care so that the health of humans, animals, and the environment are protected. Disadvantages of pesticides include their toxicity to some humans, animals, and useful plants, and the persistence (long life) of some of these chemicals in the environment.

When pesticides enter aquatic systems, the environmental costs can be high. Unintentional pesticide-related fish kills occur throughout the United States. Some of these kills have been large, involving thousands of fishes, as well as frogs, turtles, mussels, water birds, and other wildlife. Fish and other wildlife species, including rare and endangered ones like the peregrine falcon, bald eagle, and osprey, have been victims of pesticide poisoning. Pesticide use is one of many factors contributing to the decline of fish and other aquatic species.

Protection of wildlife and water quality is possible when using pesticides. If pesticides are selected wisely, used in combination with other pest control measures, and applied safely, the pollution of our surface waters and contamination of aquatic life can be avoided.

The purpose of this publication is to serve as a general guide for those who may use pesticides in or around natural wetlands, lakes, ponds, rivers, and streams. In this publication, we provide information about the toxicity and safe use of pesticides that have the potential to enter aquatic systems.

Chemical Control
Advantages Disadvantages
Simple to Apply Toxic
Rapid Effect Water-Use Restrictions
Inexpensive? Fish Kills
Wide Spectrum Retreatment Necessary
Long Lasting? Expensive
Long-Lasting
Taste Problems
Odor Problems
Registration of Pesticides:

All pesticides used in the United States must be registered according to the Federal Insecticide, Fungicide, and Rodenticide Act (FIFRA). The Environmental Protection Agency (EPA) is responsible for administering this law. The EPA has the authority to register, restrict, or prohibit the use of pesticides. Pesticide registration decisions balance the risks involved with the benefits.

The EPA decides whether to register a pesticide after considering many characteristics including:

the ingredients,
manufacturing process,
physical and chemical properties,
environmental state (mobility, volatility, breakdown rates, accumulation potential in plants and fish),
toxicity to animals, and
carcinogenic or mutagenic properties.
The EPA can approve or disapprove the registration of new pesticides, and may further restrict or cancel the registration of those in use. For example, DDT, aldrin, dieldrin, heptachlor, mirex, and toxaphene were banned from use (registration canceled) in the United States in 1972, l974, l974, l983, l977, and l982 respectively. The use of endrin was highly restricted in l979. State agencies also require the registration of pesticides used within their boundaries.

The Pesticide Label

A pesticide label containing information on use and safety must be attached to all pesticide containers. The label includes the product name, name and amount of active ingredients, EPA registration number and establishment number, name and address of the manufacturer, and net contents.

The use classification (general use or restricted use) is noted on the label. The signal word (danger, warning, or caution) provides information about hazard classification. Precautionary statements inform users of handling requirements, procedures, and special concerns. Directions for use specify legal application sites, rates, and mixing and handling instructions. The pesticide label is a binding legal agreement between the EPA, the registrant, and the user. It is illegal to use a pesticide in a way or place not specified on the label.

"Restricted-Use Pesticides" are those that must be handled with special care. A pesticide can be classified as restricted-use because it is particularly toxic to fish, birds, or mammals. They may also be so classified because of potential environmental effects. These can be used only by a trained, certified pesticide applicator.

The Pesticide Label Contains:

Trade name
Active Ingrediennt
Directions for use
Toxicity Rating
EPA Registration number
Aquatic Toxicology

Aquatic toxicology is the study of the effects of environmental contaminants on aquatic organisms, such as the effect of pesticides on the health of fish or other aquatic organisms. A pesticide's capacity to harm fish and aquatic animals is largely a function of its (1) toxicity, (2) exposure time, (3) dose rate, and (4) persistence in the environment.

Toxicity of the pesticide refers to how poisonous it is. Some pesticides are extremely toxic, whereas others are relatively nontoxic. Exposure refers to the length of time the animal is in contact with the pesticide. A brief exposure to some chemicals may have little effect on fish, whereas longer exposure may cause harm.

The dose rate refers to the quantity of pesticide to which an animal is subjected (orally, dermally, or through inhalation). A small dose of a more toxic chemical may be more damaging than a large dose of a less toxic chemical. Dosages can be measured as the weight of toxicant per unit (kilogram) of body weight (expressed as mg pesticide/kg of body weight) or as the concentration of toxicant in the water or food supply (usually expressed as parts per million, ppm or parts per billion, ppb).

A lethal dose is the amount of pesticide necessary to cause death. Because not all animals of a species die at the same dose (some are more tolerant than others), a standard toxicity dose measurement, called a Lethal Concentration 50 (LC50), is used. This is the concentration of a pesticide that kills 50% of a test population of animals within a set period of time, usually 24 to 96 hours.

Hazard ratings ranging from minimal to super toxic and LC50s for commonly used insecticides, herbicides, and fungicides are presented in Table 3, Table 4 and Table 5. For example, the 24-hour LC50 of the insecticide permethrin to rainbow trout is 12.5 ppb. This means that one-half of the trout exposed to 12.5 ppb of permethrin died within 24 hours, indicating super toxicity of this pesticide to trout.

Hazard Ratings
Toxicity LC50(mg/l)
Minimal >100
Slight 10 - 100
Moderate 1 - 10
High 0.1 - 1.0
Extreme 0.01 - 0.1
Super < 0,01
Exposure of fish and other aquatic animals to a pesticide depends on its biological availability (bioavailablility), bioconcentration, biomagnification, and persistence in the environment. Bioavailability refers to the amount of pesticide in the environment available to fish and wildlife. Some pesticides rapidly breakdown after application. Some bind tightly to soil particles suspended in the water column or to stream bottoms, thereby reducing their availability. Some are quickly diluted in water or rapidly volatize into the air and are less available to aquatic life.

Bioconcentration is the accumulation of pesticides in animal tissue at levels greater than those in the water or soil to which they were applied. Some fish may concentrate certain pesticides in their body tissues and organs (especially fats) at levels 10 million times greater than in the water.

Biomagnification is the accumulation of pesticides at each successive level of the food chain. Some pesticides bioaccumulate (buildup) in the food chain. For example, if a pesticide is present in small amounts in water, it can be absorbed by water plants which are, in turn, eaten by insects and minnows. These also become contaminated. At each step in the food chain the concentration of pesticide increases. When sport fish such as bass or trout repeatedly consume contaminated animals, they bioconcentrate high levels in their body fat. Fish can pass these poisons on to humans.

Persistence of Pesticides

Persistence refers to the length of time a pesticide remains in the environment. This depends on how quickly it breaks down (degrades), which is largely a function of its chemical composition and the environmental conditions. Persistence is usually expressed as the "half life" (T1/2) of a pesticide. Half-life is the amount of time required for half of the pesticide to disappear (the other half remains). Half-life of pesticides can range from hours or days, to years for more persistent ones.

Pesticides can be degraded by sunlight (photodecomposition), high air or water temperatures (thermal degradation), moisture conditions, biological action (microbial decay), and soil conditions (pH). Persistent (long-lasting) pesticides break down slowly and may be more available to aquatic animals.

Pesticide Formulations

The active ingredient (pesticide) is combined with other inert ingredients (carriers, solvents, propellants) to comprise the formulated pesticide product. In some cases the inert ingredients may cause concern for aquatic life. Pesticides may be purchased in solid (granules, powders, dusts) or liquid (water, oil sprays) form. A major concern in using either solid or liquid forms of pesticides is their misapplication.

Sublethal Effects

Not all pesticide poisonings result in the immediate death of an animal. Small "sublethal" doses of some pesticides can lead to changes in behavior, weight loss, impaired reproduction, inability to avoid predators, and lowered tolerance to extreme temperatures.

Fish in streams flowing through croplands and orchards are likely to receive repeated low doses of pesticides if continuous pesticide applications run-off fields. Repeated exposure to certain pesticides can result in reduced fish egg production and hatching, nest and brood abandonment, lower resistance to disease, decreased body weight, hormonal changes, and reduced avoidance of predators. The overall consequences of sublethal doses of pesticides can be reduced adult survival and lowered population abundance.

Sublethal Effects include:

Weight Loss
Low Diseases Resistance
Sterility
Reduced Egg Production
Loss of Attention
Low Predator Avoidance
Habitat Alteration

Pesticides can reduce the availability of plants and insects that serve as habitat and food for fish and other aquatic animals. Insect-eating fish can lose a portion of their food supply when pesticides are applied. A sudden, inadequate supply of insects can force fish to range farther in search of food, where they may risk greater exposure to predation.

Spraying herbicides can also reduce reproductive success of fish and aquatic animals. The shallow, weedy nursery areas for many fish species provide abundant food and shelter for young fish. Spraying herbicides near weedy nurseries can reduce the amount of cover and shelter that young fish need in order to hide from predators and to feed. Most young fish depend on aquatic plants as refuge in their nursery areas.

Aquatic plants provide as much as 80% of the dissolved oxygen necessary for aquatic life in ponds and lakes. Spraying herbicides to kill all aquatic plants can result in severely low oxygen levels and the suffocation of fish. Using herbicides to completely "clean up" a pond will significantly reduce fish habitat, food supply, dissolved oxygen, and fish productivity.

The landowner who sprays a weedy fenceline with herbicides may unintentionally kill the trumpet vine on which hummingbirds feed and the honeysuckle that nourish deer and quail. Similarly, the landowner who unnecessarily sprays his water plants kills the plants that fed the insects that fed the fish that fed the farmer. Casual use of herbicides for lake or farm pond "beautification" may reduce fish populations.

How Fish are Exposed

Fish and aquatic animals are exposed to pesticides in three primary ways (1) dermally, direct absorption through the skin by swimming in pesticide-contaminated waters, (2) breathing, by direct uptake of pesticides through the gills during respiration, and (3) orally, by drinking pesticide-contaminated water or feeding on pesticide-contaminated prey. Poisoning by consuming another animal that has been poisoned by a pesticide is termed "secondary poisoning." For example, fish feeding on dying insects poisoned by insecticides may themselves be killed if the insects they consume contain large quantities of pesticides or their toxic byproducts.

Reducing the Risk: Prior to using a pesticide, consider the following:

Use a Pesticide Only When Necessary
Is the problem bad enough to justify the use of a toxic chemical? Are there alternative ways of treating the problem? Landowners should consider the costs and consequences of pesticide treatment relative to the problem.
Use Less Toxic Pesticides
One way to reduce the effects of pesticides on aquatic systems is to use those chemicals that are least poisonous to aquatic life. The tables presented at the end of this booklet give information about the relative toxicity of many of the agricultural pesticides. Select the least toxic material.
Use Safe/Sensible Application Methods
The first rule of responsible pesticide use is to read and then reread the pesticide label and follow the directions precisely. Label instructions sometimes can be confusing. If you don't understand the instructions, contact your Extension Agent, your supplier, or the pesticide company for more information.
Pay particular attention to warning statements about environmental hazards on the label. Look for: "This product is toxic to fish." If you see such a warning, consider another pesticide or an alternative control method.
Ensure that your application equipment is in good working condition. Check for leaks, replace worn parts, and carefully calibrate your equipment.
When preparing the pesticides for application, be certain that you are mixing them correctly.
Never wash spray equipment in lakes, ponds, or rivers. If you use water from natural ponds, lakes, or streams, use an antisiphon device to prevent backflow.
If you are applying pesticides near water, check the label to find the recommended buffer zone. Buffer strip widths between the water and the treatment areas vary. Leave a wide buffer zone to avoid contaminating fish and aquatic animals.
Store and dispose of unused chemicals and their containers according to the label instructions.
Avoid pesticide drift into nontarget areas, or applications during wet, windy weather that might promote runoff to non-target streams, ponds, or lakes. Spray on calm days, or early in the morning or evening when it is less windy.
Pesticide applicators are liable for downstream fish kills and pesticide contamination.
Why Weeds:

Excess Fertility
Shallow Water
Exotic Invaders
Fast Reproduction
Types of Pesticides

Pesticides are categorized according to their target use. The three major groups of pesticides are herbicides (weed control), insecticides (insect control), and fungicides (disease control). Nematicides are pesticides used to control soil, leaf, and stem-dwelling nematodes (round worms). An acaricide is a pesticide that controls mites and ticks.

Plant Reproduction

Budding
Fragmentation
Rhizomes
Tubers
Spores
Seeds
Herbicides

Herbicides are the most commonly used pesticides in the U.S. They are widely applied to agricultural crops, forest lands, gardens, and lawns. Herbicides often are directly applied to lakes and ponds to control nuisance growths of algae (colonial, filamentous, and single cells), submersed water grasses (coontail, milfoil, naiad, pondweed), floating water plants (water lily, spatterdock, duckweed), and emergent water plants (cattails, rushes, reeds).

Dense growths of algae and rooted waterweeds can interfere with swimming, fishing, and boating. They also can discolor waters, impart unpleasant taste and odors to water supplies, and degrade property values and water quality.

Limited numbers of aquatic plants growing in ponds and lakes are beneficial. Through photosynthesis, water plants provide most of the dissolved oxygen necessary for fish and other aquatic life. They also provide food, shelter, cover, and nursery areas for sport fish and other water animals. The purpose of herbicide application is to limit plant growth. Elimination of all aquatic plants is not beneficial.

Nutrient-rich, shallow, clear waters are highly susceptible to water weed invasions. Algae and water weeds can exhibit rapid growth. Water plants can reproduce quickly because they have the ability to reproduce by seeds, fragmentation, budding, rhizomes, tubers, and spores. Some species can reproduce using several of these methods. Non-native water weeds are especially problematic because they have no native insect or animal to control their growth.

Abundant water weeds are usually a symptom of overfertilization. The lasting solution to a weed problem is to reduce fertilizer runoff. Herbicides only treat the symptoms of overfertilization (the weeds); the real cause (excessive nutrients) remains after herbicide treatment. Unless the nutrients are removed, they will endlessly stimulate successive algae blooms and rooted weed growths. In this sense, herbicides are only a short-term, cosmetic treatment.

Prevention is the best way to reduce water weed problems. Constructing ponds and lakes with steep slopes that drop quickly into deep water reduces weed growth. Construction of a sediment basin upstream from a pond or lake will help reduce the sediment and nutrient loads entering a water body.

Algae and waterweeds can be controlled by a number of nonchemical methods. Herbicides may not always be the most efficient or safest water weed control technique. Other effective water weed control methods include (1) stocking plant-eating fish like the grass carp, (2) hand or mechanical weed removal by cutting, uprooting, and harvesting, (3) dredging and deepening shallow, weedy areas, (4) lake drawdowns, (5) using chemical dyes or black plastic to eliminate light and shade-out weeds, and (6) using pond liners to prevent rooting.

Herbicides generally are less toxic to fish and aquatic life than insecticides. Many are short-lived and do not accumulate in the environment. However, some are highly toxic to aquatic animals and should be avoided or used with extreme caution near water ways and aquatic environments.

Of the approximately 200 herbicides registered by the EPA for use in the United States, only about 10 are labeled for use in aquatic systems (Table 1) and (Table 3)

Endothall compounds (Aquathol and Hydrothol) are registered by EPA as aquatic herbicides, but they are relatively toxic to fish at rates near those needed to kill water weeds. The Hydrothol formulation is the most risky to use in fish ponds. Endothall cannot be used in irrigation water, livestock water, or in food crop or food fish areas without withholding restrictions (Table 2).

Fortunately, there are a number of other less toxic, but effective, herbicides that are registered for use in aquatic systems. The five herbicides most commonly used in ponds and lakes include copper sulfate, fluridone, glyphosate, zx, and diquat (Table 3).

Chelated copper complexes and copper sulfate (Bluestone) are used to control algae, not rooted aquatic plants. Most algae species are effectively controlled by these herbicides. However, copper is a toxic metal that is long-lived (persistent) in the environment. Copper sulfate can be toxic to fish and aquatic animals at concentrations near levels used to control algae, especially in soft water. Copper toxicity increases as water hardness decreases. Copper sulfate is not as safe to use as chelated copper compounds listed above, and it should not be used in soft waters (alkalinity values less than 50 mg/L). No water-use restrictions are associated with copper compounds.

Fluridone (Sonar) is perhaps the safest of the registered herbicides to use in fish ponds. It is expensive and will not kill algae, but effectively controls submersed aquatic plants. It is a persistent, slow-acting herbicide. Sonar residue may persist for a period of 2 to 12 months, and results may take 30 to 90 days to be noticeable. Do not use Sonar-treated water for crop irrigation for 30 days after application. There are no restrictions for fishing, swimming, or livestock or human consumption.

Glyphosate (Rodeo) is best used for control of emergent and shoreline weeds such as cattail, reeds, rushes, smartweeds, and some floating-leaf plants like water lily and lotus. It is usually applied to the plant and not directly to the water. It is quickly bound to suspended particles and bottom sediments and is rapidly inactivated. It has no waiting period or withdrawal restrictions for irrigation water, livestock water, fish consumption, or swimming. Use only those glyphosate products labeled and specially-formulated for aquatic systems. Some glyphosate products contain additives that are toxic to aquatic organisms.

2,4-D (Aquacide, Aqua-Cleer, Weedar, Weed-Rhap, Weedestroy, Weedtrine ) is effective for controlling submersed aquatic plants. These compounds rapidly and completely decompose in about 3 weeks. Toxicity of these herbicides increases as pH decreases. They are less effective at pHs greater than 8, and more toxic in acidic waters (pH<6). Depending on the formulation, 2,4-D can be highly toxic to rainbow trout. 2,4-D should not be used in water for irrigation, livestock, or domestic purposes.

Diquat (Diquat, Aqua-Clear, Aqua-Quat, Watrol, Weedtrine) is a wide-spectrum herbicide that can be used to control algae and submersed weeds, but it is not especially effective on emergent weeds. A 14-day waiting period is required by law before diquat-treated water can be used for livestock consumption, crop irrigation, or drinking. There are no restrictions for fishing, but a 1-day waiting period is required before swimming. Diquat is rarely found in treated water after 10 days.

Fish kills may occur after herbicide application, even when the herbicide used is not directly toxic to fish. Fish die indirectly from suffocation, rather than herbicide poisoning, because masses of rotting water weeds killed by the herbicide decompose, reducing oxygen levels.

When using herbicides, treat one-half (or less) of the lake at a time to allow fish freedom to move to untreated, oxygen-rich areas of the pond or lake. Apply herbicides during the spring when water temperatures are cooler and dissolved oxygen levels are higher than in summer. Some herbicides are not as toxic at colder temperatures. Apply in early spring when weeds are small and not well established, and when fewer weeds are present to decompose.

Application rates in aquatic systems depend on a number of factors. Important considerations are extent of area treated, water depth, water temperature (stratification), water exchange (flow) rates, weed density, weed species, weather conditions, water clarity, and suspended particles.

Identification of the weed or pest is critical in planning an effective control strategy. The relative effectiveness of different aquatic herbicides varies depending on the weed species (Table 1) . Consult with your Extension Agent on weed identification prior to selecting a herbicide.

Applying the right amount of herbicide is especially important to achieve good control, avoid nontarget toxicity, eliminate unnecessary expense, and comply with the legal requirements. After application of a herbicide, comply with the required waiting period before using water for irrigation, livestock watering, swimming, or fishing (Table 2).

In addition to herbicides, biological control animals can be stocked to feed on water weeds. Grass carp is a fish that will eat a wide variety of submersed, emersed, and floating weeds. Some plants such as filamentous algae, cattails, rushes, and watershield are not preferred by grass carp and are not well controlled by this fish. Because grass carp is an exotic fish, most state fish and game agencies require that you obtain a permit to stock this species. Only sterile (triploid) grass carp should be stocked so that this non-native does not reproduce and outcompete native fishes. Recommended stocking rates range from 7 to 15 fish per surface acre of water.

Methods of Weed Prevention:

Stop Fertilizer Runoff
Upstream Settling Basin
Steep Shoreline Slope
Wide Buffer Zone
Exclude Livestock
Methods of Plant Control:

Hand Removal
Mechanical Harvesting
Water Level DrawDown
Hervbiverous Fish
Herbicides
Summary List of Chemicals:

Copper compounds
Copper Sulfate
Fluridone
Sonar
2,4-D
Glyphosate
Rodeo
Diquat
Weedtrine
Endothall
Aquathol
Hydrothol
Considerations for Application Timing:

Early Spring
Small Weeds
Actively Growing
Less Decay
Cool Water
Insecticides

The 1962 publication of Rachel Carson's Silent Spring directed public attention to the effects that pesticides, primarily insecticides, were having on wildlife and the environment. When this book was written, the predominant insecticides used were synthetic chemicals called organochlorine insecticides (OCs).

The most infamous OC is DDT (dichlorodiphenyl-trichloroethane). Its effect on fish, wildlife, and natural environments was devastating. Other OC insecticides, including aldrin, toxaphene, dieldrin, mirex, and heptachlor, were also very toxic to fish and wildlife, and they are banned from use in the United States. The ban on many OC insecticides in the United States has been important in the survival of fish and aquatic species and the protection of water quality.

The four main types of agricultural insecticides used today are pyrethroids (PYs), organophosphates (OPs), carbamates (CBs), and biological insecticides (BIs).

PYs, especially synthetic ones, are the most toxic group of insecticides to fish and aquatic invertebrates. They should be used with extreme caution near waterways. Despite the fact that PYs are highly toxic to aquatic animals, they seldom cause fish kills because: (1) they are strongly absorbed to bottom muds, (2) they are short lived and usually last only days, (3) they rapidly decompose in 1 to 10 days when exposed to sunlight, and (4) they usually are applied at lower rates compared to the other insecticides.

Many OP and CB insecticides are extremely hazardous to fish and wildlife. Fish kills involving these insecticides have been documented. OP insecticides can bioconcentrate in fish, frogs, tadpoles, and toads to levels that pose hazards to their predators. OP and CB insecticides are water soluble and metabolized quickly. They generally have short persistence (half-lives of days to months), and their residues do not pose long-term problems for aquatic animals. The CB insecticide carbofuran is extremely toxic to wildlife and fish.

Some BI insecticides are less hazardous to fish and other aquatic animals, because many target specific insects (narrow spectrum). BIs include microbials and insect growth regulators. For example, the microbial, Bacillus thuringiensis (BT), is a bacterium that causes disease in some insects, but does not harm other animals or plants. Insect growth regulators affect the normal growth and development of some insects. For example, Diflubenzuron (Dimilin) inhibits the formation of an insect's hard exoskeleton (outer shell). Some insect growth regulators can harm beneficial aquatic invertebrates and thus reduce the food supply for young fish.

Fungicides

Fungicides, like herbicides, generally are not as highly toxic to fish and aquatic animals as insecticides. However, some fungicides have been banned due to their adverse effects on the environment. Fungicides containing mercury were discontinued for home and agricultural use in the United States in 1976. Mercurial fungicides accumulated in the environment and concentrated up the food chain, causing fish kills.

Some currently-registered fungicides are extremely toxic to aquatic organisms. Some fungicides are poisonous to beneficial soil invertebrates. Their use should be avoided or carefully managed near aquatic systems.

Considerations for Application Rates:

Algae or Rooted Weeds
Water Depth
Weed Species
Weed Density
Water Exchange
Water Temperature
Turbidity
Weather
Detection of Fish Kills

Pesticide exposure of fish and other aquatic life may be a more widespread problem than most people realize. Most pesticide-related fish kills go unreported and, in documented cases, the number of fish killed is often underestimated. The underwater conditions, including water clarity and depth, and the small size and camouflage coloring of many fish, particularly young fish, make accurate counts difficult. Scavengers quickly remove carcasses from a kill site. Dying and stressed fish may hide in dense cover or leave the area completely.

The remoteness of many streams and wetlands often diminishes chances of detection of fish kills. When dead fish are found after a pesticide application, the incident may go unreported because it is not considered important, or because of fear of liability. Sometimes no association is made between a kill and a past pesticide application because of the amount of time that has elapsed. These factors and others tend to obscure the full impact that some pesticides are having on fish and aquatic systems.

Reporting Pesticide Spills

If you have knowledge of sick or dead fish and aquatic life that you suspect may have been poisoned by pesticides, please contact your local game warden or the United States Fish and Wildlife Service immediately. Please notify an official as soon as possible after sickened or dead wildlife are discovered. Information about possible pesticide-related incidents includes the following:
Type of pesticide product
Use rates
Weather conditions
Aquatic species involved
Extent of the problem (number of fish killed)
Location
Size of pond or lake affected
Pesticide accidents or incidents that constitute a threat to any person, to public health or safety, and/or to the environment must be reported to the responsible state agency. Initial notification must be made by telephone within 48 hours of the occurrence. A written report describing the accident or incident must be submitted within 10 days of the initial notification.

In Virginia, initial telephone contact and written reports should be directed to the Virginia Department of Agriculture and Consumer Services, Office of Pesticide Services, Enforcement and Field Operations, P.O. Box 1163, Richmond, VA 23218, call (804) 371- 6560. In the event of an emergency release which may impact others or other property, notify the Virginia Department of Emergency Services at 1-800-468-8802.

If the accident or incident involves a spill, the applicator should contact the responsible state agency to determine whether the release is governed under SARA Title III (the community Right-to-Know Law). Reporting under this regulation is determined by the chemical hazard and the volume of the released chemical. If required, the applicator must notify the National Response Center at 1-800-424-8802.

Endangered Species and Pesticides

Congress passed the Endangered Species Act (ESA) in 1973 to protect animals and plants that are in danger of becoming extinct and to protect their habitat. The ESA requires that any action authorized by a Federal agency, such as the registration of pesticides, does not harm threatened or endangered species or their habitat.

The EPA plans to identify pesticide products that have the potential to jeopardize endangered or threatened species by a statement on the label. This statement will instruct users to determine if there are any limitations on the pesticide's use in the county where it is to be applied.

Integrated Pest Management

Integrated pest management (IPM) is a system using a variety of methods, including pesticides, to reduce pest populations to acceptable levels. IPM was developed in response to overdependence on pesticides. Factors such as groundwater contamination, increasing cost of agricultural chemicals, consumer concerns about pesticide residues on foods, and concern for the environment encourage the use of IPM.

IPM strategies include:

Cultural control (crop rotation and selected planting dates to avoid pests).
Host resistance (using plants and livestock that are resistant to pests).
Mechanical control (uprooting, weed harvesting, cultivation, and use of insect traps)
Biological control (stocking grass carp to feed on water weeds)
Chemical control with pesticides
Sanitation
The key to sound pest control strategies is to determine the extent of the problem. In IPM, pesticides are not applied until pest populations reach an unacceptable (economical or aesthetic) threshold. Rather than indiscriminately applying pesticides, IPM protects naturally-occurring insect predators, parasites, and pathogens to keep pest populations at acceptable levels.

The importance of pest control exerted by naturally-occurring beneficial organisms is usually unnoticed, but its value is significant. For example, as much as 40 percent of the water weeds in a lake can be eliminated by natural plant-eating water animals (aquatic insects, crayfish, herbivores fish) or parasites. IPM takes advantage of these natural controls. IPM programs occur in many places nationwide. They may be applied in many situations ranging from home gardens to commercial water weed management.

An increased interest in sustainable agriculture is evidence of the movement toward more diverse cropping systems. Some of the benefits of diverse systems include reduced soil erosion, improved water quality, enhanced nutrient cycling, and reduced pesticide inputs. These systems are economically competitive with conventional farming systems and also good for fish and wildlife.

Many fish and wetland species live in waters that run through farmland. Activities on the farm, including pesticide use, can affect fish and water quality far downstream. Farmers and landowners who use pesticides can protect aquatic habitats by first considering whether pesticide treatment is really necessary. If pesticides must be used, use the least toxic product that will do the job and apply it according to the label. Avoid important wildlife habitats such as wetlands, stream sides, and pond and lake shores. Use the following Best Management Practices.

Water-use Restrictions

Fishing
Swimming
Irrigation
Livestock
Drinking
Best Management Practices for Protecting Water Quality

Use Integrated Pest Management (IPM) practices so chemical controls will be used only when necessary. Before using any pesticide, be sure the application is needed, and can be accomplished safely and effectively.
Evaluate chemical control options. Select the option that is least likely to have a negative impact on water quality. Select products that minimize waste and applicator exposure.
Read and follow all label directions. Use pesticides only as directed. Pay careful attention to application site requirements, methods, and rates. Pesticide label directions are not advice, they are legal requirements.
Use care when mixing and loading pesticides. Be sure the equipment is working correctly and is properly calibrated. Prepare only the amount of pesticide mix needed for the immediate application.
Apply pesticides at the proper time. Consider weather and pest life cycle when planning applications.
Store pesticides safely in a ventilated, well lighted, and secure area free from flooding.
Dispose of empty containers and rinse water properly.
Keep records of all pesticide use. Records will allow evaluation of pest control efforts and help plan future treatments.
Acknowledgments and Suggested Publications

We deeply appreciate the assistance provided by Diana Dalton and Andrew Tate, Department of Fisheries and Wildlife Sciences; P. Lloyd Hipkins, Department of Plant Pathology, Physiology and Weed Science; and Alexandra R. Spring, Soils Laboratory, Virginia Tech, in the preparation of this publication. We acknowledge the advice and guidance of Peter Bromley and William Palmer, Department of Zoology, North Carolina State University. We recognize the essential support provided by the U.S. Fish and Wildlife Service and Virginia Cooperative Extension.

Anderson R. L. 1989. "Toxicity of synthetic pyrethroids to freshwater invertebrates." Environmental Toxicological Chemistry 8: 403-410.

Extoxnet: Extension Toxicology Network. 1994. Edited by L. Seyler, D. Rutz, J. Allen, and M. Kamrin. A pesticide information project of the Cooperative Extension Offices of Cornell University, the University of California, Michigan State University, and Oregon State University.

Herbicide Handbook of the Weed Science Society of America. l989. N.E. Humberg et al., WSSA, Champlain, IL.

Farm Chemical Handbook. l995. Edited by R. Meister. C. Sine, S. Naegely, and others. Meister Publishing Co., Willoughby, Ohio.

Johnson, Waynon and M. T. Finley. l980. Handbook of Acute Toxicity of Chemicals to Fish and Aquatic Invertebrates. U.S. Fish and Wildlife Service Publication 137. Washington, D.C.

Langeland, K. A. (Editor). l990. Training Manual For Aquatic Herbicide Applicators in the Southeastern United States. Center for Aquatic Plants, University of Florida, Gainesville, Florida 32606.

Lutz, C. Greg, M. Mayeaux and M. L. Grodner. 1992. Toxicity of Selected Agricultural Pesticides to Common Aquatic Organisms in Louisiana. Publication 2416-I. Louisiana Cooperative Extension Service, Louisiana State University, Baton Rouge, Louisiana.

Mayer, Foster L., and Mark R. Ellersieck. l986. Manual of Acute Toxicity: Interpretation and Data Base for 410 Chemicals and 66 Species of Freshwater Animals. U.S. Fish and Wildlife Service. Publication l60. Washington, DC.

Palmer, William E. and Peter T. Bromley. l994. Wildlife and Agricultural Pesticide Use: A Review for Natural Resource Managers. Department of Zoology, North Carolina State University. Raleigh, North Carolina.

Schnick, R., Fred Meyer, D. Leroy Gray. l980. A Guide to Approved Chemicals in Fish Production and Fisheries Resource Management. Arkansas Cooperative Extension Service. Publication MP 241. University of Arkansas. Little Rock, Arkansas.

Spradley, J. P. l985. Toxicity of Pesticides to Fish. Arkansas Cooperative Extension Service. Publication MP330. University of Arkansas. Little Rock, Arkansas

Hudson, Rick H., Richard K. Tucker, and M.A. Haegele. 1984. Handbook of toxicity of pesticides to wildlife. USDI Fish and Wildlife Service Resource Publication Number 153. Washington, D.C.

Smith, Gregory J. 1987. Pesticide use and toxicology in relation to wildlife: Organophosphorous and carbamate compounds. USDI Fish and Wildlife Service Resource Publication 170. Washington, D.C.

Stinson, Elizabeth R., and Peter T. Bromley. l991. Pesticides and Wildlife: A Guide to Reducing Impacts on Animals and their Habitats. Virginia Cooperative Extension Publication 420-004. Virginia Tech, Blacksburg, VA.

The Royal Society of Chemistry. 1991. The Agrochemicals Handbook. Edited by K. Hamish and D. James. Cambridge, England.

United States Environmental Protection Agency. 1994. Pesticide Industry Sales and Usage: l992-1993 Market Estimates. United States Environmental Protection Agency, Publication 733-K-94-001. Washington, D.C.

Virginia Cooperative Extension. 1996. Pest Management Guide for Horticultural and Forest Crops. Virginia Cooperative Extension Publication 456-017, Virginia Tech, Blacksburg, VA.

Ware, George W. l994. The Pesticide Book. Thompson Publications

Weeks, J.A., S.B. Donahoe, G.H. Drendel, R.S. Jagan, T.E. McManus, and P.J. Sczerenie. 1988. Risk assessment for the use of herbicides in the southern region, USDA Forest Service. in: Final Environmental Impact Statement: Vegetation management in the Coastal Plain/Piedmont Volume II. USDA Forest Service, Arlington, Virginia.

Pesticide Resource Agencies

The National Response Center 1-800-424-8802

EPA National Pesticide Telecommunications Center. General Information, Corvalis, Oregon. 1-800-858-7378

U.S. Environmental Protection Agency, Office of Pesticide Programs, Ecological Effects Branch, 401 M St. H7507-C, Washington, DC 20460. Call Incident Data to (703) 305-7347

Virginia Department of Agriculture and Consumer Services. Office of Pesticide Service, Enforcement and Field Operations. P.O. Box 1163. Richmond, VA 23218, (804) 371-6560.

Virginia Department of Environmental Quality. Report all pesticide spills into water to 2111 North Hamilton Street P.O.B. 11143 Richmond, VA 23230. Call the nearest District Office: Virginia Beach (804) 552-1840; Richmond (804) 527-5020; Woodbridge (703) 490-8922; Bridgewater (540) 828-2595; Roanoke (540) 562-3666, Abingdon (540) 676-4800.

Virginia Cooperative Extension. General information. Virgina Tech Pesticide Program, Blacksburg, VA 24061 (540) 231-6543

Virginia Department of Game and Inland Fisheries. Report all wildlife and fish kills. Richmond, VA (804) 367-1000.

Virginia Department of Health. Toxicology Information, Bureau of Toxic Substances,

109 Governors Street, Room 918, Richmond, VA 23219 (804) 786-1763 Virginia Department of Emergency Services. 1-800-468-8892.

Aquatic Herbicide Sources

Athea Laboratories Inc., P.O. Box 23926 Milwaukee, WI 53223.

Albaugh Inc., 1517 N. Akeny Blvd. Suite A, Ankeny, IA 50021

Applied Biochemists, 5300 W. County Line Road, 96 North, Mequon, WI 53092

Aquacide Co.,1627 9th St., White Bear Lake, MN 55110, (800)328-9350

Aquashade Inc., 6120 W. Douglas Ave., Milwaukee, WI 53218

A & V Incorporated, N62 W22632 Village Drive, Sussex, WI 53089, (205) 288-3185

Chem One Corp., 15150 Sommermeyer, Houston, TX 77041-5308

ELF Atochem North America, 2000 Market St., Philadelphia, PA 19103, (205) 288-3185

Frank Miller & Sons Inc., 13831 S. Emerald Ave., Chicago, IL 60627

Great Lakes Biochemical Co. Inc., 6120 W. Douglas Ave., Milwaukee, WI 53218

Griffin Corporation, P.O. Box 1847, Valdosta, GA 31603, (912) 244-7954

Helena Chemical Co., 6075 Poplar Ave., Suit 500, Memphis, TN 38119.

I. Schneid Inc., 1429 Fairmont Ave., N.W., Atlanta, GA 30381.

Monsanto Agricultural Company, 700 Chesterfield Parkway North, St. Louis, MO, 631987 or 800 N. Lindbergh Blvd., St. Louis, MO 63167, (919) 556-7124

NCH Corporation. 2727 Chemsearch Blvd., Irving, TX 75062.

PBI/Gordon Corporation, 1217 W. 12th Street, P.O. Box 4090, Kansas City, MO 64101, (816) 421-4070

Phelps Dodge Refining Corporation, Box 20001, El Paso TX, 79998.

Qualis Inc., 4600 Park Ave., Des Moines, IA 50321

Riverdale Chemical Co., 425 W. l94th St., Glenwood, IL 60425, (317) 780-1944

Rhone-Poulenc Ag Company, P.O. Box 12014, 2 T. W. Alexander Drive, Research Triangle Park, NC 27709, (919) 859-6070

SEPRO Corporation, 11550 N. Meridian St., Suite 200, Carmel, IN 46032, (800)419-7779

State Chemical Manufacturing Co., 3100 Hamilton Ave., Cleveland, OH 44114.

Uniroyal Chemical Co., Inc., 74 Amity Road, Bethany, CT 06524, (919) 848-9675

Zeneca Agricultural Products, Box 15458 Wilmington, DE. 19850-5458 or 1800 Concord Pike, Wilmington, DE 19897, (800) 759-2500

Reviewed by Michelle Davis, Research Associate, Fisheries and Wildlife

Virginia Cooperative Extension materials are available for public use, re-print, or citation without further permission, provided the use includes credit to the author and to Virginia Cooperative Extension, Virginia Tech, and Virginia State University.

Issued in furtherance of Cooperative Extension work, Virginia Polytechnic Institute and State University, Virginia State University, and the U.S. Department of Agriculture cooperating. Edwin J. Jones, Director, Virginia Cooperative Extension, Virginia Tech, Blacksburg; Jewel E. Hairston, Administrator, 1890 Extension Program, Virginia State, Petersburg.

May 1, 2009

Available as:
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Diana L. Weigman
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Elizabeth R. Stinson
Other resources from:
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Virginia Cooperative Extension programs and employment are open to all, regardless of age, color, disability, gender, gender identity, gender expression, national origin, political affiliation, race, religion, sexual orientation, genetic information, veteran status, or any other basis protected by law. An equal opportunity/affirmative action employer. Issued in furtherance of Cooperative Extension work, Virginia Polytechnic Institute and State University, Virginia State University, and the U.S. Department of Agriculture cooperating. Edwin J. Jones, Director, Virginia Cooperative Extension, Virginia Tech, Blacksburg; Jewel E. Hairston, Administrator, 1890 Extension Program, Virginia State, Petersburg.

Virginia Tech - Invent the Future
Virginia State University

© 2015 Virginia Polytechnic Institute and State University
http://pubs.ext.vt.edu/420/420-013/420-013.html

in order..

1. Care.2 total opinion propaganda piece. Appeal to nature nonsense.

2. Herbicide issues in dogs. Interesting topic. Only issue is this was a thread about Glyphosate (RoundUp trade name) and since glyphosate is a non selective herbicide you wouldn't have much of a lawn. It would be dirt. This study has to look into selective herbicides, I.e. Ones who kill broadleaf weeds without harming desired turf.

3. Some herbicides, fungicides and insecticides are KNOWN to be toxic to fish. These come with labels detailing their usage and their potential harms. The label is the law. Failure to comply is breaking the law. Most farmers and horticultural professionals follow the label to a tee. They understand not only the law but are also stewards of the environment.

http://www.epa.gov/pesticides/about/#safer

http://www.epa.gov/pesticides/about/#safer

I am pretty sure I know what a pesticide is.. What is your point?

The fact is pesticides continue to evolve requiring less active ingredient to be applied less frequently to achieve the same desired results. If you are going to stick with the "all pesticides are yucky" argument then I am wasting my breath.

GMO Crops, Neonicotinoids Will Be Weeded out of U.S. Wildlife Refuges

National wildlife refuges around the country are phasing out genetically modified crops and neonicotinoid pesticides in programs meant to provide food for wildlife. A July 17 letter from James W. Kurth, chief of the national refuge system, doesn't specifically mention concerns that the pesticides or crops pose risks to wildlife bees, butterflies and other pollinators. It just says they don't fit refuge objectives, such as promoting natural ecosystems.

But it comes after a July order to phase out neonicotinoid pesticides on wildlife refuges in the Northwest and Hawaii that mentioned concerns about harm to bees and after a White House memorandum directing federal agencies to promote pollinator health after significant losses in recent decades of insects, bats and birds that pollinate fruits, nuts and vegetables.

Wildlife refuges commonly allow farmers to grow crops there if they leave some behind to feed wildlife. Most of the corn grown in the U.S. has been genetically modified to resist the herbicide glyphosate, commercially sold as Roundup. Iain Kelly, a risk assessment scientist for neonicotinoid manufacturer Bayer CropScience, said: "We don't think the science bears out that decision."

Bee deaths linked to pesticides.
See link for video:
http://www.nbcnews.com/science/environment/gmo-crops-neonicotinoids-will-be-weeded-out-u-s-wildlife-n174211

Correlation is not causation. Colony collapse is WAY bigger than just pesticides. Also for as much doom and gloom bee populations are pretty stable

Harvard Study Reveals Our Future Is At Risk, Because We're Killing Off an Unexpected Species

By Matt Essert May 18, 2014

New research from Harvard indicates that a very popular insecticide may be resulting in unintended consequences for humanity's food supply.

Neonicotionoids — among the world's most commonly used insecticides — are wreaking havoc on bees, leading to Colony Collapse Disorder (CCD), a phenomenon in which worker bees abruptly disappear from a beehive or colony. And without bees, we're in big trouble.

"If the bee disappeared off the surface of the globe then man would only have four years of life left. No more bees, no more pollination, no more plants, no more animals, no more man." This anonymous quotation sums up what scientists believe when it comes to bees as an essential link in our food chain. Somewhere between one-quarter and one-third of all the food we eat depends on bee pollination. That, along with their honey production, means a big chunk of global economies and food supplies could be in a precarious place very soon.

Over the past decade, CCD has become a major problem, leading to a 40% loss in commercial honeybees in the U.S. since 2006 and a 45% loss in the U.K. since 2010. It's believed CCD has wiped out an estimated 10 million beehives, worth $2 billion, over the past six years.

In 2007, England's National Audit Office examined data to determine the value of honeybees to the U.K. economy and found that their services equated to roughly $336 million a year. The retail value of what bees pollinate comes out to about $1.7 billion annually.

And that's just for one country. The hit would be much worse when you consider the global scope.

The University of Illinois estimates that in North America around 30% of the food humans consume is produced from bee pollinated plant life. The value of pollination by bees is estimated around $16 billion in the U.S. alone.

The science: In the Harvard research, the insecticide in question led to half the colonies studied dying. Meanwhile, none of the untreated colonies saw their bees disappear.

"We demonstrated that neonicotinoids are highly likely to be responsible for triggering 'colony collapse disorder' in honeybee hives that were healthy prior to the arrival of winter," Chensheng Lu, an expert on environmental exposure biology at Harvard School of Public Health and who led the work, told the Guardian.

Scientists had previously believed that certain insecticides were causing CCD by damaging bees' immune systems, making them more vulnerable to parasites and disease. But the new Harvard data undermines this theory and instead argues that "impairment of honey bee neurological functions, specifically memory, cognition, or behaviour, [come] as the results from the chronic sub-lethal neonicotinoid exposure."

What's most troubling is that the culprit is one of the world's most widely used insecticides; it's undoubtedly going to be very difficult to transition from this chemical any time soon. Neonicotinoids are used in over 120 countries, mainly to boost agriculture production. They make up a quarter of the world's total insecticides used around the world. Neonicotinoids are effective against plant and soil insects, and also used to control fleas on domestic animals.

Save our bees! Some people have taken their own steps to combat the problem. One group started a petition on Care2, "Tell the EPA: Save our bees and crops! Ban toxic pesticides!" SOS-Bees, an off-shoot of Greenpeace, has been rallying behind the movement to save the bees. The EU imposed a continent-wide ban on certain insecticides last year in an attempt to revitalize the waning bee population. Hopefully the rest of the world will take similar action, because if the bee population continues to decline, honey shortages will be the least of our concerns.
http://www.mic.com/articles/89557/harvard-study-reveals-our-future-is-at-risk-because-we-re-killing-off-an-unexpected-species

http://www.forbes.com/sites/jonentine/2013/04/11/science-collapse-disorder-the-real-story-behind-neonics-and-mass-bee-deaths/

Bee harming pesticides banned in Europe

http://www.theguardian.com/environment/2013/apr/29/bee-harming-pesticides-banned-europe

So public opinion and not science changed a law. Thankfully we live in a country who doesn't enact laws or remove things based on "feelings". Science rules.

"Scientists had previously believed that certain insecticides were causing CCD by damaging bees' immune systems, making them more vulnerable to parasites and disease. But the new Harvard data undermines this theory and instead argues that "impairment of honey bee neurological functions, specifically memory, cognition, or behaviour, [come] as the results from the chronic sub-lethal neonicotinoid exposure."

Science isn't ideological except when it is

http://www.forbes.com/sites/jonentine/2013/04/11/science-collapse-disorder-the-real-story-behind-neonics-and-mass-bee-deaths/

Whoops. Meant this

http://www.huffingtonpost.com/jon-entine/post_8761_b_6323626.html

http://www.beyondpesticides.org/pollinators/chemicals.php
http://switchboard.nrdc.org/blogs/jsass/nrdc_recently_filed_a_legal.html

Hahaha. Ok two ideological groups. I think I've had enough of this topic. You are clearly not going to see any pesticides as other than yucky. That is fine. I sleep well at night with science on my side. Now im off to endulge in some gmos

Hahaha. Ok two ideological groups. I think I've had enough of this topic. You are clearly not going to see any pesticides as other than yucky. That is fine. I sleep well at night with science on my side. Now im off to endulge in some gmos

+1

CD

So long!

Last word isn't winning. Science always wins. Until the next time anti science is spread. Good day. I enjoyed presenting my facts.. Um I mean my position

So Sparty, are you saying that the Earth revolves around the Sun?

And that it's really round?

So Sparty, are you saying that the Earth revolves around the Sun?

And that it's really round?

Eppur si muove

Leaked document shows EPA allowed bee-toxic pesticide despite own scientists’ red flags

By Tom Philpott

BeesmokerFollow the honey: Smoking bees makes them less mad when you move them, but leaked EPA documents might have the opposite effect.

It’s not just the State and Defense departments that are reeling this month from leaked documents. The Environmental Protection Agency now has some explaining to do, too. In place of dodgy dealings with foreign leaders, this case involves the German agrichemical giant Bayer; a pesticide with an unpronounceable name, clothianidin; and an insect species crucial to food production (as well as a food producer itself), the honeybee. And in lieu of a memo leaked to a globetrotting Australian, this one features a document delivered to a long-time Colorado beekeeper.

All of that, plus my favorite crop to fixate on: industrial corn, which blankets 88 million acres of farmland nationwide and produces a bounty of protein-rich pollen on which honeybees love to feast.

It’s The Agency Who Kicked the Beehive, as written by Jonathan Franzen!

Hive talking

An internal EPA memo released Wednesday confirms that the very agency charged with protecting the environment is ignoring the warnings of its own scientists about clothianidin, a pesticide from which Bayer racked up €183 million (about $262 million) in sales in 2009.

Clothianidin has been widely used on corn, the largest U.S. crop, since 2003. Suppliers sell seeds pre-treated with it. Like other members of the neonicotinoid family of pesticides, clothianidin gets “taken up by a plant’s vascular system and expressed through pollen and nectar,” according to Pesticide Action Network of North America (PANNA), which leaked the document along with Beyond Pesticides. That effect makes it highly toxic to a crop’s pests — and also harmful to pollen-hoarding honeybees, which have experienced mysterious annual massive die-offs (known as “colony collapse disorder”) here in the United States at least since 2006.

The colony-collapse phenomenon is complex and still not completely understood. While there appears to be no single cause for the annual die-offs, mounting evidence points to pesticides, and specifically neonicotinoids (derived from nicotine), as a key factor. And neonicotinoids are a relatively new factor in ecosystems frequented by honeybees — introduced in the late 1990s, these systemic insecticides have gained a steadily rising share of the seed-treatment market. It does not seem unfair to observe that the health of the honeybee population has steadily declined over the same period.

According to PANNA, other crops commonly treated with clothianidin include canola, soy, sugar beets, sunflowers, and wheat — all among the most widely planted U.S. crops. Bayer is now petitioning the EPA to register it for use with cotton and mustard seed.

The document [PDF], leaked to Colorado beekeeper Tom Theobald, reveals that EPA scientists have declared essentially rejected the findings of a study conducted on behalf of Bayer that the agency had used to justify the registration of clothianidin. And they reiterated concerns that widespread use of clothianidin imperils the health of the nation’s honeybees.

On Thursday, I asked an EPA press spokesperson via email if the scientists’ opinion would inspire the agency to remove clothianidin from the market. The spokesperson, who asked not to be named but who communicated on the record on behalf of the agency, replied that clothianidin would retain its registration and be available for use in the spring.

Wimpy watchdogging

Before we dig deeper into the leaked memo, it’s important to understand the sorry story of how an insecticide known to harm honeybee populations came to blanket a huge swath of U.S. farmland in the first place. It’s nearly impossible not to read it as a tale of a key public watchdog instead heeling to the industry it’s supposed to regulate.

In the EPA’s dealings with Bayer on this particular insecticide, the agency charged with protecting the environment has consistently made industry-friendly decisions that contradict the conclusions of its own scientists — and threaten to do monumental harm to our food system by wiping out its key pollinators.

According to a time line provided by PANNA, the sordid story begins when Bayer first applied for registration of clothianidin in 2003. (All of the documents to which I link below were provided to me by PANNA.) By 2003, U.S. beekeepers were reporting difficulties in keeping hives healthy through the winter, but not yet on the scale of colony collapse disorder. In February of this year, the EPA’s Environmental Fate and Effects Division (EFED) withheld registration of clothianidin, declaring that it wanted more evidence that it wouldn’t harm bee populations.

In a memo [PDF], an EFAD scientist explained the decision:

The possibility of toxic exposure to nontarget pollinators [e.g., honeybees] through the translocation of clothianidin residues that result from seed treatment (corn and canola) has prompted EFED to require field testing that can evaluate the possible chronic exposure to honeybee larvae and the queen. In order to fully evaluate the possibility of this toxic effect, a complete worker bee life cycle study (about 63 days) must be conducted, as well as an evaluation of exposure to the queen.

So, no selling clothianidin until a close, expert examination of how pollen infused with it would affect worker bees and Her Majesty the queen.

Again, that was in February of 2003. But in April of that year, just two months later, the agency backtracked. “After further consideration,” the agency wrote in another memo, the EPA has decided to grant clothianidin “conditional registration” — meaning that Bayer was free to sell it, and seed processors were free to apply it to their products. (Don’t get me started on the EPA’s habit of granting dodgy chemicals “conditional registration,” before allowing their unregulated use for years and even decades. That’s another story.)

The EPA’s one condition reflected the concerns of its scientists about how it would affect honeybees: that Bayer complete the “chronic life cycle study” the agency had already requested by December of 2004. The scientists minced no words in reiterating their concerns. They called clothianidin’s effects “persistent” and “toxic to honeybees” and noted the the “potential for expression in pollen and nectar of flowering crops.”

These concerns aside and “conditional registration” in hand, Bayer introduced clothianidin to the U.S. market in spring 2003. Farmers throughout the corn belt planted seeds treated with clothianidin, and billions — if not trillions — of plants began producing pollen rich with the bee-killing stuff.

Bee on a cornflowerA bee does what it does best — thankfully, not in a corn field.Photo: PurplekeyIn March of 2004, Bayer requested an extension on its December deadline for delivering the life-cycle study. In a March 11 memo [PDF], the EPA agreed, giving the chemical giant until May 2005 to complete the research. Clothianidin continued flowing from Bayer’s factories and from corn plants into pollen.

But the EPA also relayed a crucial decision in this memo: It granted Bayer the permission it had sought to conduct its study on canola in Canada, instead of on corn in the United States. The EPA justified the decision as follows:

[Canola] is attractive to bee [sic] and will provide bee exposure from both pollen and nectar. An alternative crop, such as corn, which is less attractive to bees as a forage crop, would provide exposure from pollen, only.

Bee experts cite three problems with this decision:

Corn produces much more pollen than does canola;
its pollen is more attractive to honey bees; and
canola is a minor crop in the United States, while corn is the single most widely planted crop.

What happened next was … not much. Bayer let the deadline for completing the study lapse; and the EPA let Bayer keep selling clothianidin, which continued to be deposited into tens of millions of acres of farmland.

Not until August of 2007, more than a year after its deadline, did Bayer deliver its study. In a November 2007 memo [PDF], EPA scientists declared the study “scientifically sound,” adding that it, “satisfies the guideline requirements for a field toxicity test with honeybees."

So what were the details of that study, on which the health of our little pollinator friends depended?

Well, the EPA initially refused to release it publicly, prompting a Freedom of Information Act by the Natural Resources Defense Council. When the EPA still refused to release it, NRDC filed suit in response. Eventually, the study was released. Here it is [PDF].

Prepared for Bayer by researchers at Canada’s University of Guelph, the study is a bit of a joke. The researchers created several 2.47-acre fields planted with clothianidin-treated seeds and matching untreated control fields, and placed hives at the center of each. Bees were allowed to roam freely. The problem is that bees forage in a range of 1.24 to 6.2 miles — meaning that the test bees most likely dined outside of the test fields. Worse, the test and control fields were planted as closely as 968 feet apart, meaning test and control bees had access to each other’s fields.

Not surprisingly, the researchers found “no differences in bee mortality, worker longevity, or brood development occurred between control and treatment groups throughout the study.”

Tom Theobald, the Colorado beekeeper who obtained the leaked memo, assessed the study harshly on the phone to me Thursday. “Imagine you’re a rancher trying to figure out if a noxious weed is harming your cows,” he said. “If you plant the weed on two acres and let your cows roam free over 50 acres of lush Montana grass, you’re not going to learn much about that weed.”

James Frazier, professor of entomology at Penn State, concurred. Frazier has been studying colony-collapse disorder since 2006. “When I looked at the study,” he told me in a phone interview, “I immediately thought it was invalid.”

Meanwhile, Bayer continued selling clothianidin under its conditional registration. Then, on April 22 of this year, the EPA finally ended clothianidin’s long period of “conditional” purgatory — by granting it full registration.

The agency gifted the bee-killing pesticide with its new status quietly; to my knowledge, the only public acknowledgment of it came through the efforts of Theobald, who is extremely worried about the fate of his own bee-keeping business in Colorado’s corn country. Theobald forwarded me a Nov. 29 email exchange with Meredith Laws, the acting chief of the EPA’s herbicide division in the Office of Pesticide Programs, to whom he’d written to enquire about clothianidin’s registration status. Laws’ reply is worth quoting in its entirety:

Clothianidin was granted an unconditional registration for use as a seed treatment for corn and canola on April 22, 2010. EPA issued a new registration notice, [but] there is no document that acknowledges the change from conditional to unconditional. This was a risk management decision based on the fulfillment of data requirements and reviews accepting or acknowledging the submittal of the data.

So, the EPA gave Bayer and its dubious pesticide a full pass without even bothering to let the public know.

Now we get to the leaked memo [PDF]. It is dated Nov. 2 — three weeks before Laws’ reply to Theobald. It relates to Bayer’s efforts to expand clothianidin’s approved use into cotton and mustard. Authored by two scientists in the EPA’s Environmental Fate and Effects Division — ecologist Joseph DeCant and chemist Michael Barrett — the memo expresses grave concern about clothianidin’s effect on honeybees:

Clothianidin’s major risk concern is to nontarget insects (that is, honey bees).

Clothianidin is a neonicotinoid insecticide that is both persistent and systemic. Acute toxicity studies to honey bees show that clothianidin is highly toxic on both a contact and an oral basis. Although EFED does not conduct … risk assessments on non-target insects, information from standard tests and field studies, as well as incident reports involving other neonicotinoids insecticides (e.g., imidacloprid) suggest the potential for long term toxic risk to honey bees and other beneficial insects.

The real kicker is that the researchers essentially invalidated the Bayer-funded study — i.e., the study on which the EPA based clothianidin’s registration as an fully registered chemical. Referring to the pesticide, the authors write:

A previous field study [i.e., the Bayer study] investigated the effects of clothianidin on whole hive parameters and was classified as acceptable. However, after another review of this field study in light of additional information, deficiencies were identified that render the study supplemental. It does not satisfy the guideline 850.3040, and another field study is needed to evaluate the effects of clothianidin on bees through contaminated pollen and nectar. Exposure through contaminated pollen and nectar and potential toxic effects therefore remain an uncertainty for pollinators. [Emphasis mine.]

So, here we have EPA researchers explicitly invalidating the study on which clothianidin gained registration for corn. But as I wrote above, despite this information’s being made public, the EPA has signaled that it has no plans to change the chemical’s status.

In the 2011 growing season, tens of millions of acres of farmland will bloom with clothianidin-laced pollen — honeybees, and sound science, be damned.

Now, in my correspondence with the EPA, the agency has denied that the downgrading of the Bayer study from “acceptable” to “supplemental” meant that the agency should be compelled to clothianidin’s approval. In a Thursday email to me, the agency delivered a limp defense of the Bayer study, contradicting its own scientists and addressing none of the critiques of it:

EPA’s evaluation of the study determined that it contains information useful to the agency’s risk assessment. The study revealed the majority of hives monitored, including those exposed to clothianidin during the previous season, survived the over-wintering period.

And it downplayed the study’s importance to Bayer’s application to register clothianidin: The study in question is “not a ‘core’ study for EPA as claimed,” the agency insisted. “It is not a study routinely required to support the registration of a pesticide.”

I ran that response by Jay Feldman of Beyond Pesticides, the group that collaborated with PANNA in publicizing the leaked document. “I find the EPA response either misinformed or misleading,” he told me. “The paper trail on this is clear. We’re talking about a bad study required by EPA [that is central] to the registration of this chemical.”

Feldman’s assessment appears to bear out. He pointed me back to the above-linked Nov. 27 document in which EPA originally accepted the Bayer study. There, on page 5, we find this statement:

Specifically, the test was conducted in response to a request by the Canadian PMRA [Pesticides and Pest Management Agency] and the U.S. EPA; as a condition for Poncho@ [clothianidin] registration in these countries, Bayer CropScience was asked to investigate the long-term toxicity of clothianidin-treated canola to foraging honey bees.

So evidently, the discredited Bayer study does lie at the heart of clothianidin’s acceptance. (I have requested an interview with an EPA official who can talk knowledgeably and on the record about these matters; the anonymous-by-request spokesperson is, at the time of publication, still looking for the “right person,” I was informed via email.)

A stinging assessment

At the very least, we have ample evidence that the EPA has been ignoring the warnings of its own staff scientists and green-lighting the mass deployment of a chemical widely understood to harm pollinators — at a time when honeybees are in grave shape.

But why? Tom Theobald, the Colorado beekeeper who broke this story, ventured an answer. “It’s corporatism, the flip side of fascism,” he said. “I’m not against corporations, I think they have a good model. But they’re like children — we have to rein them in or they get out of hand. The EPA’s supposed to do that.”

When regime change came to Washington in 2008, many of us hoped that an EPA under Barack Obama would be a better parent. EPA Director Lisa Jackson inherited quite a mess from her predecessor, and she faces the Herculean challenge of regulating greenhouse gases against fierce Republican and industry opposition.

But as concern mounts — from her own staff and elsewhere — that clothianidin is harming honeybees, there’s no excuse for Jackson’s agency to keep coddling Bayer. Frazier, the Penn State entomologist, put it to me like this: “If the Bayer study is the core study the EPA used to register clothianidin, then there’s no basis for registering it.” He urged the EPA to withdraw registration to avoid unnecessary risk to a critical player in our ecosystem — as have the governments of Germany, France, Italy, and Slovenia.

http://grist.org/article/food-2010-12-10-leaked-documents-show-epa-allowed-bee-toxic-pesticide/

http://junkscience.com/2014/12/16/paul-driessen-provides-an-essential-take-down-of-the-new-chemophobes-the-neonic-phobes/