EPA Awards Funding to Reduce Pesticide Risk Including Risks to Bees

Louisiana State, Penn State and University of Vermont at the forefront of groundbreaking technology

The U.S. Environmental Protection Agency (EPA) announced agricultural grants for Integrated Pest Management (IPM) practices to reduce the use of potentially harmful pesticides and lower risk to bees all while controlling pests and saving money.

“These collaborative projects can provide innovative solutions to reduce pesticide risks to pollinators and crops,” said James Jones, assistant administrator for the Office of Chemical Safety and Pollution Prevention. “Initiatives such as these will encourage others to adopt promising technologies and practices across the nation to reduce pesticide risks while maximizing crop production and protecting public health.”

IPM relies on easy-to-implement, environmentally-sensitive practices that prevent pests from becoming a threat. These practices involve monitoring and identifying pests and taking preventive action before pesticides are used. If pesticides are needed, methods such as targeted spraying may be used. These grants will expand public-private stewardship efforts and reduce pesticide risk in agriculture.

The Agricultural IPM Grants are awarded to:

The Louisiana State University project to minimize impacts to bees from insecticides used in mosquito control. Mosquito control is critical for public health; however, insecticides can be hazardous to bees. Bees are essential for crop production and ensuring a healthy food supply. Practices and guidelines resulting from the project will be distributed to mosquito control districts and beekeepers throughout the U.S.

The University of Vermont project to reduce pesticide use and improve pest control while increasing crop yields on 75 acres of hops in the Northeast. The awardees will also develop and distribute outreach materials to help farmers adopt these practices. The project’s goal is to reduce herbicide and fungicide applications by 50 percent while decreasing downy mildew, a plant disease.

The Pennsylvania State University project to protect bees and crops by reducing reliance on neonicotinoid pesticide seed treatments and exploring the benefits of growing crops without them. IPM in no-till grain fields will be used to control slugs and other pests that damage corn and soybeans. Researchers will share their findings with mid-Atlantic growers and agricultural professionals.


For more information on the EPA’s Regional Agricultural IPM Grants: http://www.epa.gov/pestwise/grants/regionalaggrants.html

Secure Pesticides and Chemicals during Poison Prevention Week

More than 145,000 reports made each year to poison centers involving pesticides and disinfectants

During National Poison Prevention Week, March 17-23, the U.S. Environmental Protection Agency (EPA) urges parents and caregivers to secure pesticides and other household chemicals in locked cabinets out of children's reach.

“Poison Prevention Week is a time to raise awareness and strengthen prevention efforts to empower parents and caregivers with information about simple steps that can be taken to prevent poisonings," said James Jones, acting assistant administrator for the EPA’s Office of Chemical Safety and Pollution Prevention. “EPA continues to take action to help prevent these risks to children and help ensure that the products on the market are both safe and effective for consumers. Our recent move to ban the sale of 12 D-Con mouse and rat poison products produced by Reckitt Benckiser Inc is a prime example of our commitment."

Each year, approximately 65,000 children ages 5 and younger are accidentally exposed to pesticides, and more than 10,000 of those exposures involve mouse and rat poisons. Recently, EPA took steps that, with the help of Americans who use these products around their homes, could help lower these statistics. Under new EPA safety standards, consumer use mouse and rat poison products must include a protective tamper-resistant bait station. These measures prevent children from accessing the poison.

More than 90 percent of poisonings happen in people’s homes. Parents and caregivers can protect children and loved ones against pesticide exposure.
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Poisonings are preventable. Here are some simple tips to prepare and stay safe:

• Always store pesticides and other household chemical products in a locked cabinet.
• To protect children and pets from exposure to mouse and rat poison, use products with a tamper-resistant bait station.
• Go through your home room by room to see where there are potential poisoning hazards and correct accordingly.
• Use child-resistant packaging properly by closing the container tightly after use.
• Never transfer pesticides and other household chemical products to containers that may be mistaken for food or drink.

Program the Poison Help Center number, 1-800-222-1222, in your phone.
Poison prevention tips and resources to protect your family: http://www.epa.gov/pesticides/health/poisonprevention.htm
Room by room checklist for potential poisoning hazards: http://www.epa.gov/pesticides/factsheets/roombyroom-checklist.htm
List of rat and mouse products that meet the EPA’s safety standards: http://www.epa.gov/pesticides/mice-and-rats/rodent-bait-station.html
More on National Poison Prevention Week: http://www.poisonprevention.org/index.htm

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Pesticides and Parkinson's: Researchers Uncover Further Proof of a Link

For several years, neurologists at UCLA have been building a case that a link exists between pesticide chemical exposure and Parkinson's disease. To date, paraquat, maneb and ziram — common chemicals sprayed in California's Central Valley and elsewhere — have been tied to increases in the disease, not only among farmworkers but in individuals who simply lived or worked near fields and likely inhaled drifting particles.

Now, UCLA researchers have discovered a link between Parkinson's and another pesticide, benomyl, whose toxicological effects still linger some 10 years after the chemical was banned by the U.S. Environmental Protection Agency.

Even more significantly, the research suggests that the damaging series of events set in motion by benomyl may also occur in people with Parkinson's disease who were never exposed to the pesticide, according to Jeff Bronstein, senior author of the study and a professor of neurology at UCLA, and his colleagues.

Benomyl exposure, they say, starts a cascade of cellular events that may lead to Parkinson's. The pesticide prevents an enzyme called ALDH (aldehyde dehydrogenase) from keeping a lid on DOPAL, a toxin that naturally occurs in the brain. When left unchecked by ALDH, DOPAL accumulates, damages neurons and increases an individual's risk of developing Parkinson's.

The investigators believe their findings concerning benomyl may be generalized to all Parkinson's patients. Developing new drugs to protect ALDH activity, they say, may eventually help slow the progression of the disease, whether or not an individual has been exposed to pesticides.

The research is published in the current online edition of Proceedings of the National Academy of Sciences.

Parkinson's disease is a debilitating neurodegenerative disorder that affects millions worldwide. Its symptoms — including tremor, rigidity, and slowed movements and speech — increase with the progressive degeneration of neurons, primarily in a part of the mid-brain called the substantia nigra. This area normally produces dopamine, a neurotransmitter that allows cells to communicate, and damage to the mid-brain has been linked to the disease. Usually, by the time Parkinson's symptoms manifest themselves, more than half of these neurons, known as dopaminergic neurons, have already been lost.

While researchers have identified certain genetic variations that cause an inherited form of Parkinson's, only a small fraction of the disease can be blamed on genes, said the study's first author, Arthur G. Fitzmaurice, a postdoctoral scholar in Bronstein's laboratory.

"As a result, environmental factors almost certainly play an important role in this disorder," Fitzmaurice said. "Understanding the relevant mechanisms — particularly what causes the selective loss of dopaminergic neurons — may provide important clues to explain how the disease develops."

Benomyl was widely used in the U.S. for three decades until toxicological evidence revealed it could potentially lead to liver tumors, brain malformations, reproductive effects and carcinogenesis. It was banned in 2001.

The researchers wanted to explore whether there was a relationship between benomyl and Parkinson's, which would demonstrate the possibility of long-lasting toxicological effects from pesticide use, even a decade after chronic exposure. But because a direct causal relationship between the pesticide and Parkinson's can't be established by testing humans, the investigators sought to determine if exposure in experimental models could duplicate some of the pathologic features of the disease.

They first tested the effects of benomyl in cell cultures and confirmed that the pesticide damaged or destroyed dopaminergic neurons.

Next, they tested the pesticide in a zebrafish model of the disease. This freshwater fish is commonly used in research because it is easy to manipulate genetically, it develops rapidly and it is transparent, making the observation and measurement of biological processes much easier. By using a fluorescent dye and counting the neurons, the researchers discovered there was significant neuron loss in the fish — but only to the dopaminergic neurons. The other neurons were left unaffected.

Until now, evidence had pointed to one particular culprit — a protein called α-synuclein — in the development of Parkinson's. This protein, common to all Parkinson's patients, is thought to create a pathway to the disease when it binds together in "clumps" and becomes toxic, killing the brain's neurons. (See UCLA research using "molecular tweezers" to break up these toxic aggregations.)

The identification of ALDH activity now gives researchers another target to focus on in trying to stop this disease.

"We've known that in animal models and cell cultures, agricultural pesticides trigger a neurodegenerative process that leads to Parkinson's," said Bronstein, who directs the UCLA Movement Disorders Program. "And epidemiologic studies have consistently shown the disease occurs at high rates among farmers and in rural populations. Our work reinforces the hypothesis that pesticides may be partially responsible, and the discovery of this new pathway may be a new avenue for developing therapeutic drugs."

Study: Preschoolers found to be at high risk for exposure to pesticides and toxins linked to cancer and developmental problems

Photo: Freedigitalphotos.net

In a sobering study published in the journal Environmental Health, researchers measured food-borne toxin exposure in children and adults by pinpointing foods with high levels of toxic compounds and determining how much of these foods were eaten.

The researchers found that family members in the study, and preschool children in particular, are at high risk for exposure to arsenic, dieldrin, DDE (a DDT metabolite), dioxins and acrylamide. These compounds have been linked to cancer, developmental disabilities, birth defects and other conditions.

"Contaminants get into our food in a variety of ways," said study principal investigator Irva Hertz-Picciotto, professor and chief of the Division of Environmental and Occupational Health at UC Davis. "They can be chemicals that have nothing to do with the food or byproducts from processing. We wanted to understand the dietary pathway pesticides, metals and other toxins take to get into the body."

Researchers assessed risk by comparing toxin consumption to established benchmarks for cancer risk and non-cancer health risks. All 364 children in the study (207 preschool children between two and seven and 157 school-age children between five and seven) exceeded cancer benchmarks for arsenic, dieldrin, DDE and dioxins. In addition, more than 95 percent of preschool children exceeded non-cancer risk levels for acrylamide, a cooking byproduct often found in processed foods like potato and tortilla chips. Pesticide exposure was particularly high in tomatoes, peaches, apples, peppers, grapes, lettuce, broccoli, strawberries, spinach, dairy, pears, green beans and celery.

"We focused on children because early exposure can have long-term effects on disease outcomes," said Rainbow Vogt, lead author of the study. "Currently, the U.S. Environmental Protection Agency only measures risk based on exposures of individual contaminants. We wanted to understand the cumulative risk from dietary contaminants. The results of this study demonstrate a need to prevent exposure to multiple toxins in young children to lower their cancer risk."

Perhaps most disturbing, preschool-age children had higher exposure to more than half the toxic compounds being measured. Even relatively low exposures can greatly increase the risk of cancer or neurological impairment.

"We need to be especially careful about children, because they tend to be more vulnerable to many of these chemicals and their effects on the developing brain," says Hertz-Picciotto.

Though these results are cause for concern, the study also outlines strategies to lower family exposure. For example, organic produce has lower pesticide levels. In addition, toxin types vary in different foods. Certain pesticides may be found in lettuce and broccoli, while others affect peaches and apples.

"Varying our diet and our children's diet could help reduce exposure," said Hertz-Picciotto. "Because different foods are treated differently at the source, dietary variation can help protect us from accumulating too much of any one toxin."

Families also can reduce their consumption of animal meat and fats, which may contain high levels of DDE and other persistent organic pollutants, and switch to organic milk. While mercury is most often found in fish, accumulation varies greatly by species. Smaller fish, lower on the food chain, generally have lower mercury levels. In addition, acrilomides are relatively easy to remove from the diet.

"Acrilomides come from chips and other processed grains, said co-author Deborah Bennett, associate professor of Environmental and Occupational Health at UC Davis. "Even if we set aside the potential toxins in these foods, we probably shouldn't be eating large amounts of them anyway. However, we should be eating fruits, vegetables and fish, which are generally healthy foods. We just need to be more careful in how we approach them."

The study also highlights a number of policy issues, such as how we grow our food and the approval process for potentially toxic compounds. Though the pesticide DDT was banned 40 years ago, the study showed significant risk of DDE exposure.

"Given the significant exposure to legacy pollutants, society should be concerned about the persistence of compounds we are currently introducing into the environment," said Bennett. "If we later discover a chemical has significant health risks, it will be decades before it's completely removed from the ecosystem."

While the study has profound implications for dietary habits, more work needs to be done to quantify risk. Specifically, researchers need to determine how these food-borne toxins interact collectively in the body.

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Head Injury + Pesticide Exposure = Triple the Risk of Parkinson’s Disease

A new study shows that people who have had a head injury and have lived or worked near areas where the pesticide paraquat was used may be three times more likely to develop Parkinson’s disease.

Paraquat is a herbicide commonly used on crops to control weeds. It can be deadly to humans and animals.

“While each of these two factors is associated with an increased risk of Parkinson’s on their own, the combination is associated with greater risk than just adding the two factors together,” said study author Beate Ritz, MD, PhD, of UCLA’s Fielding School of Public Health.

“This study suggests that the physiological process that is triggered by a head injury may increase brain cells’ vulnerability to attacks from pesticides that can be toxic to the brain or the other way around, for example, chronic low dose exposure to pesticides may increase the risk of Parkinson’s after a head injury.”

The study involved 357 people with Parkinson’s disease and 754 people without the disease, all of whom lived in an agricultural area in central California. The participants reported any head injuries they had ever received with a loss of consciousness for more than five minutes.

The researchers determined participants’ exposure to the weed killer based on a 500-meter area around their home and work addresses, using a geographic information system (GIS) that combined data on paraquat use collected by the state of California’s Pesticide Use Reporting system with land use maps.

People with Parkinson’s disease were twice as likely to have had a head injury with loss of consciousness for more than five minutes as people who did not have the disease. Of the 357 people with Parkinson’s disease, 42, or 12 percent, reported ever having had such a head injury, compared to 50 of the 754 people without the disease, or 7 percent.

People with Parkinson’s disease were 36 percent more likely to have exposure to paraquat than those who did not have the disease. Of those with Parkinson’s, 169 had exposure to the weed killer, or 47 percent, compared to 291 of those without the disease, or 39 percent.

The study was published in medical journal of the American Academy of Neurology.


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