PESTICIDES & PARKINSON’S COMMITTEE
Pesticides and suicide:
more on the relation between pesticides and PD
glyphosate creating havoc in some parts of Argentina
CDC (Center of Disease Control) pesticides interactive map
NEW! Major Pesticides are more toxic to human cells than their declared active principles
GLYPHOSATE (in Round Up): NEW!
a) FROM REUTERS’ JOURNAL:
April 25 (Reuters) – Heavy use of the world’s most popular herbicide, Roundup, could be linked to a range of health problems and diseases, including Parkinson’s, infertility and cancers, according to a new study.
The peer-reviewed report, published last week in the scientific journal Entropy, said evidence indicates that residues of “glyphosate,” the chief ingredient in Roundup weed killer, which is sprayed over millions of acres of crops, has been found in food.
Those residues enhance the damaging effects of other food-borne chemical residues and toxins in the environment to disrupt normal body functions and induce disease, according to the report, authored by Stephanie Seneff, a research scientist at the Massachusetts Institute of Technology, and Anthony Samsel, a retired science consultant from Arthur D. Little, Inc. Samsel is a former private environmental government contractor as well as a member of the Union of Concerned Scientists.
“Negative impact on the body is insidious and manifests slowly over time as inflammation damages cellular systems throughout the body,” the study says.
We “have hit upon something very important that needs to be taken seriously and further investigated,” Seneff said.
Environmentalists, consumer groups and plant scientists from several countries have warned that heavy use of glyphosate is causing problems for plants, people and animals.
The EPA is conducting a standard registration review of glyphosate and has set a deadline of 2015 for determining if glyphosate use should be limited. The study is among many comments submitted to the agency.
Monsanto is the developer of both Roundup herbicide and a suite of crops that are genetically altered to withstand being sprayed with the Roundup weed killer.
These biotech crops, including corn, soybeans, canola and sugarbeets, are planted on millions of acres in the United States annually. Farmers like them because they can spray Roundup weed killer directly on the crops to kill weeds in the fields without harming the crops.
Roundup is also popularly used on lawns, gardens and golf courses.
Monsanto and other leading industry experts have said for years that glyphosate is proven safe, and has a less damaging impact on the environment than other commonly used chemicals.
Jerry Steiner, Monsanto’s executive vice president of sustainability, reiterated that in a recent interview when questioned about the study.
“We are very confident in the long track record that glyphosate has. It has been very, very extensively studied,” he said.
Of the more than two dozen top herbicides on the market, glyphosate is the most popular. In 2007, as much as 185 million pounds of glyphosate was used by U.S. farmers, double the amount used six years ago, according to Environmental Protection Agency (EPA) data.
b) THE STUDY ITSELF:
Source: http://www.mdpi.com/1099-4300/15/4/1416 (download the PDF file)
Entropy 2013, 15, 1-x manuscripts; doi:10.3390/ e140x000x
Entropy ISSN 1099-4300
Review (an in depth study of 48 pages)
Glyphosate’s Suppression of Cytochrome P450
Enzymes and Amino Acid Biosynthesis by the Gut
Microbiome: Pathways to Modern Diseases
This paper presents an exhaustive review of the toxic effects of the herbicide, glyphosate, the active ingredient in Roundup®, in humans, and demonstrates how glyphosate’s adverse effects on the gut microbiota, in conjunction with its established ability to inhibit the activity of cytochrome P450 enzymes, and its likely impairment of sulfate transport, can remarkably explain a great number of the diseases and conditions that are prevalent in the modern industrialized world. Its effects are insidious, because the long-term effects are often not immediately apparent. The pathologies to which glyphosate could plausibly contribute, through its known biosemiotic effects, include inflammatory bowel disease, obesity, depression, ADHD, autism, Alzheimer’s disease, Parkinson’s disease, ALS, multiple sclerosis, cancer, cachexia, infertility, and developmental malformations. Glyphosate works synergistically with other factors, such as insufficient sun exposure, dietary deficiencies in critical nutrients such as sulfur and zinc, and synergistic exposure to other xenobiotics whose detoxification is impaired by glyphosate. Given the known toxic effects of glyphosate reviewed here and the plausibility that they are negatively impacting health worldwide, it is imperative for more independent research to take place to validate the ideas presented here, and to take immediate action, if they are verified, to drastically curtail the use of glyphosate in agriculture. Glyphosate is likely to be pervasive in our food supply, and, contrary to being essentially nontoxic, it may in fact be the most biologically disruptive chemical in our environment.
META ANALYSIS ON PESTICIDES & PARKINSON’S
1. UCLA research
Public release date: 3-Jan-2013
Contact: Mark Wheeler
University of California – Los Angeles
Pesticide exposure may not just increase the risk of Parkinson’s disease, but may actually start a cascade of events that directly cause the disease.
Over the past several years, UCLA researchers have successively established a link between exposure to various pesticides and Parkinson’s disease, including the common agricultural chemicals maneb, paraquat and ziram. This link is seen among both farm workers and those living or working near agricultural fields.
Researchers sought to determine whether there might be a link between Parkinson’s and benomyl, a pesticide that was banned in the United States in 2001 after 30 years of use, after it was linked to cancer, brain defects, liver tumors and reproductive damage. The researchers confirmed in a laboratory study that dopaminergic neurons were damaged or destroyed upon exposure to benomyl. This destruction occurred because benomyl blocked the action of an enzyme known as ALDH, which normally interferes with the action of a naturally occurring brain toxin called DOPAL. Without ALDH, DOPAL builds up and destroys the dopaminergic cells. ALDH had never before been linked to Parkinson’s disease, which was believed instead to be caused by a protein called a-synuclein. If the study’s findings are correct, ALDH disruption may turn out to be a cause of the disease even in people who have not been exposed to pesticides.
2. PESTICIDE-INDUCED DISEASES DATABASE (FOR PARKINSON’S DISEASE): (references to scientific studies, from Beyond Pesticides)
3. PESTICIDES AND PARKINSON’S: UCLA RESEARCHERS UNCOVER FURTHER PROOF OF A LINK
link between Parkinson’s and benomyl (banned in 2001 after 30 years of use, after it was linked to cancer, brain defects, liver tumors and reproductive damage). The researchers confirmed in a laboratory study that dopaminergic neurons were damaged or destroyed upon exposure to benomyl. This destruction occurred because benomyl blocked the action of an enzyme known as ALDH, which normally interferes with the action of a naturally occurring brain toxin called DOPAL. Without ALDH, DOPAL builds up and destroys the dopaminergic cells. ALDH had never before been linked to Parkinson’s disease, which was believed instead to be caused by a protein called a-synuclein. If the study’s findings are correct, ALDH disruption may turn out to be a cause of the disease even in people who have not been exposed to pesticides.
This work was funded in part by National Institute of Environmental Health Sciences grants P01ES016732, R01ES010544, 5R21ES16446-2 and U54ES012078; National Institute of Neurological Disorders and Stroke grant NS038367; the Veterans Affairs Healthcare System (Southwest Parkinson’s Disease Research, Education, and Clinical Center); the Michael J. Fox Foundation; the Levine Foundation; and the Parkinson Alliance.
4. PESTICIDE EXPOSURE TIED TO PD RISK
By Kathleen Struck, Senior Editor, MedPage Today
Published: May 28, 2013
Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner
In sensitivity analyses on high-quality studies of more than 200 cases, the risks of Parkinson’s related only to rural living became significant.
Primary source: Neurology
Pezzoli G, Cereda E “Exposure to pesticides or solvents and risk of Parkinson disease” Neurology 2013; 80: 2035-2041.
Exposure to pesticides and solvents appears to be a risk factor for Parkinson’s disease, a meta-analysis found.
Based on an analysis of 89 prospective and case-control studies, exposure to bug or weed killers and solvents increased the risk of developing Parkinson’s disease by 33% to 80%, reported Gianni Pezzoli, MD, of the Parkinson Institute, Istituti Clinici di Perfezionamento in Milan, and Emanuele Cereda, MD, PhD, IRCCS University Hospital San Matteo Foundation in Pavia, Italy
5. 11 FEB 2011: NIH STUDY FINDS TWO PESTICIDES ASSOCIATED WITH PARKINSON’S DISEASE
Speaker:Freya Kamel, Ph.D.,
Staff Scientist, Epidemiology Branch
New research shows a link between use of two pesticides, rotenone and paraquat, and Parkinson’s disease. People who used either pesticide developed Parkinson’s disease approximately 2.5 times more often than non-users.
The study was a collaborative effort conducted by researchers at the National Institute of Environmental Health Sciences (NIEHS), which is part of the National Institutes of Health, and the Parkinson’s Institute and Clinical Center in Sunnyvale, Calif.
“Rotenone directly inhibits the function of the mitochondria, the structure responsible for making energy in the cell,” said Freya Kamel, Ph.D., a researcher in the intramural program at NIEHS and co-author of the paper appearing online in the journal Environmental Health Perspectives. “Paraquat increases production of certain oxygen derivatives that may harm cellular structures. People who used these pesticides or others with a similar mechanism of action were more likely to develop Parkinson’s disease.”
There are no home garden or residential uses for either paraquat or rotenone currently registered. Paraquat use has long been restricted to certified applicators, largely due to concerns based on studies of animal models of Parkinson’s disease. Use of rotenone as a pesticide to kill invasive fish species is currently the only allowable use of this pesticide.
6. PESTICIDES, COUNTRY LIVING MAY INCREASE RISK OF PARKINSON’S DISEASE
Those exposed to various pesticides, and people who live in rural areas, were a third to 80 percent more likely to develop Parkinson’s disease, according to studies analyzed by the American Academy of Neurology. But urban dwellers face their own health risks.
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By Jeffrey Kopman, Everyday Health Staff Writer
MONDAY, May 27, 2013 — Bug and weed killers are designed to attack bugs and weeds, not farmers and those who live in the country. Unfortunately, pesticides and rural living may lead to a higher risk of Parkinson’s disease, according to an analysis published today in Neurology.
The analysis took data from 104 studies that used questionnaires to determine chemical exposure and Parkinson’s disease diagnoses. Subjects were broken down by their exposure to chemicals, where they lived and various lifestyle choices, such as whether they farmed for a living or typically drank well water.
Researchers found that exposure to different chemicals and solvents was linked to an increased risk for Parkinson’s disease ranging from 33 to 80 percent. Study subjects exposed to pesticides were two-thirds more likely to develop the disease than those who weren’t exposed.
Rural living was tied to a 75 percent overall increased risk for Parkinson’s disease, and well water drinking was linked to a 66 percent increase.
Researchers hope their findings will lead to further investigation into the cause and effect relationship of pesticides and Parkinson’s disease.
“We didn’t study whether the type of exposure, such as whether the compound was inhaled or absorbed through the skin and the method of application, such as spraying or mixing, affected Parkinson’s risk,” said study author Emanuele Cereda, MD, PhD, with the IRCCS University Hospital San Matteo Foundation in Pavia, Italy. “However, our study suggests that the risk increases in a dose response manner as the length of exposure to these chemicals increases.”
The Big City’s Bothers Versus The Countryside’s Chronic Conditions
While country living frees people of some environmental hazards – including pollution from traffic that can increase risk of diabetes, COPD, and asthma, according to recent research – studies have shown that it’s not all green grass and sunshine.
Rural living has been linked to higher rates of chronic diseases compared to people living in cities. This factor could be attributed to the gap in care: Rural areas of the United States often have fewer healthcare options, and live further away from the doctors and hospitals that do exist.
Farmers and their families face another unique health problem: Agricultural industrial hazards, like tractors and machinery, lead to thousands of children being hospitalized per year.
“People that live in rural areas are more likely to be around farming activities. It is thought that this leads to a higher exposure to pesticides,” said Gary W. Miller, Ph.D., Rollins School of Public Health, Emory University in Atlanta, Georgia.
Exposure to these chemicals has been linked to an increased risk for developing ADHD, prostate cancer, and now Parkinson’s disease.
Pesticides are not as big of a problem for city slickers, but exposure to overcrowded public transportation systems and crowded streets can lead to an exceptional spreading of germs and viruses, like the flu scare of 2012-2013.
Ultimately, while the cleaner air and open space might seem like a healthier alternative to skyscrapers and cement, both rural and urban living carry their own unique health risks.
“Both [country and city living] have pluses and minuses,” said Dr. Miller. “In my opinion the country is superior from a health perspective. People tend to be more active and have lower exposure to pollution.”
7. STUDY LINKS EXPOSURE TO BUG AND WEED KILLERS TO HIGHER RISK FOR PARKINSON’S
Study Links Exposure to Bug and Weed Killers to Higher Risk for Parkinson’s
David H. Lewis / Getty Images
Who doesn’t want a pristine lawn free of annoying weeds and bugs? But some of those pest-fighting strategies may come with a price — to your health.
A new study published in the journal Neurology found that pesticides, which have already been linked to a range of health complications from allergies to lower IQ levels, may also play a role in the development of Parkinson’s.
Parkinson’s is a neurological disease in which motor nerves in the brain lose their ability to function, leading to uncontrolled movements, tremors and difficulty in walking and speaking. While genes play some role in the condition, more research is connecting lifestyle and environmental factors to a higher risk of disease.
In the latest review, the researchers reviewed 104 studies that analyzed exposure to pesticides and solvents that kill weeds, fungus, rodents and bugs, and the risk of Parkinson’s disease. The trials measured things such as whether the participants lived in close proximity to farms or other agricultural plots that use a higher volume of such chemicals, the likelihood of well-water consumption, rural living and various occupations that put an individual at a greater or lower risk of exposure.
(MORE: Study: Flavonoids May Help Protect Against Parkinson’s)
They found that exposure to bug and weed killers and solvents was linked to a 33% to 80% greater risk of developing Parkinson’s disease. In some studies, individuals who came in contact with the weed killer paraquat or the fungicides maneb and mancozeb were twice as likely to develop Parkinson’s.
Unfortunately, the trials did not all address how the participants were exposed, so the scientists could not determine if certain routes, like inhaling the chemicals, was more dangerous than absorbing them through the skin. The investigation did conclude, however, that risk appears to increase the longer people are exposed. But more studies are needed to figure out whether there is a threshold for when the chemicals become most harmful to the brain.
The scientists also acknowledge that some of the data is conflicting; while the studies they analyzed showed a strong association between solvents and well water and a higher risk of Parkinson’s, the same elevated risk didn’t appear for insecticides.
Despite that, the results add to growing research about how exposure to environmental factors may play a role in diseases like Parkinson’s. “I think the study is actually a big advance in our research knowledge of the relation between chemical exposures and the basic neurological injuries,” Dr. Arch Carson of the University of Texas School of Public Health in Houston told MedPage Today. “This report is the first to show that there is a positive relationship between not only insecticides and herbicides but also some other solvent chemicals to which many people are exposed and the development of Parkinson’s syndrome.”
Uncovering and understanding these links could not only help prevent some cases of disease, but also lead to more targeted ways of intervening with effective treatments.
8. THE BIG PICTURE: STUDYING POPULATIONS TO UNDERSTAND PARKINSON’S
By Beate Ritz, M.D., Ph.D.
Despite the significant progress we have made in diagnosing and treating Parkinson’s disease (PD), many basic questions remain unanswered. Among them: How many people have Parkinson’s disease? What puts people at risk of developing PD? Are there some groups — for example, people who live in certain geographic locations, or are of particular ethnic backgrounds — who are more likely than others to develop PD? Are people being diagnosed with Parkinson’s more frequently than before? Are there toxins in the environment, or aspects of people’s lifestyle, that contribute to PD? And the elusive “holy grail,” is there anything that could prevent it?
Epidemiologists approach these problems by studying large groups of people over long periods of time. They use these data to formulate a picture of who gets certain health conditions, and to investigate whether chemicals, or foods and health habits, among other things, might cause disease or protect against it. The answers they receive can help us to understand, treat and — in the long run — prevent many health conditions, including Parkinson’s disease.
Getting at PD Risk and Protective Factors
Through epidemiological studies of this kind, we do already have some basic information about how many people live with Parkinson’s, and who has a higher risk of developing it.
For example, in the United States, studies have shown that in the population aged 60 years or more, about one percent — or five to 10 adults per thousand — have Parkinson’s. That makes PD the second most common neurodegenerative disease after Alzheimer’s.
We know some other things about people who are more or less likely to develop Parkinson’s disease. These factors include the following:
Age is the chief risk factor for Parkinson’s. As the number of people over age 60 increases, an increasing number of people will be diagnosed with PD.
PD is more common in men. About 60 percent of people with PD are male and 40 percent are female.
PD is more common among whites than it is among blacks, or among people of Asian ancestry.
People who have Parkinson’s report that they smoke less and drink less coffee than do other people. But we do not know whether long-term use of caffeine or nicotine may prevent PD or whether people with PD may simply stop drinking coffee or smoking in the early (or preclinical) phase of PD. Or could it be that these behaviors are part of what some doctors hypothesize to be “a Parkinson’s personality?”
Research has suggested other factors that may reduce PD risk, although these are not proven. They include taking anti-inflammatory medications and statins; exhibiting high blood levels of uric acid; and eating foods rich in antioxidants, or taking supplements. Research also suggests factors that may increase the risk of developing PD, including living in a rural area, working as a farmer, and drinking well water. Stronger evidence points to occupational and general exposure to pesticides, and perhaps exposure to certain metals and to PCBs (organic chemicals), as increasing the risk of PD.
We discovered these associations by looking at behavioral and health data, from thousands of people, that originally had been collected over many decades for another purpose altogether. In one example of this type of research, researchers set about gathering health information regularly on more than 8,000 men of Japanese ancestry who lived in Hawaii in 1964, with the purpose of studying heart disease. But the scientists also followed these men for other aspects of health, including Parkinson’s diagnoses. In the 1990s, looking back at almost 30 years of records, researchers compared the 149 men who had developed PD with others in the group. They found that the men who were smokers or who consumed caffeine at the beginning of the study were less likely to have developed PD than were the others. Later studies bolstered these observations.
It is important to remember that these risk factors, generally do not necessarily cause Parkinson’s disease. But they can help us understand how it develops. Knowing the agents that may be harmful to dopamine neurons may help us find ways to reduce our exposure to them. It can help us to better understand how toxins may increase the risk of developing PD, and thereby help us to identify new targets for treatments.
The Importance of Disease Registries
So far, epidemiologists interested in PD have had to rely mainly on large long-term studies that were designed to study other illnesses. Why are there so few studies and databases designed for Parkinson’s?
One reason is that in the United States, there is no centralized place for recording cases of Parkinson’s as there are for many other diseases. A second reason is that gathering information about cases of PD is more difficult than for many other diseases. For example, if you want to find out the ages at which people die from strokes, you can look at death certificates. If you want to see who has cancer, the diagnoses will be confirmed by pathologists’ reports. But PD often is not listed on death certificates and PD diagnoses are not always accurate. Unless a person with PD has been diagnosed by an experienced movement disorder specialist, there’s a strong chance of PD being confused with diseases such as Multiple system atrophy (MSA), Progressive supranuclear palsy (PSP), or Essential Tremor.
In countries with national health care, it is theoretically easier to assess the prevalence of PD. But even here there are problems — for example, numbers cannot be easily compared country-to-country because different methods have been used to identify PD. Even in a small country like Norway, which has universal health care, centralized record-keeping and well-trained physicians, a recent study showed that tremor disorders were often misdiagnosed as PD by non-specialists.
To truly understand PD, we need a focused approach — ideally, a disease registry that includes confidential information on health and other characteristics (for example, employment and residence) for everyone with PD who lives in a large county, state or country.
California Parkinson’s Disease Registry
In 2004, in an effort to begin gathering data on PD in a well-defined US population, I worked with a group of collaborators — including Greg and Ann Wasson, Mark Siegel, and Drs. Caroline Tanner and J. William Langston — to pass a law establishing the California Parkinson’s Disease Registry. The law mandates the Department of Health to register cases of PD in a confidential database, and it requires health care providers to report cases to the registry. But it too has faced challenges — a key one being that the law forbids the expenditure of state funds to run the registry itself!
In 2007, with many colleagues, I began a pilot project to develop this registry. We focused on three counties in California’s Central Valley, which is the nation’s most productive agricultural region. We chose this area in part because we wanted to investigate a suspected association between pesticide exposure and PD. It took months of legwork to contact health care facilities and physicians treating people with PD; to encourage their participation; and then to recruit people in the registry to participate in our research.
Following up on mounting evidence that pesticide exposure increases PD risk, one of our first projects with the registry was to look at people who live close to fields that had been sprayed with the fungicide maneb and the herbicide paraquat. We found that these people had an increased risk of developing PD. In a later study, we found that people whose workplaces were near fields sprayed with these pesticides, as well as the fungicide ziram, had an increased PD risk. People who both lived and worked near fields sprayed with pesticides had the highest PD risk. People who were diagnosed with PD at younger ages had higher exposures to pesticides — both at workplaces and at home.
In another project, we followed 233 people recently diagnosed with PD for five years, to investigate why it is that some people with Parkinson’s live for many years without much change in their movement symptoms, whereas others decline rapidly. This long-term study allowed us to compare the genes of “fast progressors” and “slow progressors.” One important result of the study was the identification of genetic variations that may help predict the course of a person’s PD and suggest a way in which we can identify people with PD who will benefit the most from early treatment.
In a fairly short time, with a PD registry representing only part of our state, we have already accumulated strong scientific evidence both to support changes in environmental regulations and to suggest pathways to developing neuroprotective agents (that is, agents that can protect neurons from dying in PD). These results underscore the need for more comprehensive PD registries in California and elsewhere.
What You Can Do
If you are a person with PD, you can make a contribution to research by contacting a PD registry, if there is one near you (see box at right). If you live in the majority of states that don’t have registries, you can volunteer for studies and encourage people without PD to do the same. The biggest impediment to observational studies is recruiting volunteers who don’t have PD. We need to include their survey responses and DNA samples, so that we can compare their histories to those of people with PD and find the differences.
Studying populations makes it possible to get at some of the most fundamental questions of research — the who, when and why of Parkinson’s — and you can be a part of this process. We cannot do it without you!
Dr. Ritz is Professor of Epidemiology at the University of California, Los Angeles Fielding School of Public Health and School of Medicine.
Conclusions Our data show an increased PD mortality in California counties using agricultural pesticides. Unless all of our measures of county pesticide use are surrogates for other risk factors more prevalent in pesticide use counties, it seems important to target this prevalent exposure in rural California in future studies that use improved case finding mechanisms and collect pesticide exposure data for individuals.
about Beate Ritz, M.D., Ph.D.
Chair and Professor, Epidemiology
Professor, Environmental Health Sciences, Neurology
Member, JCCC Molecular Epidemiology Program Area, Center for Neurodegenerative Disease Studies.
Work Phone Number: (310) 206-7458
Email Address: email@example.com
Research Interests: Her research focuses on the health effects of occupational and environmental toxins such as pesticides, ionizing radiation, and air pollution on chronic diseases including neurodegenerative disorders (Parkinson’s disease), cancers, and adverse birth outcomes and asthma. She previously investigated the causes of cancer in chemical toxin and radiation exposed workers and assessed the impact of ergonomic work-place factors on musculo-skeletal disorders. For the past decade, she studied the effects of air pollution on adverse birth outcomes as well as asthma in children in Southern California. In 2006, she received the Robert M Zweig Memorial award for outstanding achievement in air quality and medicine from the South Coast Air Quality Management District. She also spend the past 15 years investigating the long-term effects of pesticide exposures on Parkinson’s disease and cancers and is currently conducting a project to implement a Parkinson’s disease registry required by a new law in California. In her research she uses geographic information system (GIS) modeling of environmental exposures including pesticide use and traffic related air pollution in California and investigates links between genetic susceptibility factors and environmental exposures in populations. She is directing and collaborating in a large number of federally (NIH, DOD), state (California Air Resources Board), and foundation (Michael J Fox Foundation) funded research projects.
9. WELL-WATER CONSUMPTION AND PARKINSON’S DISEASE IN RURAL CALIFORNIA
In conclusion, our study, the first of its kind to apply a semiquantitative approach to estimating pesticide exposure in well water, contributes evidence that consumption of well water potentially contaminated with pesticides may play a role in the etiology of PD.
10. THREATS TO HEALTHY AGING WITH A CLOSER LOOK AT ALZHEIMER’S & PARKINSON’S DISEASES
environmental Factors in the Development of parkinson’s Disease Page 145 (chapter 8)
11. INTERACTION BETWEEN ABCB1 AND PROFESSIONAL EXPOSURE TO ORGANOCHLORINE INSECTICIDES IN PARKINSON DISEASE (JAMA neurology)
12. CYP2D6 POLYMORPHISM, PESTICIDE EXPOSURE, AND PARKINSON’S DISEASE.
13. PROFESSIONAL EXPOSURE TO PESTICIDES AND PARKINSON DISEASE
Our results support an association between PD and professional pesticide exposure, and show that some pesticides (ie, organochlorine insecticides) may be more particularly involved. Ann Neurol 2009;66:494–504
14. ENVIRONMENTAL-GENETIC INTERACTIONS IN THE PATHOGENESIS OF PARKINSON’S DISEASE
Recent studies have revealed that certain interactions promote the development of PD: between the CYP2D6 and SLC6A3 genes and insecticide exposure; between the MAO-B and GST genes and smoking; between the ADORA2A andCYP1A2 genes and caffeine consumption; and between the PON-1 gene and organic phosphate exposure.
15. INDUSTRIAL CLEANER LINKED TO INCREASED RISK OF PARKINSON’S DISEASE
Published Tuesday, February 9, 2010 4:00 am
16. AGENT ORANGE COMPONENT LINKED TO PARKINSON’S DISEASE
Published Monday, September 14, 2009 4:00 am
17. IDENTIFYING RISK FACTORS IN PD
In general, genetic and physical states probably affect each person’s likelihood of developing Parkinson’s disease differently, making them more or less vulnerable to certain common exposures, such as pesticides or solvents.
18. PARKINSON’S DISEASE RISK FROM AMBIENT EXPOSURE TO PESTICIDES
Due to the heavy and expanding agricultural use of neurotoxic pesticides suspected to affect dopaminergic neurons, it is imperative to closely examine the role of pesticides in the development of Parkinson’s disease (PD).
19. NEW STUDIES SUPPORT LINK BETWEEN CHEMICALS AND PARKINSON’S DISEASE
20. PESTICIDE USE UPS PARKINSON’S IN MEN
21. PESTICIDES & PARKINSON’S: WHAT EVERYONE SHOULD KNOW (APDA)
Studies of people living near the Central Valley in California and who were exposed to both maneb and the herbicide paraquat were at a much higher risk of developing Parkinson’s disease (PD) than those who were exposed to only one of the two chemicals. Farmers who use pesticides and their spouses have been found to be 2.5 times more likely to develop PD.
22. INTERACTION BETWEEN ABCB1 AND PROFESSIONAL EXPOSURE TO ORGANOCHLORINE INSECTICIDES IN PARKINSON DISEASE
Objective To study the association between Parkinson disease (PD) and 2 polymorphisms in ABCB1among subjects enrolled in the French health system for agricultural workers (Mutualité Sociale Agricole), as well as the interaction between ABCB1 and organochlorine insecticides.
23. CYP2D6 POLYMORPHISM, PESTICIDE EXPOSURE, AND PARKINSON’S DISEASE.
Source: National Institute of Health and Medical Research (INSERM) Unit 360, Hôpital de la Salpêtrière, 47 boulevard de l’Hôpital, 75651 Paris Cedex 13, France. elbaz@chups,jussieu.fr
We performed a case-control study of Parkinson’s disease (PD) in a population characterized by a high prevalence of pesticide exposure and studied the joint effect of pesticide exposure and CYP2D6. Although they are based on a small group of subjects with the joint exposure, our findings are consistent with a gene-environment interaction disease model according to which (1) pesticides have a modest effect in subjects who are not CYP2D6 poor metabolizers, (2) pesticides’ effect is increased in poor metabolizers (approximately twofold), and (3) poor metabolizers are not at increased PD risk in the absence of pesticide exposure.
24. RESEARCHERS SAY PESTICIDE EXPOSURE AND HEAD TRAUMA ARE FACTORS IN PARKINSON’S DISEASE
25. TOXICANT AND DISEASE DATABASE AND PARKINSON’S DISEASE / MOVEMENT DISORDERS
26. WORLD HEALTH ORGANIZATION:
more researches at world level at: http://www.who.int/heli/risks/toxics/chemicalsdirectory/en/index1.html
27. NIH DATA BASE
28. IS PESTICIDE USE RELATED TO PARKINSON DISEASE? SOME CLUES TO HETEROGENEITY IN STUDY RESULTS
29. PESTICIDE ASSESSMENT: PROTECTING PUBLIC HEALTH ON THE HOME TURF
Pesticide regulation is examined in the context of Health Canada’s Pest Management Regulatory Agency’s assessment of the chlorophenoxy herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) for turf. 2,4-D is the most common herbicide used to kill weeds in grass.
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