New Research Shows Two of the Leading Killers in America Might be Linked

“We know there’s a link,” says Heather Snyder, senior associate director of Medical and Scientific Relations for the Alzheimer’s Association. “What we’re trying to find out is the why.”

Snyder is speaking of two of this country’s worst scourges: Alzheimer’s disease and diabetes. Both are major killers. According to the Centers for Disease Control and Prevention, they are, respectively, the sixth and seventh leading causes of death in the U.S.

Now, research has begun to suggest that they share something else besides a capacity for death—namely, a common organic thread. For that reason, research into one may lead to successful means of dealing with the other.

To begin with, 26 million people in the U.S. have diabetes, 7 million of whom don’t even know they are affected, according to the National Institute of Diabetes and Digestive and Kidney Disease. But regardless of awareness, diabetes remains a condition whereby too much sugar builds up in the bloodstream because the body cannot use insulin effectively. That is, the body stops producing sufficient insulin to help cells absorb sugar and turn it into energy.

Certain segments of the population have a disproportionate rate of diabetes, including Hispanic, African, Asian and Native Americans. According to the National Institutes of Health, 8.3 percent of the U.S. population have diabetes, but more than 16.1 percent of the adult population of American Indians and Alaska Natives have been diagnosed with it. The rates of diabetes vary by region, with American Indians in southern Arizona suffering the highest rates in the country at 33.5 percent.

Diabetes and Alzheimer’s have several links. For example, insulin resistance and type 2 diabetes increase the risk of both heart disease and stroke. Damaged blood vessels can result from either of these conditions, and researchers believe that damaged vessels in the brain may well contribute to Alzheimer’s.

Further, our brain cells use a high level of energy, which can be affected by diabetes because the disease retards the body’s ability to absorb sugar to generate the necessary energy. Healthy brain function also depends on a symphony of many different chemicals working in concert. Too much insulin can throw off the balance of these chemicals and potentially trigger Alzheimer’s. Finally, high blood sugar causes inflammation, which could damage brain cells and help Alzheimer’s develop.

Tackling the connection between diabetes and Alzheimer’s disease may ultimately involve a better understanding of vascular dementia, a disease with the same symptoms as Alzheimer’s. But as Snyder puts it, “Of the top 10 causes of death in the United States, Alzheimer’s is the only one without any way to prevent, cure or slow its progression.” Vascular dementia, by contrast, can be prevented or managed through many of the same healthy habits that can also reduce the risk of diabetes.

“[Vascular dementia] results from hypertension, a high-fat diet, smoking and uncontrolled diabetes,” says Carson Henderson, associate director of Two Hawk Institute, an Indian-owned and -operated corporation focused on health education, training and research in Indian country. “If you exercise, eat right, and don’t smoke, you might be able to prevent vascular dementia as you age.”

Vascular dementia is caused by low blood flow to the brain, often as the result of a stroke or series of strokes. “With vascular dementia, your brain cells are dying, because small, tiny blood vessels in the brain are being blocked, and the cells below are not receiving blood or oxygen,” explains Carson Henderson’s husband, Neil Henderson, Oklahoma Choctaw, who directs the American Indian Diabetes Prevention Center at the University of Oklahoma Health Sciences Center’s College of Public Health. “Vascular dementia looks a lot like Alzheimer’s disease, but it is not the same causation. You still get memory loss and confused thinking.”

The latest link between diabetes and dementia was established by a recent study undertaken by Kyushu University in Japan. Researchers analyzed “1,017 community-dwelling dementia-free subjects” over the course of 15 years and found that Alzheimer’s disease and vascular dementia “were significantly higher in subjects with diabetes then in those with normal glucose tolerance.”

Snyder puts the significance of the finding this way: “Diabetes affects your heart, and there are links between cardiovascular health and brain health. The brain uses 25 percent of the oxygen in blood for its functions, if the heart isn’t healthy, the brain won’t be healthy, either.”

So the ties between diabetes and heart disease and stroke continue to be uncovered. Now, with the possibility that diabetes might be among the causes of one of America’s most lethal diseases, organizations like the Alzheimer’s Association are doing everything they can to spread awareness—and prevention.

Source: A Deadly Duo: New Research Shows Two of the Leading Killers in America Might be Linked
By ICTMN Staff December 14, 2011

“We know there’s a link,” says Heather Snyder, senior associate director of Medical and Scientific Relations for the Alzheimer’s Association. “What we’re trying to find out is the why.”

Snyder is speaking of two of this country’s worst scourges: Alzheimer’s disease and diabetes. Both are major killers. According to the Centers for Disease Control and Prevention, they are, respectively, the sixth and seventh leading causes of death in the U.S.

Now, research has begun to suggest that they share something else besides a capacity for death—namely, a common organic thread. For that reason, research into one may lead to successful means of dealing with the other.

To begin with, 26 million people in the U.S. have diabetes, 7 million of whom don’t even know they are affected, according to the National Institute of Diabetes and Digestive and Kidney Disease. But regardless of awareness, diabetes remains a condition whereby too much sugar builds up in the bloodstream because the body cannot use insulin effectively. That is, the body stops producing sufficient insulin to help cells absorb sugar and turn it into energy.

Certain segments of the population have a disproportionate rate of diabetes, including Hispanic, African, Asian and Native Americans. According to the National Institutes of Health, 8.3 percent of the U.S. population have diabetes, but more than 16.1 percent of the adult population of American Indians and Alaska Natives have been diagnosed with it. The rates of diabetes vary by region, with American Indians in southern Arizona suffering the highest rates in the country at 33.5 percent.

Diabetes and Alzheimer’s have several links. For example, insulin resistance and type 2 diabetes increase the risk of both heart disease and stroke. Damaged blood vessels can result from either of these conditions, and researchers believe that damaged vessels in the brain may well contribute to Alzheimer’s.

Further, our brain cells use a high level of energy, which can be affected by diabetes because the disease retards the body’s ability to absorb sugar to generate the necessary energy. Healthy brain function also depends on a symphony of many different chemicals working in concert. Too much insulin can throw off the balance of these chemicals and potentially trigger Alzheimer’s. Finally, high blood sugar causes inflammation, which could damage brain cells and help Alzheimer’s develop.

Tackling the connection between diabetes and Alzheimer’s disease may ultimately involve a better understanding of vascular dementia, a disease with the same symptoms as Alzheimer’s. But as Snyder puts it, “Of the top 10 causes of death in the United States, Alzheimer’s is the only one without any way to prevent, cure or slow its progression.” Vascular dementia, by contrast, can be prevented or managed through many of the same healthy habits that can also reduce the risk of diabetes.

“[Vascular dementia] results from hypertension, a high-fat diet, smoking and uncontrolled diabetes,” says Carson Henderson, associate director of Two Hawk Institute, an Indian-owned and -operated corporation focused on health education, training and research in Indian country. “If you exercise, eat right, and don’t smoke, you might be able to prevent vascular dementia as you age.”

Vascular dementia is caused by low blood flow to the brain, often as the result of a stroke or series of strokes. “With vascular dementia, your brain cells are dying, because small, tiny blood vessels in the brain are being blocked, and the cells below are not receiving blood or oxygen,” explains Carson Henderson’s husband, Neil Henderson, Oklahoma Choctaw, who directs the American Indian Diabetes Prevention Center at the University of Oklahoma Health Sciences Center’s College of Public Health. “Vascular dementia looks a lot like Alzheimer’s disease, but it is not the same causation. You still get memory loss and confused thinking.”

The latest link between diabetes and dementia was established by a recent study undertaken by Kyushu University in Japan. Researchers analyzed “1,017 community-dwelling dementia-free subjects” over the course of 15 years and found that Alzheimer’s disease and vascular dementia “were significantly higher in subjects with diabetes then in those with normal glucose tolerance.”

Snyder puts the significance of the finding this way: “Diabetes affects your heart, and there are links between cardiovascular health and brain health. The brain uses 25 percent of the oxygen in blood for its functions, if the heart isn’t healthy, the brain won’t be healthy, either.”

So the ties between diabetes and heart disease and stroke continue to be uncovered. Now, with the possibility that diabetes might be among the causes of one of America’s most lethal diseases, organizations like the Alzheimer’s Association are doing everything they can to spread awareness—and prevention.

Authors: ICTMN Staff December 14, 2011

Republished by courtesy of Indian Country Today Media Network
Original Source: A Deadly Duo: New Research Shows Two of the Leading Killers in America Might be Linked
Twitter: Indian Country

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Children in rural communities get a “double-dose” of the pesticide chlorpyrifos from food and drift from neighboring fields

Washington, DC — As children settle into the new school year, health professionals are demanding that the Environmental Protection Agency (EPA) ban the neurotoxic chemical chlorpyrifos, a pesticide used on farms throughout the country and the same chemical that the agency banned some ten years ago for use in homes.

In a letter to be submitted to EPA tomorrow, over two dozen health professionals cite new science showing the health impacts of chlorpyrifos, including lowering IQs and increasing the risk of ADHD and learning disabilities among children.

“EPA should follow the science and take this brain toxin completely off the market” said Dr. David Carpenter, MD, Director Institute for Health & The Environment, University at Albany. “Chlorpyrifos poses serious threats to children’s health and doesn’t belong in our homes, on our farms, or on our cafeteria trays.”

The recent studies show that exposure to chlorpyrifos in the womb and in early childhood, during critical development “windows,” can lead to lasting effects on the brain. Researchers now say that as many as 25% of all U.S. children may have IQs several points lower due to eating foods treated with chlorpyrifos and similar pesticides.

“Fruits and vegetables are essential for healthy children but shouldn’t be grown with chlorpyrifos,”said Ted Schettler, MD, MPH, Science Director of the Science and Environmental Health Network, and one of the letter’s signatories. “Children in rural communities face a double dose of this brain poison. They are exposed to chlorpyrifos drifting from neighboring fields, and again when the pesticide is on their food.”

Chlorpyrifos was banned for use in homes over ten years ago because of it’s potential harm to children. But ten million pounds of chlorpyrifos are still used on agricultural fields each year. Air monitoring, biomonitoringand poisoning data confirm that extensive human exposure to chlorpyrifos is linked to its continued use in agriculture. According to data from the Centers for Disease Control,the vast majority of us — including children — carry breakdown products of the chemical in our bodies.

Children living in farm communities are at especially high risk. In addition to exposure from food they may also be breathing in particles that drift into their classrooms and homes from nearby farms. Farmworker children are exposed even more, as parents sometimes carry residues of the pesticide home at the end of the day on clothing and shoes.

“Chlorpyrifos drift poses serious threats to communities like mine,” said Luis Medellin, of the community organization El Quinto Sol de America. Luis grew up in homes next to farms using chlorpyrifos in California’s San Joaquin Valley. “The realities on the ground show that this brain toxin can’t be used safely and should not be used in the fields.”

At age 17, Luis began using Pesticide Action Network’s Drift Catcher to document chemical drift from neighboring citrus fields, finding that a majority of samples contained chlorpyrifos. Residents also sampled chlorpyrifos in their urine, and all but one had levels above what EPA considers “acceptable.”

In their letter to EPA (pdf), health professionals are demanding that EPA ban all uses of chlorpyrifos. In their letter they state:

We urge EPA to act now on the weight of scientific evidence of health harms of chlorpyrifos for children and fetuses. It is time that EPA take action to protect the public health and provide a healthy legacy for our children and for future generations. We call on EPA to cancel all uses of pesticide chlorpyrifos.

Other letters with a similar demand were delivered to EPA from environmental health groups nationwide, including a petition signed by more than 6,000 concerned citizens across the country.

Author:

PAN, Toxic Brain Chemical Must Be Banned: Health Professionals Demand EPA Take Action, October 5, 2011

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Several experts from different European countries agree that Electromagnetic Hypersensitivity is a real, physical illness and for some of them this condition seems to be strictly related to Multiple Chemical Sensitivity (MCS). This is what came out of the congress “Mobile Telephony, Wi-Fi, Wi-Max: Are there Health Risks?”, held at Palazzo Marini – Chamber of Deputees in Rome on 14 June 2011. The event, organized by the Association for Environmental and Chronic Toxic Injury (A.M.I.C.A.), was meant to give an overview on the health dangers linked to the use of wireless devices.

Prof. Dominique Belpomme, Oncologist, Professor of the Centre Hospitalier Universitaire Necker-Enfants Malades, Chairman of Research for Anti-Cancer Therapeutics (ARTAC), in his lecture “Diagnostic and Therapeutic Protocols for Electromagnetic Fields Intolerance”, showed the results of a clinical observation on more than 450 patients enrolled from 2008 to 2011. He and his team use a new technique to make the diagnosis to people reporting reactions to electromagnetic fields, a condition that he prefers to define as “Electromagnetic Fields Intolerance” or “EFI Syndrome” rather than “Electromagnetic Hyper-Sensitivity”.

The new technique is the “Pulsed Eco-Doppler” of the brain that combines the eco-doppler with a computer to evaluate brain perfusion. Unlike some other methods, this one is not dangerous and it does not involve any ionizing radiation. The results show that people with Electromagnetic Fields Intolerance have a reduced perfusion in the brain, particularly in the left part of the limbic area of the brain, compared to the control group. This is a very particular area, because it is the “ancient” part of the brain that controls many body functions.

“These results are very important – Belpomme said at the congress – because for the first time we are able to define the Electromagnetic Fields Intolerance as a physical illness based on objective tests”.

His team uses also other tests, such as the dosage of histamine, of protein S100B, and of heat shock proteins hsp70 and hsp27 in the blood. The 70% of the group of patients observed showed a serious reduction of vitamin D, about 1-2% of the patients showed an increase of proteins hsp27 and hsp70, while more than the 40% of the sample had increased histamine, a fact that is fully compatible with a physiological interpretation of this syndrome.

About 10% of the patients had an increased protein S100B, which is a marker for Blood Brain Barrier (BBB) permeability. In one third of the sample, a reduction of melatonin in urine was found, and this can explain symptoms such as fatigue, insomnia and depression in these patients.

These alterations are quite similar to the ones found in patients with Multiple Chemical Sensitivity (MCS), particularly regarding the brain perfusion reduction, the neurogenic inflammation, the oxidative stress increase, and the reduction of the defense mechanism. The fact that EMF induces the opening of the BBB may interfere with the brain protection from toxic chemicals. It is not uncommon, in fact, that patients with EFI Syndrome have MCS symptoms, while many patients with MCS also react to EMF.

The increase of oxidative stress in electrosensitive patients was found also by Dr. Valeria Pacifico, who lectured in Rome about “Metabolic biomarkers of oxidation-reduction imbalance and susceptibility to non-ionizing radiation”. She works in the team of Dr. Chiara De Luca at the Experimental Laboratory BILARA at Istituto Dermopatico of Immaculata in Rome that published several works on the role of oxidative stress in environmental sensitivities. (1, 2)

“To make a diagnosis of this syndrome we need to listen first to patients and we need to verify if the symptoms improve or disappear when they stay away from EMF sources”, Prof. Belpomme explained. In order to demonstrate if the electromagnetic fields were the real cause of the alterations found in these patients, the patients had to repeat the tests before and after a period of avoidance of EMF for three months. The results show that after the period of avoidance the levels tend toward the normal standard.

Given the strong correlation found by six epidemiologic studies on EMF exposure and Alzheimer Disease (AD), Prof. Belpomme believes that any electrosensitive patient with memory dysfunctions should be evaluated also for AD. He stresses the fact that AD is a loss of long term memory while EFI Syndrome often involves the loss of short term memory, but this symptom may be considered as a pre-Alzheimer condition.

Prof. Olle Johansson, Assoc. Prof., The Experimental Dermatology Unit, Department of Neuroscience, Karolinska Institute; Professor, The Royal Institute of Technology, Stockholm, talked in Rome about “The precautionary principle: from Bioinititive to the Seletun consensus”. He dedicated his lecture to people affected by EHS and MCS because “they have a very difficult life”.

He is one of the most dedicated scientists in the promotion of new biologically-based safety guidelines for EMF. He was in Benevento for the ICEMS resolution in 2006, then in London in 2007 for a new resolution, and he was also member of the group of independent scientists that published the famous Bioinitiative Report in 2007, which had strong ecological concern in the political agenda. Thanks to this report, in fact, the European Parliament signed a resolution on September 4, 2008 to state that the actual safety limits for EMF are obsolete and to warn EU governments about the increase of new environmental illnesses such as EHS, MCS and Dental Amalgam Mercury Syndrome.

More recently, Prof. Johansson was part of the group of scientists who prepared the Seletun Consensus, published last February in Reviews on Environmental Health (3). It states that present standards do not protect global human population from electromagnetic fields and all EMF should be reduced now instead of waiting for a definitive proof of danger. It also states that people reporting EHS symptoms should be considered as having a functional disability.

In Sweden, for example, EHS, MCS and fibromyalgia are already classified as functional disabilities. This means that people affected by these conditions are not considered patients, but it’s the environment that creates limitations for them so it’s the environment that has to be changed. This kind of classification represents the full concretization of the UN Convention on the Rights of Persons with Disabilities, signed by governments on March 30, 2007. This convention should be enough to push all governments to find the right accommodation and the best welfare strategies for people with environmental sensitivities, and put an end to discrimination.

Author: Francesca Romana Orlando, journalist and Vice President of A.M.I.C.A.

Literature:

1. De Luca C. et al., Biological definition of multiple chemical sensitivity from redox state and cytokine profiling and not from polymorphisms of xenobiotic-metabolizing enzymes, Toxicology and Applied Pharmacology, YTAAP-11818; No. of pages: 8; 4C.
2. De Luca C. et al., The Search for Reliable Biomarkers of Disease in Multiple Chemical Sensitivity and Other Environmental Intolerances, Int. J. Environ. Res. Public Health 2011, 8, 2770-2797; doi:10.3390/ijerph8072770
3. Fragopoulou A ed al., Scientific panel on electromagnetic field health risks: consensus points, recommendations, and rationales, Rev Environ Health. 2010 Oct-Dec; 25(4):307-17.

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Were pesticides to blame for the death of Knut, the polar bear?

Many thousands of people mourn the sudden death of Knut, the polar bear. He was the darling at a German zoo. Why did Knut die? Initial autopsy results showed that Knut, the polar bear, suffered from a brain disease. A former animal keeper at a zoo reported the death of gorilla babies dying from pesticide use. The keeper herself fell ill and nearly died. Were pesticides the cause of death of the polar bear, Knut? Recent scientific research has shown that pesticides cause different brain diseases. What caused Knut’s brain disease will require further investigation. It is possible, because pesticides are used regularly in zoos to keep the zoo animals free of vermin.

All mourn the loss of Knut, the polar bear

In the media, on Twitter and Facebook, the death of Knut, the polar bear , remains the main topic for days now. The sweet polar bear was raised by a nurse with a bottle in the German zoo after his mother abandoned him. The little polar bear in no time, won the hearts of all the visitors. Now the sadness is great, and the cause of Knut’s brain disease is still under investigation. Zoo visitors witnessed the polar bear turning itself around several times and falling into the pond. Over 500 people observed the death of this polar bear and reported that he had an epileptic-like seizure before he sank into the water in his polar bear enclosure. Knut’s keeper also died suddenly at the age of 44 from a heart attack in 2008.

Dream job, but health went downhill

The young woman worked in one of the biggest zoos in Germany. She loved her job as a veterinary nurse above everything. She was responsible for the gorillas. With the bottle, she helped gorilla babies grow when needed. Most of all, she never wanted to go home after work because she loved her job so much. During her training, her health was deteriorating. The reason for her health decline was first discovered years later. Several radiological studies including SPECT, CT, and MRT scans of her brain showed severe brain damage and atrophy. Pesticides were the reason the keeper’s health went downhill.

Gorilla babies dead due to the use of pesticides

During training, the young keeper had to deal with pesticides during the spraying of the gorilla’s sleeping quarters. The pesticide nerve agents, pyrethroids and organophosphates were used. The young woman had to spray the sleeping caves. As she kneeled in front of the caves, she couldn’t avoid breathing in the poison. “The gorilla babies died, and now I know it was because they were exposed to the pesticides,” she told me several years ago when we met at a special clinic. Her immune and nervous system were severely damaged, and she had problems with her muscles and her heart was weakening. Her hair was falling out and she had the typical nerve agent seizures. She stated, “I initiated a workers’ compensation lawsuit and won.” There was no question that the health of the animal keeper was destroyed by pesticides.

Knut died from pesticide exposure?

We do not know exactly which brain disease Knut, the public’s favorite animal in the Berlin Zoo, suffered from, but further studies will hopefully determine the nature and cause of his brain disease. Pesticides may well be on the short list, because they are regularly used in zoos to keep the zoo animals free of fleas and other parasites. Certain herbicides, which are often used on pavements and along roadsides in zoos in order to be kept free of weeds, are quite capable of causing life-threatening seizures.

Author: Silvia K. Müller, CSN – Chemical Sensitivity Network, March 21, 2011

Translation: Thanks to Christi Howarth.

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Nutritional supplementation with Spirulina, a nutrient-rich, blue-green algae, appeared to provide neuroprotective support for dying motor neurons in a mouse model of amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, University of South Florida neuroscientists have found. Although more research is needed, they suggest that a spirulina-supplemented diet may provide clinical benefits for ALS patients.

A spirulina dietary supplement was shown to delay the onset of motor symptoms and disease progression, reducing inflammatory markers and motor neuron death in a G93A mouse model of ALS. Spirulina, an ancient food source used by the Aztecs, may have a dual antioxidant and anti-inflammatory effect on motor neurons, the researchers said.

Their study is published (pdf) in the current issue of The Open Tissue Engineering and Regenerative Medicine Journal (3:36-41).

“ALS is a degenerative motor neuron disease,” said the study’s lead author, Svitlana Garbuzova-Davis, PhD, DSc, assistant professor in the Department of Neurosurgery and Brain Repair at USF. “Most available treatments relieve symptoms without altering the underlying disease. However, evidence for oxidative stress has been associated with ALS and, in our past studies, we demonstrated potent decreases in markers of oxidative damage and inflammation in aged rats fed diets supplemented with spirulina or spinach. In this initial study, the diet supplement was fed only to pre-symptomatic mice. Further studies showing the diet supplement’s effect on the lifespan of symptomatic ALS mice are needed to prove the treatment’s effectiveness.”

Specifically, when the USF researchers tested compounds found in blueberries and spirulina for effectiveness in animal models of stroke and aging in past experiments, they noted neuroprotective effects of the nutritional supplements.

The current study compared ALS mice receiving a spirulina-supplemented diet over a 10-week period with mice that did not receive the diet supplementation. The spirulina-fed ALS mice showed reduced inflammatory markers and motor neuron degeneration over that period.

“The focus of our future ALS experiments will include motor neuron counts and an examination of lifespan following dietary spirulina supplementation in symptomatic ALS mice,” said study co-author Paula C. Bickford, PhD, a professor in the USF Department of Neurosurgery and Brain Repair and a senior research biologist at the James A. Haley Veterans’ Hospital in Tampa.

Reference:

University of South Florida (USF Health), Blue-green algae tested for treating ALS, 21-Dec-2010

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Urgent action needed on dioxins, says toxicologist

The environmental scientist whose work on dioxins last year prompted governments around the world to suspend the use of some pesticides says there is more to the problem and authorities need to act urgently.

Although dioxins have been banned from the ingredients of pesticides in Australia for more than a decade, many dioxins emerged in the manufacturing process and there was no end-stage monitoring to protect consumers and the public, said University of Queensland scientist Dr Caroline Gaus.

Numerous environmental and health issues were associated with undeclared dioxin impurities, said Dr Gaus, an environmental toxicologist with the National Research Institute for Environmental Toxicology (ENTOX).

Little information was available about the impurities because they were created during the production process so were not original ingredients.

“We estimate that the amount of these impurities is relatively high compared to other current dioxin sources, but this cannot be adequately quantified due to the commercial protection of data on pesticides use in Australia and internationally,” Dr Gaus said.

She said pesticides with impurities used in high volumes represented a previously neglected but significant and concerning source of dioxins in the environment. They also posed a risk to the health of people handling pesticides, and to consumers.

“Some of these pesticides contained high concentrations of dioxins, comparable to those known from pesticides which are banned or restricted for use in most countries since the 1980s and 90s,” she said.

Dioxins are linked to a range of cancers and are considered one of the most toxic man-made chemicals. They can cause adverse health effects in humans and wildlife including cancer, and act on development, reproduction and the endocrine system.

Research by Dr Gaus and PhD student Eva Holt last year showed that a wide range of currently used and globally marketed pesticides contained dioxin impurities, despite the widespread belief that modern pesticides were no longer a significant dioxin source.

As a result of their work, a new wave of suspensions, recalls, restrictions and government reviews on pesticide formulations is under way worldwide, including in the United States, Canada, New Zealand and Australia.

The study analysed 23 different pesticide formulations, containing 15 different active ingredients currently used in Australia (plus four formulations that are no longer registered for use in Australia), including insecticides, herbicides and fungicides. Dioxins were detected in all samples, including some commonly used products. Researchers estimate approximately 200 pesticides have the potential to contain dioxins.

The pesticides are used on crops including cotton, potatoes, lettuce, tomatoes, beans and peanuts, as well as in parks and recreation areas, at turf farms and plant nurseries.

“In view of the global manufacturing, distribution and use of pesticides, international regulation and monitoring strategies should be developed and implemented to identify, evaluate, and target pesticide dioxin sources at the manufacturing stage,” Dr Gaus said.

Some Recent Restrictions

The Australian Pesticides and Veterinary Medicines Authority (APVMA) suspended all formulations containing quintozene (pentachloronitrobenzene) from use in April this year due to risk to workers applying the pesticide, which was commonly used on golf courses. The fungicide is under review in New Zealand where it is used on bulbs and turf. The manufacturer recently initiated a voluntary recall of product containing quintozene. The APVMA has recently suspended the pesticide PCNB from sale and a stop sale order has been issued by the US Environmental Protection Agency.

About Dioxins

• Dioxins are toxic compounds which have adverse health effects in humans and wildlife. They can elicit adverse health effects at low levels (cancer, immunotoxicity, reproduction, endocrine function, development).
• These toxicants are managed under the international Stockholm Convention treaty which aims to protect human health and the environment by reducing and eliminating dioxin release to the environment. More than 150 countries, including Australia, have ratified the Stockholm Convention treaty since 2004.
• Most chlorinated pesticides have the potential to contain dioxins if manufactured under certain conditions and processes (e.g. > 150 ºC, alkaline conditions, process including chlorine) – the US EPA lists 161 chemicals (but it is not complete – PCNB for example is not listed). Thus, pesticides were considered historical sources of dioxins and contemporary monitoring data in most current-use pesticides are lacking.
• Dioxin impurities can vary between manufacturing facility, batch, year and country due to variations in production processes and conditions.

About the Research

• 23 different formulations containing 15 different active ingredients currently used in Australia (plus 4 formulations that are no longer registered for use in Australia), including insecticides, herbicides and fungicides, were analysed. Dioxins were detected in all samples. These include commonly used pesticides, such as PCNB, MCPA, 2,4-D, chlorothalonil and triclopyr/picloram. Others are Fluroxypyr, Mecoprop, Flumetsulam, Imazamox, Prochloraz, Fenamisphos, Chlorpyrifos, Lindane; 2,4-D; 2,4-DB; Chlorthal amd Quintozene.
• Some of these pesticide formulations contained high concentrations of dioxins, comparable to those known from pesticides which are banned or restricted for use in most countries since the 1980/90s.
• Highest dioxin (1,100-2,000 mg/tonne AI) and TEQ (2,400-5,700 µg/tonne AI) concentrations were found in the fungicide quintozene (also known as pentachloronitrobenzene (PCNB)).
• Dioxin concentrations in PCNB are comparable to those known from the banned pesticides 2,4,5-T (trichlorophenoxyacetic acid; the key ingredient of Agent Orange). Note: TEQ concentrations in PCNB are at the lower end for those known for 2,4,5-T (approaching the 7,000 µg/tonne used under the Stockholm Convention to estimate historical dioxin releases via past use of 2,4,5-T).
• There are about 6000 pesticide products on the market in Australia (containing ~2000 different active ingredients) – the UQ/ENTOX scientists analysed only a small proportion (0.4 per cent) of these.
• Dioxin concentrations in other pesticides analysed ranged from 61-190 ug TEQ/tonne AI. Impurity concentrations may vary considerably depending on the conditions employed during pesticide production and should therefore be monitored regularly.
• As many pesticides are used in high volumes, they can represent previously neglected but important sources of dioxins to the environment and pose a risk to the health of people handling pesticides.
• Based on these findings, the APVMA have recently suspended the pesticide PCNB, due to dioxin contamination and the associated risks to pesticide applicators. Similarly, the US EPA have issued a stop sale order for PCNB.
• The estimated release of dioxins from the use of PCNB is 27 g TEQ/year (10-90th percentile range: 14-110 g TEQ/year). The dioxin release from this pesticide alone ranks among the top 5 dioxin sources to land in Australia (range 28-110 g TEQ/year).
• The greatest source of uncertainty with these estimates is the lack of information on pesticide use volumes in Australia, which is commercial in confidence and thus not publicly available. This is why the dioxin release associated with many of the pesticides analysed by the UQ/ENTOX scientists could not be estimated to date (has to be modelled)
• The cumulative dioxin release associated with high volume-use of different pesticides may be an important source of dioxins, even if pesticides contain lower dioxin levels than PCNB, e.g. if all pesticide products were contaminated at levels ranging from 100-10,000 µg TEQ/tonne AI and used at a total of 200,000 tonnes per year, then the annual dioxin release would be between 20 and 2000 g TEQ/year.

Note: data on the amount of pesticides used in Australia is not publicly available (commercial in confidence), total pesticide use may be considerably higher than 200,000 tonnes (approximately 2.25 million tonnes of pesticides a year are used in the USA, including 1.18 million tonnes per year of chlorine and hypochlorite pesticides).

The study was funded by an Australian Research Council Discovery Grant and undertaken by the National Research Institute for Environmental Toxicology, University of Queensland (Eva Holt, Caroline Gaus) in collaboration with the National Measurement Institute in Sydney (Gavin Stevenson) and collaborators from Germany (Roland Weber).

The United Nations Environmental Protection Agency has used the data from the study to develop a burden of toxicology measure for use worldwide. It helps identify and prioritise dioxin sources.

Reference:

University of Queensland, Urgent action needed on dioxins, says toxicologist, December 6, 2010

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• Chemical Threat: Groups call for Pesticide Ban
• Anxiety in adult female mice following perinatal exposure to Chlorpyrifos
• EFSA publishes European overview of Dioxin Levels in Food and Feed

Consumers, Parents, Health Advocates, Farm Workers and Others Target Widely Used Pesticides Linked to Attention and Learning Problems

(Yakima, WA) 13,000 individuals and organizations from across the U.S. sent a letter to the U.S. Environmental Protection Agency (EPA) today calling for a ban on the pesticide chlorpyrifos and a phase out of other organophosphate (OP) pesticides.

Dr. Theo Colborn’s organization TEDX (The Endocrine Disruption Exchange) concurrently announced the addition of chlorpyrifos to their publicly-accessible on-line database, Critical Windows of Development, spotlighting animal research that links prenatal, low dose chlorpyrifos exposure to altered health outcomes in the brain and other organs.

“Human studies have now linked prenatal exposure to chlorpyrifos with mental and developmental delays emphasizing even more the urgency to remove the product from the market,” said Colborn, President of TEDX and a signatory on the letter. “Chlorpyrifos illustrates the urgent need to be cautious, prevent further exposure and protect our children from the time they are conceived onward,” she said.

Dr. David Carpenter, M.D. and Director of the Institute for Health and the Environment at the University of Albany said, “It is unacceptable that farm worker children, and children in the general population continue to be exposed to these neurotoxins.”

“As more families cope with the suffering and costs of learning and developmental disabilities and attention problems, EPA must prevent further exposures to neurotoxic pesticides,” said Maureen Swanson of the Learning Disabilities Association of America. “EPA needs to protect people, especially children and pregnant women, from any chemical that threatens brain development. In addition to banning neurotoxic pesticides, we must reform the Toxic Substance Control Act to require EPA to address the many neurotoxic chemicals in our everyday products,” she said.

“The last time EPA reviewed these pesticides, its own scientists complained that the Agency was not assuring adequate protection of the nation’s children, and that it was unduly influenced by those it regulates,” said Dr. William Hirzy, a professor at American University in Washington D.C. and a former EPA chemist. While at EPA, Hirzy was involved in a letter raising these concerns sent to management by six unions representing 9000 EPA scientists and other staff, as the Agency was finalizing its Cumulative Risk Assessment for organophosphates in 2006. “Five years later, with even more sobering studies in hand, will EPA finally act to protect children?” Hirzy asked.

“The warning signs have been obvious for decades, yet EPA has allowed generation after generation to suffer exposures and consequences,” said Carol Dansereau, Executive Director of the Farm Worker Pesticide Project, a Washington State farm worker organization that initiated the letter to EPA. “EPA is promising to better protect children and other vulnerable people, but that promise is meaningless as long as it keeps reregistering chlorpyrifos and other organophosphates, ” she said. FWPP and others are asking the public to contact EPA and join in demanding a ban, and precaution-based policies.

“Unfortunately chlorpyrifos and other organophosphates do not stay where sprayed. They evaporate and move with wind and fog. That’s how they contaminated our fields,” said Larry Jacobs of Jacobs Farm/Del Cabo, an organic grower in California. “There are better ways to manage insect pests than depending on organophosphates like chlorpyrifos. We signed onto the letter to EPA to protect our health and to protect our farm.”

EPA is in the process of considering re-registration for chlorpyrifos, one of the most widely used pesticides in agriculture in the US and worldwide.

More Information:

Fact Sheets: On Health Effects, Industry Influence on EPA, Regulatory Status, Use/Exposures/Alternatives, the Letter and Signers

Literature:

United Farm Workers, Chemical Threat: Groups Call for Pesticide Ban – Consumers, Parents, Health Advocates, Farm Workers and Others Target Widely Used Pesticides Linked to Attention and Learning Problems, 10/13/2010

Related articles:

• Prenatal Exposure to Pesticides linked to ADHD
• Groups Seeking Ban on Organophosphate Pesticide Go to Federal Court
• President’s Cancer Panel: Organic Foods reduce Environmental Risks
• Earthday – Ontarion Lawns and Gardens getting Greener and Pesticide free

Daily chemical exposures at low doses can affect our health

ROME – On September 24, 2010, from 8:30 a.m. to 5:30 p.m., the congress “New Environmental Diseases” was held at the Chamber of Deputees Congress Hall in Rome. The event was organized by A.M.I.C.A. (Association for Environmental and Chronic Toxic Injury), the Italian organization that works for the rights of people with MCS and EHS, and it was supported by Mep Domenico Scilipoti, an oncologist, holistic doctor, and rapporteur of a draft to become law on environmental diseases and disabilities and also for the phasing out of dental amalgam.

“More and more scientific evidence shows how daily chemical exposures at low doses can affect our health. With this event we would like to create a bridge between science and politics in order to have a new legislation, particularly for the protection of those affected by Multiple Chemical Sensitivity, Electromagnetic Hyper Sensitivity, Chronic Fatigue Syndrome and Fibromyalgia. These diseases seem to be correlated one to another,” Francesca Romana Orlando, Vice President of A.M.I.C.A., commented. She has just published the book Il Cerchio Perfetto (The Perfect Circle) about the link between industry, politics, academics, and media and its role in the hiding of toxic dangers to the public.

“Just a few weeks ago, at the Senate Commission for Health, the debate about the draft to become law for the recognition of MCS as an epidemic disease started. The prevalence of this illness is about 10% of the population and in Italy the patients still don’t have any hospital to receive any medical treatment in a proper environment,” Silvia Bigeschi, Vice President of A.M.I.C.A., adds.

There are ten projects to become law for the recognition of MCS as an epidemic disease at the Italian Parliament and, just the day before of the congress, A.M.I.C.A. presented a petition with more than 10,000 signature asking for the approval of a law for MCS and also a petition to the Ministry of Health for the total phase out of dental mercury (amalgam), since many cases of MCS, CFS and EHS seem to be triggered by amalgam fillings.

The congress was divided in four sessions. The first one was about “Diagnostic approaches” for MCS, CFS and FM. Prof. Giuseppe Genovesi of the University of Rome La Sapienza and Dr. Chiara De Luca, Head of the Laboratory BILARA at the Dermatological Institute Immacolata of Rome, presented the results of a study on oxidative stress and genetics in MCS patients, that was recently published on Toxicology Applied Pharmacology (Apr. 26, 2010).

While Dr. De Luca focused on the clear evidence of oxidative stress in these patients, such as the lack of enzyme catalysis and GST, Prof. Genovesi stressed the fact that the results don’t show the prevalence of one specific genetic polymorphism, but most of the patients had one or more genetic factors inducing a lower detoxification. He also announced that they are going to test the genetic predisposition of the enzyme catalysis, since this is so typically low in MCS patients.

Dr. Alberto Migliore, the chief of Rheumatology Department at the S. Pietro Fatebenefratelli Hospital in Rome, published a study about the comorbidity of MCS and Sjogren Syndrome. Dr. Lorenzo Bettoni presented a lecture about the environmental causes of CFS and FM, with an hypothesis about the role of chemicals, EMF pollution, and physical/mental stress on the triggering of these illnesses.

Dr. Giacomo Rao, who works for the Italian National Insurance of Workers (INAIL, the public institute that gives compensation and pension to the workers injured at workplace), talked about the legal aspects of the recognition of these illnesses as a disability. He showed that there are several impact life factors to consider and that in Italy there are now many MCS disability certificates, even if it is always very difficult to convince the commissions about the severity of this illness. He added that the final judgment depends only on the good will of the commissioners to study a new issue.

In the second session entitled “New Paradigms of Toxicology and Environmental Medicine,” Martin L. Pall, Professor Emeritus of Biochemistry and Basic Medical Sciences, Washington State University, presented his theory about the biochemical vicious cycle ON/ONOO – induced by the combination of high NOS activity and Tetrahydrobiopterin (BH4) depletion – and how it is able to explain not only MCS, CFS or FM, but also other emerging neuro-degenerative illnesses such AD, Parkinson or ALS. He commented that the De Luca – Genovesi study about oxidative stress represents a full confirmation of his theory.

Dr. Peter Ohnsorge, President of the European Academy for Environmental Medicine (EUROPAEM), has already applied Pall’s theory to his clinical approach in order to reduce NMDA in the cerebral metabolism. He proceeds in treating inflammation first, by supplementing enzymes, antioxidants, minerals and Vitamins. Then, he offers a chelation therapy, when possible, and also hemapheresis (Membrane Differential Filtration), gut therapy and detoxification. He also uses sauna therapy since the heat helps to increase BH4 and to oppose the vicious NO/ONOO cycle.

Recently, Dr. Ohnsorge was commissioned by the German Ministry of Health and Social Affairs, to do a controlled randomized study about the efficacy of therapies for MCS patients with the double aim of detoxification of lipophilic toxins and improving the complaints. He found out that using a complex therapeutic regime usually allows the patients to recover slowly, but surely.

The MCS people in the audience asked him several questions, for example about the bad secondary effects of supplementation of glutathione (GSH) and about the tests of compatibility of drugs and dental materials. He explained that supplementation has to be given always with very low doses at the beginning in order to avoid violent breaks in the detoxification mechanisms. Moreover, he suggested using the Lymphocyte Transformation Test (LTT) to find out reactions to drugs, metals, plastics and environmental toxins, while the basophil degranulation test is suggested when inflammation is suspected induced by metals, like in the case of titanium implants.

In the same second session, Dr. Ernesto Burgio, Coordinator of the Scientific Committee of ISDE Italia (Doctors for the Environment), gave a lecture about the epigenetic damages caused by environmental toxins and EMFs. The epigenome represents the interface between the information from the environment and the genome, and even in the absence of chromosomal or gene mutations, there still can be a change in the expression of the gene (DNA Methylation) because of an epigenetic injury. “With a few exceptions, cellular differentiation almost never involves a change in the DNA sequence itself,” commented Dr. Burgio.

Since the environment changed too quickly in the latest decades, the capacity of adaptation of the (epi) genome is not enough to compensate it. Thus, a toxic exposure from the parents, in the womb, or during the early childhood can induce a chronic disabling illness later in life.

New studies are being explored on how a lead exposure in infants can be associated to Alzheimer’s disease (AD)-like symptoms years later or how the mother’s exposure to high levels of folic acid, vitamin B12 or to cigarette smoke can induce epigenetic changes that can repress gene transcription and, then, induce phenotypes of asthma (i.e. allergic airway inflammation) in the offspring. These findings could lead to the conclusion that our society is on the edge of a “disevolution.”

In the third section on “Heavy Metals Toxicity,” Dr. Raimondo Pische, President of the International Academy of Bio-Dentistry (AIOB) talked about the risks associated with the exposure to the metals of dental amalgam. In particular, he presented a video of an amalgam fillings showing how mercury vapors are easily released by the amalgam. He underlined the fact that the dentists are the first ones at risk when they pose and remove amalgam fillings and that dental mercury represents the main source of exposure to mercury vapors in not occupational environments. This is no longer acceptable since mercury is the most toxic element in nature after the radioactive elements.

Dr. Antonello Maria Pasciuto, Italian member of the European Academy for Environmental Medicine (EUROPAEM), talked about the LTT-MELISA, the Lymphocyte Transformation Test for the proof of late allergy to metals (type IV). This kind of allergy was observed in patients with MCS, CFS, MS, FM, ALS and autoimmune diseases and it usually improves, as well as the symptoms, after the safe removal of dental metals.

Dr. Gianpaolo Guzzi of the Italian Organization for the Research on Metals and Biocompatibility (A.I.R.M.E.B.) talked about the side effects of chelation therapies. His group studied hundreds of patients with amalgam toxic load and they reviewed the effects of EDTA, DMPS, DMSA and Glutathione. EDTA seems to redistribute metals without really getting rid of them, while DMPS seems more effective on treating elemental mercury, but with severe side effects in some cases. DMSA works to detoxify from methyl mercury and it can also get rid of elemental mercury stocked in the kidneys. Recently Dr. Guzzi’s research group is testing the efficacy of Glutathione in metal detoxification since there aren’t studies about it.

In the last session about “EMF and Health”, Dr. Fiorenzo Marinelli, researcher of the Institute of Molecular Genetics (IGM) in Bologna talked about wireless technologies such as mobile phones, Wi-Fi and Wi-Max. He pointed out the fact that thermal effects are only a part of the biological effects of EMFs, but still these are the only ones considered by international safety standard limits. There are also other effects induced by the signal information in itself. This explains why, even though UMTS has usually a lower intensity of the signal compared to GSM, it uses a wider band of frequencies, then involving a greater risk of damage in the DNA, as the recent European Reflex study showed. His research group has recently studied the effects of radars and Wi-Fi and the preliminary findings show that both these kind of EMFs promote cell proliferation (2010).

Since scientific literature clearly demonstrates that EMF in our everyday life can induce DNA breakage, genetic deregulation as well as chromosomal breakage, increase of free radicals, alteration of neurotransmitters, memory loss, hypersensitivity-allergy, aging and possibly cancer, Dr. Marinelli supports the reduction of the safety limit of exposure to 0,6 V/m, as requested by the International Commission for the Electromagnetic Safety (ICEMS) since 2002.

Finally, Prof. Olle Johansson, associate professor at The Experimental Dermatology Unit – Department of Neuroscience of the Karolinska Institute, and Professor at The Royal Institute of Technology, Sweden, also member of the famous Bioinitiative Working group, presented a lecture about Electro-Hyper-Sensitivity, which is fully recognized as a functional impairment in Sweden. He explained not only the bioeffects of EMF on EHS people, but also the social problem of disability in our modern societies. “Disability is everywhere and it can happen to anyone: I myself have a disability when I am in Italy because I can not speak Italian,” Prof. Johansson commented. He reminded that all modern democracies signed international equal rights UN treaties, but still they leave these principles un-realized when it comes to environmental disability.

Reference:

A.M.I.C.A. congress shows how environmental and chemical pollution cause health injuries and disabilities, Rome, September 25th, 2010

Photo: AMICA

Contact:

Francesca Romana Orlando
Vice President of AMICA
Associazione Malattie da Intossicazione Cronica e/o Ambientale
(Association for Environmental and Chronic Toxic Injury)
P.O. Box 3131, 00121 Rome – Italy
www.infoamica.it amica(at)infoamica.it

Related articles:

• Predictions of Multiple Chemical Sensitivity Mechanism confirmed by Roman Study
• Martin Pall about genetic evidence and Multiple Chemical Sensitivity
• Italian Parties united under the MCS cause
• An Italian law proposal for Environmental Illness and Disability

A $634,000 grant from the Department of Defense is allowing researchers at the University at Buffalo to investigate a trio of environmental factors and their influence on the progression of multiple sclerosis.

The two-year project, headed by Murali Ramanathan, PhD, tests the hypothesis that nicotine metabolism, the byproducts of vitamin D metabolism and increased levels of anti-Epstein-Barr virus (EBV) each interact with variations in specific genes to cause increased neurodegeneration and increased lesions in MS patients.

Ramanathan is a professor of pharmaceutical sciences and neurology in the School of Pharmacy and Pharmaceutical Sciences and the School of Medicine and Biomedical Sciences, respectively.

The study is a collaboration between the UB and investigators from Charles University in Prague, Czech Republic, and will be conducted on samples obtained at both universities’ MS centers.

The research aims to identify gene-environmental interactions between key molecules in the vitamin D pathway, anti-Epstein-Barr virus antibodies, cigarette smoking and key genetic variants that are implicated in conversion of patients with clinically isolated syndrome (CIS) to definite MS.

They will assess the risk of developing clinically definite MS and the time to progression, as well as the neurodegeneration in the brain of MS patients, as measured by brain atrophy, and the extent of brain injury caused by lesions.

“We will use a novel approach to measure the levels of vitamin D and its metabolites, EBV exposure and nicotine metabolites from cigarette smoking,” says Ramanathan. “We have developed sensitive and selective measurements for key metabolites in the vitamin D and nicotine metabolism pathways using mass spectrometry, a method that has not been used previously to study vitamin D metabolism.

The novel study design will include the genetic variations that were associated with the risk of developing MS, as well as genes that determine the levels and responses to environmental factors. MS patients will be divided into two equal groups: a training group that will be used to identify gene-environmental interactions, and a group that will be used to replicate the training group result.

“Identifying gene-environmental interactions is critical for developing better strategies for slowing the progression of MS, because it could enable patients with preexisting genetic risk factors to reduce the rate of disease progression through lifestyle modification,” Ramanathan says.

The study results will identify the gene-environment interactions that promote disease progression in MS and facilitate the development of preventive and therapeutic interventions for MS that disrupt these interactions, notes Ramanathan.

Bianca Weinstock-Guttman, MD, Robert Zivadinov, MD, PhD, and Jun Qu, PhD, all of UB, are study co-principal investigators. Dana Horakova, MD, PhD, and Eva Havrdova, MD, PhD, are collaborators at Charles University in Prague.

The University at Buffalo is a premier research-intensive public university, a flagship institution in the State University of New York system and its largest and most comprehensive campus. UB’s more than 28,000 students pursue their academic interests through more than 300 undergraduate, graduate and professional degree programs. Founded in 1846, the University at Buffalo is a member of the Association of American Universities.

Reference: University at Buffalo, Study to Look at Environmental Factors, MS Progression, September 21, 2010.

Berkeley — Children who were exposed to organophosphate pesticides while still in their mother’s womb were more likely to develop attention disorders (ADHD) years later, according to a new study by researchers at the University of California, Berkeley.

The new findings, to be published Aug. 19 in the journal Environmental Health Perspectives (EHP), are the first to examine the influence of prenatal organophosphate exposure on the later development of attention problems. The researchers found that prenatal levels of organophosphate metabolites were significantly linked to attention problems at age 5, with the effects apparently stronger among boys.

Earlier this year, a different study by researchers at Harvard University associated greater exposure to organophosphate pesticides in school-aged children with higher rates of attention deficit hyperactivity disorder (ADHD) symptoms.

“These studies provide a growing body of evidence that organophosphate pesticide exposure can impact human neurodevelopment, particularly among children,” said the study’s principal investigator, Brenda Eskenazi, UC Berkeley professor of epidemiology and of maternal and child health. “We were especially interested in prenatal exposure because that is the period when a baby’s nervous system is developing the most.”

The study follows more than 300 children participating in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), a longitudinal study led by Eskenazi that examines environmental exposures and reproductive health. Because the mothers and children in the study are Mexican-Americans living in an agricultural community, their exposure to pesticides is likely higher and more chronic, on average, than that of the general U.S. population.

Yet, the researchers pointed out that the pesticides they examined are widely used, and that the results from this study are a red flag that warrants precautionary measures.

“It’s known that food is a significant source of pesticide exposure among the general population,” said Eskenazi. “I would recommend thoroughly washing fruits and vegetables before eating them, especially if you’re pregnant.”

Organophosphate pesticides act by disrupting neurotransmitters, particularly acetylcholine, which plays an important role in sustaining attention and short-term memory.

“Given that these compounds are designed to attack the nervous system of organisms, there is reason to be cautious, especially in situations where exposure may coincide with critical periods of fetal and child development,” said study lead author Amy Marks, who was an analyst at UC Berkeley’s School of Public Health at the time of the study.

Many of these same UC Berkeley researchers are also finding that children with certain genetic traits may be at greater risk, a finding that is being published the same day in a separate EHP paper. That study found that 2-year-olds with lower levels of paraoxonase 1 (PON1), an enzyme that breaks down the toxic metabolites of organophosphate pesticides, had more neurodevelopmental delays than those with higher levels of the enzyme. The authors suggest that people with certain PON1 genotypes could be particularly vulnerable to pesticide exposure.

In the study on attention problems, researchers tested for six metabolites of organophosphate pesticides in mothers twice during pregnancy and in the children several times after birth. Together, the metabolites represent the breakdown products of about 80 percent of all the organophosphate pesticides used in the Salinas Valley.

The researchers then evaluated the children at age 3.5 and 5 years for symptoms of attention disorders and ADHD using maternal reports of child behavior, performance on standardized computer tests, and behavior ratings from examiners. They controlled for potentially confounding factors such as birthweight, lead exposure and breastfeeding.

Each tenfold increase in prenatal pesticide metabolites was linked to having five times the odds of scoring high on the computerized tests at age 5, suggesting a greater likelihood of a child having clinical ADHD. The effect appeared to be stronger for boys than for girls.

While a positive link between prenatal pesticide exposure and attention problems was seen for 3.5-year-olds, it was not statistically significant, a finding that did not surprise the researchers.

“Symptoms of attention disorders are harder to recognize in toddlers, since kids at that age are not expected to sit down for significant lengths of time,” said Marks. “Diagnoses of ADHD often occur after a child enters school.”

The UC Berkeley researchers are continuing to follow the children in the CHAMACOS study as they get older, and expect to present more results in the years to come.

The findings add to the list of chemical assaults that have been linked to ADHD in recent years. In addition to pesticides, studies have found associations with exposure to lead and to phthalates, which are commonly used in toys and plastics.

“High levels of the symptoms of ADHD by age 5 are a major contributor to learning and achievement problems in school, accidental injuries at home and in the neighborhood, and a host of problems in peer relationships and other essential competencies,” said UC Berkeley psychology professor Stephen Hinshaw, one of the country’s leading experts on ADHD, who was not part of this study. “Finding preventable risk factors is therefore a major public health concern.”

Literature: University of California – Berkeley, Prenatal exposure to pesticides linked to attention problems, 19-Aug-2010.

Related Articles:

• Pesticides in kids linked to ADHD- Attention-Deficit/Hyperactivity Disorder, study finds
• Western Diet linked to ADHD
• Groups Seeking Ban on Organophosphate Pesticide Go to Federal Court
• Common household pesticides linked to childhood cancer cases in Washington area
• Anxiety in adult female mice following perinatal exposure to Chlorpyrifos