THE GUARDIAN, UNITED KINGDOM
Tuesday, December 1, 2009
British Medical Journal
Women who use insect repellents during the first three months of pregnancy are more likely to give birth to baby boys with a genital defect, according to researchers. Insecticides used in gardening and agriculture may also be linked to genital malformations in boys.
What do we know already?
Hypospadias is a birth defect that affects boys' penises. It causes the opening to appear on the underside of their penis, rather than the tip. Boys born with hypospadias usually have an operation to correct it in the first few years of their life. Hypospadias probably affects about 1 or 2 out of 500 boys, but not much is known about the causes. Researchers have been looking at whether contact with everyday chemicals during pregnancy is linked to a higher risk of having a baby boy with the condition. In a study published last year, researchers interviewed the mothers of 471 boys born with hypospadias in the South East of England. Women who had regular contact with hairspray, such as those working as hairdressers, had a higher chance of having a boy with hypospadias. Researchers have looked again at the same group of women, this time looking at exposure to insect repellents, normally used on the skin, and insecticides, such as sprays used in gardening and agriculture. Other research has already found that high doses of some insect repellents, such as DEET, can have harmful effects on pregnant rats. So far, studies looking at humans have found either no or low risks from using insect repellents. However, it's impossible to rule out any risk without larger studies.
What does the new study say?
Women who had a son with hypospadias were more likely to have used insect repellents during early pregnancy, compared with women who had a healthy baby. However, the researchers didn't ask about the specific products women used, so it's impossible to say whether or which individual repellents might be linked to the increased risk. Different active ingredients include DEET and permethrin, while natural repellents contain essential oils of citronella or eucalyptus.
The researchers also looked at whether insecticides might be linked to birth defects. They looked at whether women lived near farmland, used pesticides in the garden, used fly sprays or ant powder, treated pets for fleas, or used nit shampoo. No single one of these things was linked to a higher risk, but women who had a combination of several were more likely to have a son with hypospadias.
How reliable are the findings?
Studies like this one can't prove that insect repellents or insecticides are the cause of birth defects. We only know there's a link. Women who use insect repellents may be different in lots of ways from women who don't, so there could be other factors that play a part. However the researchers did adjust their findings to take account of other things which could affect the risk of hypospadias, such as smoking, the mother's age, income, and the infant's birth weight.
Where does the study come from?
The study appeared in a journal called Occupational and Environmental Medicine, which is published by the BMJ Group.
What does this mean for me?The researchers say that more research needs to be done on insect repellents before we can draw firm conclusions. There are probably several things that increase the risk of genital defects in boys, with smoking being another likely factor. It's difficult to know just how big a part insect repellents or insecticides might play.
What should I do now?
There hasn't been much research looking at whether individual insect repellents are safe during pregnancy. So it's hard to know for certain what's best at this stage. There may be times when you need to use them, for example if you're travelling in a malarial area. Talk to your doctor if you're in any doubt.
Research done last year suggested that taking folic acid supplements when trying to get pregnant might help protect your baby from hypospadias. Folic acid also helps prevent major birth defects like spina bifida. Official advice recommends you take a 400 microgram folic acid supplement (also called vitamin B9) from the time when you stop using contraception up to week 12 of your pregnancy.
From:
Dugas J, Nieuwenhuijsen MJ, Martinez D, et al. Use of biocides and insect repellents and risk of hypospadias. Occupational and Environmental Medicine. Published online 1 December 2009.
(Beyond Pesticides, October 26, 2009) A new study conducted in China finds that people with organophosphate pesticides in their homes are more likely to have suicidal thoughts. According to the study, "Pesticide exposure and suicidal ideation in rural communities in Zhejiang province, China," published in the October issue of the WHO Bulletin, there is biological evidence that chronic low-grade exposure to organophosphate pesticides, which are very easily absorbed into the body through the skin and lungs, may have adverse effects on mental health.
The study was carried out in the central/coastal region of China, a relatively wealthy area with a rapidly developing economy. In a very large survey of mental health in rural community residents, participants were also asked about how they stored pesticides. The study found that people who stored pesticides at home, i.e. those with more exposure, were more likely to report recent suicidal thoughts. Supporting this, the survey also found suicidal thoughts to be associated with how easily accessible these pesticides were in the home and that the geographic areas with highest home storage of pesticides also had highest levels of suicidal thoughts in their populations.
"Organophosphate pesticides are widely used around the world. They are particularly lethal chemicals when taken in overdose and are a cause of many suicides worldwide," stated one of the study researchers, Dr. Robert Stewart. "Our research findings that suggest that higher exposure to these chemicals might actually increase the risk of suicidal thoughts provides further support for calls for tighter international restrictions on agricultural pesticide availability and use."
The analysis involved data from a survey of a representative sample of 9,811 rural residents in Zhejiang province who had been asked about the storage of pesticides at home and about whether or not they had considered suicide within the two years before the interview. The Chinese version of the 12-item General Health Questionnaire (GHQ) was administered to screen for mental disorder.
According to the study findings, the odds ratio for the association between pesticides stored at home and suicidal ideation over the 2 years prior to the study was more than double. Of the pesticides stored at home, nearly 87 percent comprised or included organophosphates. The most commonly stored pesticide was methamidophos, which was present in 63 percent of households that stored pesticides.
Previous studies have shown that farmers often have higher rates of depression than other population groups. A study published in 2008, "Depression and pesticide exposures among private pesticide applicators enrolled in the Agricultural Health Study," found that both acute high-intensity and cumulative pesticide exposure contribute to depression in pesticide applicators. Another 2008 study "A cohort study of pesticide poisoning and depression in Colorado farm residents," found adverse effects on mental health such as irritability were associated with pesticide poisoning.
A 2002 study found that farmers poisoned by agricultural pesticides containing organophosphates are nearly six times as likely to suffer depression in their lifetimes as compared to their counterparts. The study showed that populations exposed to the agricultural pesticides also face long-term risks of anxiety, irritability, restlessness and depression. In the study, 69 participants reported having been sickened by pesticide poisoning. Other study findings include that the Colorado farm population was more likely to have high depressive symptoms if they were female and in poor physical health and younger farmers were more likely to have high depressive symptoms compared to older farmers.
Organophosphates are a family of insecticides that are derived from World War II nerve agents. They are cholinesterase inhibitors, meaning that they bind irreversibly to the active site of an essential enzyme for normal nerve impulse transmission, acetylcholine esterase (AchE), inactivating the enzyme.
(Beyond Pesticides, October 30, 2009) A recent study shows that women who use insecticides are at elevated risk for autoimmune diseases such as rheumatoid arthritis and lupus. The results of the yet unpublished study were presented on October 17, 2009 at the American College of Rheumatology annual meeting in Philadelphia, PA.
The study, which looked at more than 75,000 women, shows that those who spray insecticides at least six times per year have almost two and a half times the risk of developing lupus and rheumatoid arthritis versus those who do not use insecticides. The risk doubles if insecticides were used in the home for 20 years or more.
Hiring a gardener or commercial company to apply insecticides also resulted in a doubling of risk, but only if they were used long-term, says Christine G. Parks, PhD, an epidemiologist with the National Institute of Environmental Health Sciences in Research Triangle Park, N.C., one of the lead researchers who analyzed data from the Women's Health Initiative (WHI) Observational Study.
"Our new results provide support for the idea that environmental factors may increase susceptibility or trigger the development of autoimmune diseases in some individuals," said Dr. Parks. While the study does not confirm cause and effect, Dr. Parks added, "We need to start thinking about what chemicals or other factors related to insecticide use could explain these findings."
Of the 76,861 postmenopausal, predominantly white women, ages 50 to 79, in the WHI study, 178 of them had rheumatoid arthritis and 27 had lupus. An additional eight women had both disorders. As part of the study, the women were asked a number of questions relating to farming and insecticide use. "Importantly, the relationships we observed were not explained by other factors that we considered, including farm history, age, race, ethnicity, socioeconomic factors such as education and occupation, smoking and other risk factors for disease," Dr. Parks said.
"The findings are fairly compelling" because they show the greater and longer the exposure, the greater the risk," said Darcy Majka, MD, assistant professor of medicine at Northwestern Univ\ersity Feinberg School of Medicine, another researcher who analyzed the WHI data.
According to Dr. Parks, studies show that up to three fourths of U.S. households reported using insecticides in either or both the home and garden, and 20% of the households had applied insecticides within the last month. "Insecticide exposure in the home can be quite persistent because [the chemicals] don't break down in the home environment."
Source: WebMD Health News
By CHARLES DUHIGG
The New York Times
October 7, 2009
The Environmental Protection Agency plans to conduct a new study about the potential health risks of atrazine, a widely used weedkiller that recent research suggests may be more dangerous to humans than previously thought.
Atrazine - a herbicide often used on corn fields, golf courses and even lawns - has become one of the most common contaminants in American drinking water.
For years, the E.P.A. has decided against acting on calls to ban the chemical from environmental activists and some scientists who argued that runoff was polluting ecosystems and harming animals.
More recently, new studies have suggested that atrazine in drinking water is associated with birth defects, low birth weights and reproductive problems among humans, even at concentrations that meet current federal standards.
The E.P.A. is expected to announce on Wednesday that it will conduct a new evaluation of the pesticide to assess any possible links between atrazine and cancer, as well as other health problems, such as premature births. The E.P.A. may determine that new restrictions are necessary.
The decision by E.P.A.'s administrator, Lisa P. Jackson, who took over the agency in January, is a significant departure from the policies of the E.P.A. under President George W. Bush.
For years, agency officials said that atrazine in drinking water posed almost no risk to humans or the environment. As recently as this summer, E.P.A. staff members argued that current regulations were adequate.
"We're going to use our scientific resources in a new and more aggressive way regarding atrazine," said Stephen A. Owens, who was recently confirmed as E.P.A. assistant administrator for prevention, pesticides and toxic substances.
"There are new scientific findings that deserve attention, and we're going to engage our scientific panels in actively reviewing the work of this office under previous administrations," he added. "We have a question: Did the decisions made in previous administrations use all the available science?"
A representative of atrazine's largest manufacturer, the Swiss company Syngenta, said that she had not been fully briefed on the E.P.A.'s announcement. However, the spokeswoman, Sherry Ford, said, "we expect a positive outcome for atrazine at the end of this process."
Ms. Ford added that the company "stands behind the safety of atrazine, which has undergone extensive testing. We are a science-based company, and we expect the E.P.A. to make sound decisions based on science, no matter which administration is currently in power."
Observers say the E.P.A.'s announcement signals a significant shift.
"This is a dramatic change," said Linda Birnbaum, director of the National Institute of Environmental Health Sciences, part of the Department of Health and Human Services. "There is growing evidence that atrazine could be a hazard to human health. This is a strong signal that the world is changing for some of the most widely used chemicals."
Atrazine has become a lightning rod in disputes over how the E.P.A. has used scientific findings to regulate chemicals and toxins.
The agency was sued in 2003 by an environmental advocacy organization, the Natural Resources Defense Council, amid claims that regulators had ignored studies showing that atrazine was dangerous to some animals.
In August, The New York Times reported on recent epidemiological studies that suggested small amounts of atrazine in drinking water, including levels considered safe by federal standards, might be associated with birth defects - including skull and facial malformations and misshapen limbs - as well as premature births and low birth weights in newborns.
E.P.A. officials said those studies, as well as recent papers reviewing numerous studies that showed that atrazine interferes with the development and hormone systems of some animals, played a role in their decision to re-evaluate the chemical.
A Times analysis of E.P.A. records also found that in some American towns, atrazine concentrations in drinking water had spiked sharply, sometimes for as long as a month. Though the E.P.A. and Syngenta were aware of those spikes, they often did not promptly warn local water systems, and the reports produced by local regulators and distributed to residents often failed to reflect those higher concentrations. Interviews with local water officials indicated that many of them were unaware that atrazine concentrations sometimes jumped sharply in their communities.
But officials in other communities have grown concerned. Water systems in six states - Illinois, Indiana, Iowa, Kansas, Mississippi and Ohio - recently sued atrazine's manufacturers to force them to pay for removing the chemical from drinking water.
The E.P.A. is expected to announce on Wednesday four meetings over the coming year of the agency's independent scientific advisory panel that will focus on atrazine.
(Beyond Pesticides, September 18, 2009) Previously documented in the Potomac River, which flows through downtown Washington, DC, the occurrence of "intersex" fish is now found to be nationwide. U.S. Geological Survey (USGS) researchers published their study, "Widespread occurrence of intersex in black basses from U.S. rivers" in the online edition of Aquatic Toxicology.
USGS researchers examined 16 different species of fish across the U.S. between 1995 and 2004. The condition of intersex fish, male fish producing eggs, is most commonly found in smallmouth and largemouth bass. One third of male smallmouth bass and one fifth of the male largemouth bass are intersex.
Scientists tested sites in the Apalachicola, Colorado, Columbia, Mobile, Mississippi, Pee Dee, Rio Grande, Savannah, and Yukon River basins. Research shows intersex fish in approximately one-third of all examined sites. The only site where researchers found no intersex fish is the Yukon River basin.
While the study did not look for the causes for intersex fish, scientists believe endocrine disruptors, chemicals that interfere with the body's hormonal systems, are certainly to blame.
"We know that endocrine-active compounds have been associated with intersex in fish, but we lack information on which fish species are most sensitive to such compounds, the way that these compounds interact to cause intersex, and the importance of environmental factors," said Jo Ellen Hinck, the lead author of the paper and a biologist at the USGS Columbia Environmental Research Center. "Proper diagnosis of this condition in wild fish is essential because if the primary causes are compounds that disrupt the endocrine system, then the widespread occurrence of intersex in fish would be a critical environmental concern."
While the government knows something is going wrong, it has yet to take any action to stop the contamination of water with endocrine disrupting chemicals. Environmentalists believe that given the severity of the situation, the Environmental Protection Agency (EPA), in consultation with USGS, should take a precautionary approach and begin phasing out suspected endocrine disruptors that contaminate the U.S. water supply while research continues. EPA announced in April 2009 that it is finally moving forward with the process, which experts call flawed, for screening endocrine disrupting chemicals, nearly 11 years after its deadline mandated by the Food Quality Protection Act of 1996. Beyond Pesticides believes the time for action is now.
Most scientists have suspected endocrine disruptors and synthetic estrogens, such as pesticides and birth control pills, from the beginning. Endocrine disruptors are a diverse group of several thousands of chemicals that are used in everything from pesticides and flame retardants to cosmetics and pharmaceuticals. Endocrine disruptors may be mistaken for hormones by the body and thus their presence may alter the function of hormones, either blocking their normal action or interfering with how they are made in the body. Since hormones regulate things like growth and body development, there is great potential for damage. In particular, some endocrine disruptors are mistaken for the female hormone estrogen. These estrogen mimics interfere with the reproductive system, causing infertility, malformed sexual organs, and cancer of sensitive organs.
When intersex fish were first discovered in the Potomac River, the USGS identified: atrazine, a common herbicide used in agriculture and on lawns that is already linked to sexual abnormalities in frogs; insecticides chlorpyrifos and endosulfan; the herbicide metolachlor; and two chemicals used to add fragrance to perfumes, soaps and other products, tonalide and galaxolide.
Disturbingly, there are many commonly used pesticides that are known or suspected endocrine disruptors, such as atrazine, 2,4-D, lindane, and permethrin. A recent study found that the commonly used lawn pesticide formulation Round-up, with the active ingredient glyphosate, causes damaging endocrine effects in fetuses. EPA does not currently evaluate or consider the endocrine disrupting properties of pesticides during registration or reregistration.
The environmental effects of these chemicals has been well-established: pseudo-hermaphrodite polar bears with penis-like stumps, panthers with atrophied testicles, hermaphroditic deformities in frogs, and male trout with eggs growing in their testes have all been documented as the probable result of endocrine-disrupting chemicals in the environment. Many scientists believe that wildlife provides early warnings of effects produced by endocrine disruptors, which may as yet be unobserved in humans.
Source: USGS Press Release News Room
(Beyond Pesticides, September 16, 2009) A new study published in the September issue of Archives of Neurology reports that the risk of Parkinsonism doubled with increased occupational exposure to pesticides, including eight agents associated with experimental Parkinsonism. These data add to the growing number of studies that lend credence to a causative role of certain pesticides in neurological disorders.
The study, "Occupation and Risk of Parkinsonism: A Multicenter Case-Control Study," set out to investigate occupations, specific job tasks, or exposures and risk of parkinsonism in collaboration with eight movement disorders centers in North America including, the Parkinson's Institute, CA, Department of Neurology, Baylor College of Medicine and Department of Neurology, Beth Israel Medical Center, New York. The investigation focused on five occupations previously suggested as posing an increased risk of Parkinsonism: agriculture, education, healthcare, welding, and mining. This examination of toxicant exposures included solvents and pesticides putatively associated with Parkinsonism. 519 people with Parkinson's disease and 511 similar people who did not have Parkinson's were studied.
Overall, the study finds that those whose jobs involve using pesticides are 80 percent more likely to develop the condition. The data reveals that any exposure to the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) almost triples the risk of Parkinsonism compared with individuals who report no exposure to the agent. The herbicide paraquat and the insecticide permethrin are also associated with a more than three-fold increased risk of Parkinson's disease.
"Occupational pesticide exposure emerges as the most consistent etiologic association with Parkinsonism," Caroline M. Tanner, MD, PhD, of the Parkinson's Institute in Sunnyvale, CA. Those who worked in agriculture, education, health care, or welding but who had not been exposed to pesticides through their work were not likely to develop the disease. The researchers note that while they did not look at pesticide exposures such as hobby gardening or residential exposure, "because these exposures may affect many more subjects, future attention is warranted."
Previous studies have linked pesticide exposure to the onset of Parkinson's disease (PD), including several published this year alone. A similar study conducted by French researchers found that farmworkers who used insecticides had over a two-fold increase in the risk of PD. Another recent publication found that rural residents who drank contaminated well water had an increased (up to 90 percent) risk of developing PD. Exposure to the pesticides, paraquat and maneb, within 500 meters of an individual's home, increased the risk of developing Parkinson's by 75 percent, according to a University of California, Berkeley study. The Institute of Medicine (IOM) found suggestive but limited evidence that exposure to Agent Orange and other herbicides used during the Vietnam War is associated with an increased chance of developing ischemic heart disease and Parkinson's disease in Vietnam veterans.
Parkinson's Disease is the second most common neurodegenerative disease affecting more than one million people in the U.S. Parkinson's disease occurs when nerve cells in the substantia nigra region of the brain are damaged or destroyed and can no longer produce dopamine, a nerve-signaling molecule that helps control muscle movement. All three pesticides in this study; 2,4-D, paraquat and permethrin, have effects on dopaminergic neurons. All three pesticides are currently registered for use in the U.S. 2,4-D is a herbicide most commonly found in many popular lawn care products, while permethrin is an insecticide (synthetic pyrethroid) found in many mosquito products and residential bug sprays. Both chemicals are already linked to cancer, endocrine disruption and other reproductive and developmental effects. Paraquat is a restricted-use pesticide (RUP) used primarily in agriculture.
For more on Parkinson's disease, please read "Pesticides Trigger Parkinson's Disease," a review of published toxicological and epidemiological studies that link exposure to pesticides, as well as gene-pesticide interactions, to Parkinson's disease and published in Pesticides and You (spring 2008).
Source: Reuters
Contact Information:
U.S. Department of the Interior, U.S. Geological Survey
Office of Communication
119 National Center
Reston, VA 20192
Intersex in smallmouth and largemouth basses is widespread in numerous river basins throughout the United States is the major finding of the most comprehensive and large-scale evaluation of the condition, according to U.S. Geological Survey (USGS) research published online in Aquatic Toxicology.
Of the 16 fish species researchers examined from 1995 to 2004, the condition was most common by far in smallmouth and largemouth bass: a third of all male smallmouth bass and a fifth of all male largemouth bass were intersex. This condition is primarily revealed in male fish that have immature female egg cells in their testes, but occasionally female fish will have male characteristics as well.
Scientists found intersex fish in about a third of all sites examined from the Apalachicola, Colorado, Columbia, Mobile, Mississippi, Pee Dee, Rio Grande, Savannah, and Yukon River basins. The Yukon River basin was the only one where researchers did not find at least one intersex fish.
Although intersex occurrence differed among species and basin, it was more prevalent in largemouth bass in southeastern U.S., where it occurred at all sites in the Apalachicola, Savannah, and Pee Dee river basins, said Jo Ellen Hinck, the lead author of the paper and a biologist at the USGS Columbia Environmental Research Center. The researchers also documented intersex in channel catfish for the first time.
"Although the USGS has already documented the severity of intersex in individual basins such as the Potomac, this study reveals the prevalence of intersex is more widespread than anyone anticipated, said Sue Haseltine, associate director for biology at the U.S. Geological Survey. "This research sends the clear message that we need to learn more about the hormonal and environmental factors that cause this condition in fish, as well as the number of fish afflicted with this condition."
The study, said Hinck, presents the observed occurrence of intersex in a variety of freshwater fish species, but not potential causes. "This study adds a lot to our knowledge of this phenomena, but we still don't know why certain species seem more prone to this condition or exactly what is causing it. In fact, the causes for intersex may vary by location, and we suspect it will be unlikely that a single human activity or kind of contaminant will explain intersex in all species or regions," she said.
For example, said Hinck, at least one of their sites with a high prevalence of intersex—the Yampa River at Lay, Colo.—did not have obvious sources of endocrine-active compounds, which have been associated with intersex in fish. Such compounds are chemical stressors that have the ability to affect the endocrine system and include pesticides, PCBs, heavy metals, household compounds such as laundry detergent and shampoo, and many pharmaceuticals. Yet other study sites with high occurrence of intersex were on rivers with dense human populations or industrial and agricultural activities, which are more generally associated with endocrine-active compounds.
"We know that endocrine-active compounds have been associated with intersex in fish, but we lack information on which fish species are most sensitive to such compounds, the way that these compounds interact to cause intersex, and the importance of environmental factors," Hinck said. "Proper diagnosis of this condition in wild fish is essential because if the primary causes are compounds that disrupt the endocrine system, then the widespread occurrence of intersex in fish would be a critical environmental concern."
Specific river basin results include:
Federal agencies have released the seven draft reports required by President Obama's Executive Order, which contain a range of proposed strategies for accelerating cleanup of the Bay and its vast watershed. The draft reports and an executive summary are available at http://executiveorder.chesapeakebay.net
The draft reports collectively call for increased accountability and performance from pollution control, habitat protection and land conservation programs at all levels of government, including an expanded use of regulatory authorities to address pollution control and additional voluntary and market-based solutions – particularly when it comes to habitat protection and land conservation programs. Federal agencies are also proposing new ways to harness the latest innovations in science and technology.
The draft reports are the first step in the creation of a new strategy for restoration and protection. The reports include a variety of strategies and options for addressing issues such as water quality, public access, landscape conservation, climate change, scientific monitoring and the protection of living resources.
During the past 120 days, 10 federal agencies collaborated to develop the draft reports. The recommendations in the reports were shaped by consultations with the six states in the Chesapeake Bay watershed and the District of Columbia, as well as suggestions from stakeholders and the public. During the next 60 days, the Federal Leadership Committee will evaluate the proposals and consult with Bay jurisdictions to refine the recommendations. On November 9, the Federal Leadership Committee will release a draft strategy that integrates the seven reports. Release of a draft strategy and revised reports will initiate a public comment period that concludes in early 2010. A final strategy will be completed by May 12, 2010.
Executive Summary Draft Reports EO 13508.pdf (356.15 kb)
202(a) define the next generation of tools and actions to restore water quality
202(b) target resources to better protect the Chesapeake Bay and its tributary waters
202(c) strengthen storm water management practices
202(d) assess the impacts of a changing climate
202(e) expand public access to waters and open spaces
202(f) strengthen scientific support for decisionmaking
202(g) develop focused and coordinated habitat and research activities
Cardin Releases Details of Chesapeake Bay Program Reauthorization Bill
U.S. Senator Benjamin L. Cardin (D-MD), chairman of the Environment and Public Works Water and Wildlife Subcommittee that has jurisdiction over the Environmental Protection Agency's Chesapeake Bay Program, this week released details of the Chesapeake Bay Ecosystem Restoration Act of 2009. The Cardin-authored reauthorization gives state and local governments of the Chesapeake Bay Watershed Area strong new enforcement tools and more than $1.5 billion in new grant authority to restore the Bay's health and — for the first time — sets a firm deadline of May 2020 for all restoration efforts to be in place.
The bill also establishes a flexible pollution trading program that is designed to lower compliance costs while also providing Bay watershed farmers with added financial incentives to implement conservation practices on their lands. In addition, the bill puts the force of law behind a recent Executive Order from President Obama that requires every federal department to work toward Bay restoration.
(Beyond Pesticides, August 26, 2009) The commonly used herbicide atrazine can spike at extremely high levels which go undetected by regular monitoring, according to new report by the Natural Resources Defense Council (NRDC), Poisoning the Well. Currently, the U.S. Environmental Protection Agency (EPA) considers an annual average atrazine level of below 3 parts per billion to be acceptable for human consumption, although studies have shown adverse health impacts below EPA's "safe" levels. The analysis by NRDC discovered that in the 139 municipal water systems from which EPA collected data on a biweekly basis in 2003 and 2004, atrazine is found 90% of the time. Furthermore, 54 of these water systems have at least one spik e above 3 parts per billion.
"The data shows that EPA is unable to adequately regulate atrazine and protect the public from this hazardous herbicide in our drinking water," said Jay Feldman, executive director of Beyond Pesticides. "With studies showing hormonal and other adverse effects at extremely low levels, any level of atrazine in our drinking water is dangerous and spikes above EPA's 3 ppb threshold are completely unacceptable. EPA must put public health first and ban this toxic chemical."
Under the federal Safe Drinking Water Act, municipal water supplies are tested for chemicals about four times a year. Because this is done so infrequently, EPA mandates that companies manufacturing a chemical—in this case, Syngenta for atrazine—must monitor drinking water in a sample pool of towns as much as once a week. A New York Times investigation finds, however, that too often reports of these spikes of atrazine in the drinking water go unreported to residents or fail to reflect the higher concentrations.
The town of Piqua, Ohio was found to have concentrations of atrazine at 59.57 parts per billion in April of 2005 by Syngenta, with similar levels in 2004 and 2007. In a report sent to citizens in 2005, though, the highest level was said to be 11.6 parts per billion. Residents were also not told when or for how long these peaks occurred. Syngenta claims that they provided city officials in Piqua with results, yet city officials are unaware of this.
EPA asserts that it does not believe these one-time spikes are of concern to human health; however, plenty of evidence exists suggesting otherwise.
"Our biggest concern is early-life-stage development," says Jennifer Sass, senior scientist at NRDC. "…These endocrine disruptors act in the body at extremely low levels. These spikes matter."
Earlier this year, a study published in the medical journal Acta Paeditrica found that the highest rates of birth defects for U.S. babies occur when conception occurs in the spring and summer months, when the highest concentrations of pesticides are found in surface waters. The correlation between the month of the last menstrual period and higher rates of birth defects is statistically significant for half of the 22 categories of birth defects reported in the Centers for Disease Control database from 1996 to 2002, including spina bifida, cleft lip, clubfoot and Down's syndrome.The study relies on findings by the U.S. Geological Survey, the EPA and other agencies on the seasonal variations in nitrates, atrazine and other pesticides in the surf ace water.
Even at levels considered "safe" by EPA drinking water standards, atrazine is linked to endocrine-disrupting effects. Research by UC Berkeley professor, Tyrone Hayes, Ph.D., demonstrates that exposure to doses of atrazine as small as 0.1 parts per billion, turns tadpoles into hermaphrodites - creatures with both male and female sexual characteristics.
Atrazine has also been implicated in a study as a possible cause for male infertility, blocking the action of the male sex-hormone testosterone and could impact the development of male reproductive organs in humans.
In yet another study last year by Dr. Rick Relyea, Ph.D., an associate professor of biological sciences in the University of Pittsburgh's School of Arts and Sciences, a mixture of small amounts of ten of the most commonly used pesticides, including atrazine killed 99 percent of the leopard frog tadpoles that he was testing.
While EPA is aware of these new studies, the agency will not review the research until sometime next year, and in the meantime has not warned pregnant women about the risks of atrazine or to use a simple carbon water filter.
"The public believes that the EPA has carefully reviewed all the chemicals that are used and has the authority it needs to deal with risks, but that's often not the case," says Erik D. Olson, director of food and consumer product safety at the Pew Charitable Trusts.
While atrazine is one of the most common agricultural pesticides in the U.S., runoff from lawns and gardens is a serious concern. Dr. David Skelley, Ph.D. a professor of ecology at the Yale School of Forestry and Environmental Studies, discovered last year that intersex frogs are more common in suburban areas than agricultural areas. His research focused on specific chemicals, such as atrazine which is increasingly used to manicure home lawns and gardens.
Pesticides, such as atrazine, even at low levels, have been associated with reproductive and developmental effects as well as endocrine disruption. Atrazine is the most commonly detected pesticide in rivers, streams and wells, with an estimated 76.4 million pounds of atrazine applied in the U.S. annually. Atrazine has a tendency to persist in soils and move with water, making it a common water contaminant.
By Kari Lydersen
The Washington Post
Tuesday, August 25, 2009
Published: August 22, 2009
Mark Lyons for The New York Times
In Piqua, Ohio, the city manager, Frederick Enderle, left, said he was unaware of spikes in atrazine. Residents like Jeff Lange are angry about the risks.
But atrazine often washes into water supplies and has become among the most common contaminants in American reservoirs and other sources of drinking water.
Now, new research suggests that atrazine may be dangerous at lower concentrations than previously thought. Recent studies suggest that, even at concentrations meeting current federal standards, the chemical may be associated with birth defects, low birth weights and menstrual problems.
Laboratory experiments suggest that when animals are exposed to brief doses of atrazine before birth, they may become more vulnerable to cancer later.
An investigation by The New York Times has found that in some towns, atrazine concentrations in drinking water have spiked, sometimes for longer than a month. But the reports produced by local water systems for residents often fail to reflect those higher concentrations.
Officials at the Environmental Protection Agency say Americans are not exposed to unsafe levels of atrazine. They say that current regulations are adequate to protect human health, and that the doses of atrazine coming through people’s taps are safe even when concentrations jump.
But some scientists and health advocates disagree. They argue that the recent studies offer enough concerns that the government should begin re-examining its regulations. They also say that local water systems which have primary responsibility for the safety of drinking water should be forced to monitor atrazine more frequently, in order to detect short-term increases and warn people when they occur.
The E.P.A. has not cautioned pregnant women about the potential risks of atrazine so that they can consider using inexpensive home filtration systems. And though the agency is aware of new research suggesting risks, it will not formally review those studies until next year at the earliest. Federal scientists who have worked on atrazine say the agency has largely shifted its focus to other compounds.
Interviews with local water officials indicate that many of them are unaware that atrazine concentrations have sometimes jumped sharply in their communities. But other officials are concerned. Forty-three water systems in six states Illinois, Indiana, Iowa, Kansas, Mississippi and Ohio recently sued atrazine’s manufacturers to force them to pay for removing the chemical from drinking water.
Representatives of the E.P.A. and Syngenta, the company that manufactures most of the atrazine sold, say that current federal standards are based on hundreds of studies showing Americans are safe. In a written statement, the E.P.A. said that it applied large safety buffers in regulating atrazine and continued to monitor emerging science.
“The exposure that the agency allows under its atrazine drinking water regulations is at least 300 to 1,000 times lower than the level where the agency saw health effects in the most sensitive animal species tested,” the statement said. New studies, while raising important issues, do not “suggest a revision to E.P.A.’s current regulatory approach, which has been built on the review and consideration of hundreds of studies, including animal toxicity and human epidemiological studies dealing with atrazine,” the agency said.
Syngenta said the lawsuits were baseless.
But the head of another government agency voiced apprehension. “I’m very concerned about the general population’s exposure to atrazine,” said Linda S. Birnbaum, director of the National Institute of Environmental Health Sciences, a division of the Department of Health and Human Services. “We don’t really know what these chemicals do to fetuses or prepubescent children.”
“At a minimum, pregnant women should have access to accurate information about what’s in their drinking water,” Dr. Birnbaum added.
Critiques of the E.P.A.
Atrazine is just one example of what critics say are regulatory weaknesses in the protections of America’s drinking water. Health and environmental advocates argue that the laws safeguarding drinking water and policing toxins are insufficient, and that the E.P.A. is often too slow in evaluating emerging risks, not cautious enough and too unwilling to warn the public when health concerns arise.
In January, a Government Accountability Office report said that the E.P.A.’s system for assessing toxic chemicals was broken, and that the agency often failed to gather adequate information on whether chemicals posed health risks.
Forty percent of the nation’s community water systems violated the Safe Drinking Water Act at least once last year, according to a Times analysis of E.P.A. data, and dozens of chemicals have been detected at unsafe levels in drinking water.
In interviews, some E.P.A. officials conceded that they were frustrated by the limitations they face in scrutinizing chemicals like atrazine. An estimated 33 million Americans have been exposed to atrazine through their taps, according to data from water systems nationwide.
“The public believes that the E.P.A. has carefully reviewed all the chemicals that are used and has the authority it needs to deal with risks, but that’s often not the case,” said Erik D. Olson, director of food and consumer product safety at the Pew Charitable Trusts, and a former lawyer at the E.P.A. and for the Senate Committee on the Environment and Public Works.
“The E.P.A. is working with weak laws, basic research at the agency is often seriously underfunded, and in some cases there’s institutional inertia against change,” he added. “That’s contributed to a sense that the agency is often slow to react to new science showing risks.”
Though the hazards posed by atrazine are far from clear, some scientists and health advocates argue that the chemical deserves special scrutiny because it is so widely used. The European Union, for instance, has banned atrazine as part of a precautionary policy that prohibits pesticides that easily contaminate groundwater. (European regulators did not evaluate the chemical’s health risks.)
Atrazine, which is sold under various brand names including AAtrex, is most commonly used on corn in farming states. But it can also be found on lawns, gardens, parks and golf courses. Sometimes, the only way to avoid atrazine during summer months, when concentrations tend to rise as cropland is sprayed, is by forgoing tap water and relying on bottled water or using a home filtration system.
E.P.A. officials note that anyone using atrazine must complete a short training course and is warned to wear long-sleeve shirts and pants, as well as chemical-resistant gloves and shoes, when spraying. The chemical cannot be applied near lakes, reservoirs or other bodies of water. And local water systems must produce an annual report detailing the highest concentrations of atrazine and other chemicals detected over the previous year.
Some high-ranking E.P.A. officials say there are concerns over atrazine, and that it, among other chemicals, is likely to be closely re-examined by the new E.P.A. administrator, Lisa P. Jackson.
“Atrazine is obviously very controversial and in widespread use, and it’s one of a number of substances that we’ll be taking a hard look at,” said Stephen A. Owens, who was recently confirmed as the E.P.A.’s assistant administrator for prevention, pesticides and toxic substances.
He went on: “I can’t say whether the outcome will be any different, but Administrator Jackson has made clear that we need to take a close look at decisions made in the previous administration, and be certain about the science behind those judgments.”
The New Science
Some of the current regulations governing atrazine in drinking water were established in the 1990s. Critics say that science has changed since then but that the regulations have not.
Recent studies suggest that when adults and fetuses are exposed to even small doses of atrazine, like those allowed under law, they may suffer serious health effects. In particular, some scientists worry that atrazine may be safe during many periods of life but dangerous during brief windows of development, like when a fetus is growing and pregnant women are told to drink lots of water.
“There are short, critical times like when a fetus’s brain is developing when chemicals can have disastrous impacts, even in very small concentrations,” said Deborah A. Cory-Slechta, a professor at the University of Rochester in New York who has studied atrazine’s effects on the brain and serves on the E.P.A.’s science advisory board. “The way the E.P.A. tests chemicals can vastly underestimate risks.”
“There’s still a huge amount we don’t know about atrazine,” she added.
In recent years, five epidemiological studies published in peer-reviewed journals have found evidence suggesting that small amounts of atrazine in drinking water, including levels considered safe by federal standards, may be associated with birth defects including skull and facial malformations and misshapen limbs as well as low birth weights in newborns and premature births. Defects and premature births are leading causes of infant deaths.
Some of those studies suggest that as atrazine concentrations rise, the incidence of birth defects grows. One study by researchers at Purdue University, published in the journal Environmental Health Perspectives suggests that concentrations as small as 0.1 parts per billion may be associated with low birth weights.
The E.P.A. generally does not require water systems to notify residents unless the yearly average of atrazine in drinking water exceeds 3 parts per billion, and under a determination made earlier this decade, the agency considers one-day exposures of up to 297 parts per billion safe.
Another study suggests that concentrations of atrazine in drinking water below the E.P.A. thresholds may disrupt menstrual cycles.
Many of those studies examined large populations that are already exposed to atrazine and sought to exclude the effects of other contaminants and environmental or health factors. However, such epidemiological studies cannot prove that atrazine causes specific diseases. Definitive scientific proof would probably require unethical experiments, like exposing pregnant women to the chemical in controlled settings. Some research found that other pesticides may have also contributed to health problems.
Agency and Industry Rebuttal
In written statements, the E.P.A. and Syngenta argued there were problems with all of the studies suggesting health risks from low doses of atrazine.
Agency officials pointed out that epidemiological findings cannot fully differentiate between multiple influences, and that they only highlight associations, and do not demonstrate a cause-and-effect relationship, and that the “E.P.A. has required and extensively reviewed laboratory studies on atrazine and developmental effects.”
“Data from these studies,” the E.P.A. said, “do not suggest that birth defects, small-for-gestational-age, or effects on limb development would occur as a result of exposure to levels of atrazine found in the environment.” Officials added that the agency evaluates all studies as they appear and takes appropriate actions.
Syngenta said in a written statement that “the evidence is overwhelming that atrazine does not cause adverse health effects at levels to which people are normally exposed,” and that “studies have shown that atrazine does not cause birth defects and does not cause reproductive effects.”
But six researchers asked by The Times to review the epidemiological studies said the results were troubling. “These suggest real reasons for concern,” said Melissa Perry, an associate professor at the Harvard School of Public Health. “The results need to be replicated, but they suggest there are real questions for policy makers about what constitutes safe levels of atrazine.”
Concerns have also been raised by researchers at the E.P.A. itself. Since 2003, for instance, research published by agency scientists in journals like Toxicology and Applied Pharmacology has shown that when rats are exposed to brief doses of atrazine as fetuses, some experience delayed puberty and their mammary glands change in ways that could make them more vulnerable to cancer later in life.
“The morphological changes we see look similar to those caused by other compounds that make tissue more susceptible to carcinogens,” said Suzanne Fenton, an E.P.A. scientist who has written about atrazine. “This theory hasn’t been tested for atrazine. There’s still a lot that we don’t know.”
E.P.A. and Syngenta representatives said that experiments showing changes in rats used higher doses than found in drinking water and that those studies did not provide the scientific confidence required for regulation. Outside scientists, in interviews, said other research suggested that similar effects could be observed at lower doses.
Dr. Fenton says she is no longer working on atrazine. Other E.P.A. employees also said they had been encouraged to redirect their energies to other chemicals, because of insufficient resources and competing priorities.
E.P.A. officials said that other researchers were currently working on atrazine and that the agency intended to convene a panel by 2011 to evaluate epidemiological and other studies.
Below the Radar
The federal Safe Drinking Water Act was created, in part, with cities like Piqua, Ohio, in mind. A town of 20,500, it has its own water system, and thanks to federal right-to-know laws created to warn residents about chemicals in their drinking water, Piqua’s officials must test for atrazine and other substances and inform people of the highest concentrations detected.
But when spikes in atrazine occur in Piqua and elsewhere, residents often do not learn of them, a review of E.P.A. and state data shows.
Since local water systems test for atrazine as infrequently as once a year, the E.P.A. has required that the companies manufacturing the chemical, primarily Syngenta, monitor the drinking water of a sample of towns as many as 154 communities as often as once a week. The companies submit that data to federal officials. The E.P.A. says those tests indicate that few towns have violated Safe Drinking Water limits for atrazine.
However, a Times review of Syngenta’s data shows that some communities had large spikes of atrazine in their drinking water, sometimes for months at a time. But residents were not warned.
For instance, in April 2005, the drinking water in Piqua contained atrazine concentrations of 59.57 parts per billion. The residents of Piqua were also exposed to elevated concentrations of atrazine in 2004 and 2007. Data shows similar patterns in dozens of other cities, like Versailles, Ind., and Evansville, Ill.
But the people of Piqua never learned about those spikes from local water officials or the E.P.A. City officials test for atrazine only once a month in the spring, and the annual report sent to residents in 2005 said the highest level of atrazine detected was only 11.6 parts per billion 80 percent lower than the peak measured by Syngenta. Residents were also not told when peaks had occurred or how long they lasted or whether there were multiple spikes.
Syngenta said the company regularly provided city officials with testing results. Piqua officials were largely unaware of or did not use those notifications.
“I didn’t know that we got any information about atrazine besides our own testing,” said Frederick E. Enderle, Piqua’s city manager since 2005. “I’m not even sure what we would do with it.”
Some residents are angry.
“This makes my blood boil,” said Jeff Lange, a Piqua resident and environmental activist. “I have friends and family drinking this water. How are pregnant women or sick people supposed to know when to avoid it?”
Drinking water experts say atrazine spikes most likely occur in many other towns that are not monitored by Syngenta. In those areas, there is essentially no way for residents or officials to monitor how high levels go.
E.P.A. officials said that under the Safe Drinking Water Act, the data collected by third parties, like Syngenta, did not fall under right-to-know provisions and that Piqua was required only to notify residents based on the city’s testing.
But residents, including Mr. Lange, said Syngenta’s findings should have at least prompted the city to test more frequently, or led the E.P.A. to tell the city to change its testing schedule.
E.P.A. officials also said they do not believe that atrazine spikes like those in Piqua are dangerous. “A one-time reading of 59 parts per billion in finished water does not pose a risk to human health,” the agency wrote.
However, studies like the one at Purdue suggest there are health risks at much smaller concentrations, and other studies suggest those risks rise as exposures grow.
Critics contend that atrazine is just one of the many chemicals the E.P.A. has not regulated with sufficient caution.
The Natural Resources Defense Council, an environmental advocacy group, is expected to release a report on Monday saying that weak E.P.A. regulation of atrazine poses risks to humans and the environment. Other organizations have made similar charges about a variety of chemicals, including fuel additives, dry cleaning and manufacturing solvents, and industrial waste dumped into water supplies.
“There’s pretty broad consensus that the laws regarding toxic substances need to be modernized and overhauled, and that the E.P.A. needs more resources,” said Mr. Olson of Pew, who added that the agency’s new leadership had begun addressing many issues.
“But in the meantime, people are getting exposed to dangerous chemicals,” Mr. Olson said. “And the E.P.A. isn’t responding swiftly enough.”
(Beyond Pesticides, August 17, 2009) The four-day testing period the U.S. Environmental Protection Agency (EPA) commonly uses to determine ‘safe' levels of pesticide exposure for humans and animals could fail to account for the long-term effects of toxic chemicals, University of Pittsburgh researchers report in the September edition of Environmental Toxicology and Chemistry. The team found that the highly toxic pesticide endosulfan, a neurotoxin banned in several nations but still used extensively in U.S. agriculture, can exhibit a "lag effect" with the fallout from exposure not surfacing until after direct conta ct has ended. The findings build on a 10-year effort by Rick Relyea, Ph.D., an associate professor of biological sciences in Pitt's School of Arts and Sciences, to understand the potential links between the global decline in amphibians, routine pesticide use, and the possible threat to humans in the future.
The team exposed nine species of frog and toad tadpoles to endosulfan levels "expected and found in nature" for the EPA's required four-day period, then moved the tadpoles to clean water for an additional four days, Jones reported. Although endosulfan was ultimately toxic to all species, three species of tadpole showed no significant sensitivity to the chemical until after they were transferred to fresh water. Within four days of being moved, up to 97 percent of leopard frog tadpoles perished along with up to 50 percent of spring peeper and American toad tadpoles.
Of most concern, explained Dr. Relyea, is that tadpoles and other amphibians are famously sensitive to pollutants and considered an environmental indicator species. The EPA does not require testing on amphibians to determine pesticide safety, but Dr. Relyea previously found that endosulfan is 1,000-times more lethal to amphibians than other pesticides. Yet, he said, if the powerful insecticide cannot kill one the world's most susceptible species in four days, then the four-day test period may not adequately gauge the long-term effects on larger, less-sensitive species.
"When a pesticide's toxic effect takes more than four days to appear, it raises serious concerns about making regulatory decisions based on standard four-day tests for any organism," Dr. Relyea said. "For most pesticides, we assume that animals will die during the period of exposure, but we do not expect substantial death after the exposure has ended. Even if EPA regulations required testing on amphibians, our research demonstrates that the standard four-day toxicity test would have dramatically underestimated the lethal impact of endosulfan on even this notably sensitive species."
Andrew Blaustein, a professor in Oregon State University's nationally ranked Department of Zoology, who is familiar with the Pitt study, said the results raise concerns about standards for other chemicals and the delayed dangers that might be overlooked. Some of the frog eggs the Pitt team used had been collected by Blaustein's students for an earlier unrelated experiment, but he had no direct role in the current research.
"The results are somewhat alarming because standards for assessing the impacts of contaminants are usually based on short-term studies that may be insufficient in revealing the true impact," Blaustein said. "The implications of this study go beyond a single pesticide and its effect on amphibians. Many other animals and humans may indeed be affected similarly."
Tadpoles in the Pitt project spent four days in 0.5 liters of water containing endosulfan concentrations of 2, 6, 7, 35, 60, and 296 parts-per-billion (ppb), levels consistent with those found in nature. The team cites estimates from Australia-where endosulfan is widely used-that the pesticide can reach 700 ppb when sprayed as close as 10 meters from the ponds amphibians typically call home and 4 ppb when sprayed within 200 meters. The EPA estimates that surface drinking water can have chronic endosulfan levels of 0.5 to 1.5 ppb and acute concentrations of 4.5 to 23.9 ppb.
Leopard frogs, spring peepers, and American toads fared well during the experiment's first four days, but once they were in clean water, the death rate spiked for animals previously exposed to 35 and 60 ppb. Although the other six species did not experience the lag effect, the initial doses of endosulfan were still devastating at very low concentrations. Grey and Pacific tree frogs, Western toads, and Cascades frogs began dying in large numbers from doses as low as 7 ppb, while the same amount killed all green frog and bullfrog tadpoles.
A second paper by Dr. Relyea and Devin Jones, a recent Pitt biological sciences graduate, also in the current Environmental Toxicology and Chemistry expands on one of Dr. Relyea's most notable investigations, a series of findings published in Ecological Applications in 2005 indicating that the popular weed-killer Roundup®(active ingredient glyphosate is "extremely lethal" to amphibians in concentrations found in the environment. The latest work determined the toxicity of Roundup Original Max for a wider group of larval amphibians, including nine frog and toad species and four salamander species.
In November 2008, Dr. Relyea reported in Oecologia that the world's 10 most popular pesticides-which have been detected in nature-combine to create "cocktails of contaminants" that can destroy amphibian populations, even if the concentration of each individual chemical is within levels considered safe to humans and animals. The mixture killed 99 percent of leopard frog tadpoles and endosulfan alone killed 84 percent.
A month earlier, Dr. Relyea published a paper in Ecological Applications reporting that gradual amounts of malathion, one of the most popular insecticides in the U.S., too small to directly kill developing leopard frog tadpoles instead sparked a biological chain reaction that deprived them of their primary food source. As a result, nearly half the tadpoles in the experiment did not reach maturity and would have died in nature.
Source: University of Pittsburgh
(Beyond Pesticides, August 12, 2009) A new study examining the effects of the mosquito repellent DEET on insects, mice and human proteins reports that the chemical interferes with a prominent central nervous system enzyme. This effect is magnified when exposure to DEET is combined with exposure to certain other pesticides.
Entitled, "Evidence for inhibition of cholinesterases in insect and mammalian nervous systems by the insect repellent deet," and published in BioMed Central (BMC) Biology, the study utilized toxicological, biochemical and electrophysiological techniques to show that DEET is not simply a behavior-modifying chemical, but that it also inhibits cholinesterase activity in both insect and mammalian neuronal preparations. The researchers examined DEET's effects on mosquitoes, cockroach nerves, mouse muscles, and enzymes purified from fruit flies and humans. Applications of DEET slowed or halted the actions of the enzyme acetylcholinesterase. This enzyme is crucial for regulating nerve impulses in both insects and mammals, and once its functions are disrupted, neuromuscular paralysis, leading to death by asphyxiation result. In humans, symptoms include headache, exh austion and mental confusion together with blurred vision, salivation, chest tightness, and muscle twitching and abdominal cramps.
The study also investigated the consequences of DEET interactions with carbamate insecticides on the cholinergic system, and found that DEET has the capacity to strengthen the toxicity of carbamates, a class of insecticides known to block acetylcholinesterase.
The results are consistent with previous studies, says Mohammed Abou-Donia, PhD, of the Duke University Medical Center in Durham, N.C, who was not involved in the new work. "DEET is a good chemical for protection against insects," Dr. Abou-Donia says. "But prolonged exposure results in neurological damage, and this is enhanced by other chemicals and medications."
In light of these recent findings, SC Johnson, manufacturer of a variety of DEET repellent products released a statement claiming that such concerns were "unfounded." However, this is not the first study that has highlighted the adverse impacts associated with DEET and its use with other pesticides. Several studies done by a team of Duke University researchers suggest that DEET, in conjunction with permethrin-impregnated clothing, may be linked to Gulf War Syndrome.
DEET (N,N-diethyl-meta-toluamide) is commonly used as an insect repellent but its use has become highly controversial. Scientists have raised concerns about the use of DEET and seizures among children, even though the U.S. Environmental Protection Agency (EPA) claims that there is not enough information to implicate DEET with these incidents. DEET is quickly absorbed through the skin and has caused adverse effects including severe skin reactions including large blisters and burning sensations. Laboratory studies have found that DEET can cause neurological damage, including brain damage in children. DEET was originally developed for military use in 1946 and was then registered for use on the general public in 1957. According to the EPA, more than one third of the U.S. population uses DEET-containing products every year.
However, safer alternatives to DEET include citronella and other essential oils, like oil of lemon eucalyptus which has been recommended as an efficacious alternative by the Center for Disease Control and prevention (CDC). For more information on safer methods to protect yourself from mosquitoes and other insects, please visit Beyond Pesticides' fact sheet on mosquito repellents.
Source: U.S. News & World Report.
(Beyond Pesticides, July 29, 2009) A new study by researchers at the Lombardi Comprehensive Cancer Center at Georgetown University finds a higher level of common household pesticides in the urine of children with acute lymphoblastic leukemia (ALL), a cancer that develops most commonly between three and seven years of age. The findings are published in the August issue of the journal Therapeutic Drug Monitoring.
Researchers, in the study entitled, "Pediatric Acute Lymphoblastic Leukemia and Exposure to Pesticides," caution that these findings, which do not establish a cause-and-effect relationship, suggest an association between pesticide exposure and development of childhood ALL.
"In our study, we compared urine samples from children with ALL and their mothers with healthy children and their moms. We found elevated levels of common household pesticides more often in the mother-child pairs affected by cancer," says the study's lead investigator, Offie Soldin, Ph.D., an epidemiologist at Lombardi. Dr. Soldin cautions, "We shouldn't assume that pesticides caused these cancers, but our findings certainly support the need for more robust research in this area." Previous studies have found that exposures to certain pesticides increases the risk of developing certain cancers and degenerative diseases.
The study was conducted between January 2005 and January 2008 with volunteer participants from Lombardi and Children's National Medical Center who live in the Washington metropolitan area. It included 41 pairs of children with ALL and their mothers (cases), and 41 pairs of healthy children and their mothers (controls). For comparison purposes, the case pairs were matched with control pairs by age, sex and county of residence. Previous studies in agricultural areas of the country have suggested a relationship between pesticides and childhood cancers, but researchers say this is the first study conducted in a large, metropolitan area.
Urine samples were collected from all child-mother pairs and analyzed by the Centers for Disease Control and Prevention to look for evidence of organophosphates (OP), the chemical name of some household pesticides. The body breaks down OP into metabolites which can be tracked in urine samples. The researchers say pesticides were detected in the urine of more than half of the participants, but levels of two common OP metobolites, diethylthiophosphate (DETP) and diethyldithiophosphate (DEDTP), were higher in the children with ALL compared to the control children (p<0.03 and p<0.05).
As a part of the study, the mothers completed a questionnaire to collect information about the family's exposure to pesticides, their medical history, home and neighborhood characteristics, diet, and history of smoke exposure. More case mothers (33 percent) than controls (14 percent) reported using insecticides in the home (p<0.02), however there was no correlation found between high levels of the OP metabolites in urine and reported use of pesticides.
"We know pesticides – sprays, strips, or ‘bombs,' are found in at least 85 percent of households, but obviously not all the children in these homes develop cancer. What this study suggests is an association between pesticide exposure and the development of childhood ALL, but this isn't a cause-and-effect finding," Dr. Soldin explains. "Future research would help us understand the exact role of pesticides in the development of cancer. We hypothesize that prenatal exposure coupled with genetic susceptibility or an additional environmental insult after birth could be to blame."
Children are more vulnerable to the negative effects of pesticide exposures. EPA concurs that children take in more pesticides relative to body weight than adults and have developing organ systems that are more vulnerable and less able to detoxify toxic chemicals. The National Academy of Sciences reports that children are more susceptible to chemicals than adults and estimates that 50% of lifetime pesticide exposure occurs during the first five years of life.
Source: Lombardi Comprehensive Cancer Center, Georgetown University Medical Center, Press Release
(Beyond Pesticides, July 28, 2009) A new study by researchers at the National Food Institute, Technical University of Denmark shows that exposure to a mixture of pesticides and other chemicals has a synergistic effect on the development of male sex organs. Synergy occurs when the effect of multiple chemicals is greater than the sum of the individual effects. The study, "Synergistic Disruption of External Male Sex Organ Development by a Mixture of Four Antiandrogens," was published July 15, 2009 in the online edition of Environmental Health Perspectives.
The researchers designed their study to determine the consequences of simultaneous exposure to multiple "antiandrogens." An antiandrogen, or androgen antagonist, is any of a group of hormone receptor antagonist compounds that are capable of preventing or inhibiting the biologic effects of androgens, male sex hormones, on normally responsive tissues in the body. Disrupting the action of androgens during gestation, certain chemicals present in food, consumer products and the environment can induce irreversible malformations of sex organs among male offspring.
The team investigated the effects of mixtures of a widely used plasticizer, di(2-ethylhexyl) phthalate (DEHP), used in medical devices such as IV bags and tubing, beauty products, PVC toys, vinyl shower curtains, car seats, wallpaper and more; two fungicides present in food, vinclozolin and prochloraz; and, a pharmaceutical, finasteride, on landmarks of male sexual development in rats. These chemicals were chosen because they disrupt androgen action according to differing mechanisms of action.
According to the study results, combined exposure on malformations of external sex organs was synergistic, and the observed responses were greater than would be predicted from the toxicities of the individual chemicals. In relation to other hallmarks of disrupted male sexual development, including changes in anogenital distance, retained nipples, and sex organ weights, the combined effects were dose additive. When the four chemicals were combined at doses equal to no-observed-adverse effect levels estimated for nipple retention, significant reductions in anogenital distance were observed in male offspring.
The authors believe that current methods of chemical risk assessment "may lead to considerable underestimations of risks associated with exposures to chemicals that disrupt male sexual differentiation."
(Beyond Pesticides, July 27, 2009) A mother's exposure to urban air pollutants known as polycyclic aromatic hydrocarbons (PAHs) can adversely affect a child's intelligence quotient or IQ, according to the new study "Prenatal Airborne Polycyclic Aromatic Hydrocarbon Exposure and Child IQ at Age 5 Years." PAHs are widespread in urban environments and throughout the world as they have many sources, several of which are related to pesticides, including creosote used for wood preservation, burning pesticide-laden grass seed fields, and exposure to organochlorine pesticides whether banned, yet ubiquitous DDT or the still used insecticide dicofol. Other sources include synthetic turf fields and the burning of coal, diesel, oil and gas, or other organic substances such as tobacco. PAHs have been known to be bioaccumulative, carcinogenic and disrupt the endocrine system.
The new study, funded by the National Institute of Environmental Health Sciences (NIEHS), a branch of the National Institutes of Health, the U.S. Environmental Protection Agency and several private foundations, found that children exposed to high levels of PAHs in New York City had full scale and verbal IQ scores that were 4.31 and 4.67 points lower than those of less exposed children. High PAH levels were defined as above the median of 2.26 nanograms per cubic meter (ng/m3). A difference of four points, which was the average seen in this study, could be educationally meaningful in terms of school success, as reflected, for example, in standardized testing and other measures of academic performance. However, the researchers point out that the effects may vary among individual children.
"This research clearly shows that environmental PAHs at levels encountered in an urban setting can adversely affect a child's IQ," said Linda Birnbaum, Ph.D., director of NIEHS. "This is the first study to report an association between PAH exposure and IQ, and it should serve as a warning bell to us all. We need to do more to prevent environmental exposures from harming our children."
The study was conducted by scientists from the Columbia University Center for Children's Environmental Health. It included children who were born to non-smoking black and Dominican-American women age 18 to 35 who resided in Washington Heights, Harlem or the South Bronx in New York. The children were followed from utero to 5 years of age. The mothers wore personal air monitors during pregnancy to measure exposure to PAHs and they responded to questionnaires.
At 5 years of age, 249 children were given an intelligence test known as the Wechsler Preschool and Primary Scale of the Intelligence, which provides verbal, performance and full-scale IQ scores. The test is regarded as a validated, reliable and sensitive instrument for assessing intelligence. The researchers developed models to calculate the associations between prenatal PAH exposure and IQ. They accounted for other factors such as second-hand smoke exposure, lead, mother's education and the quality of the home caretaking environment. Study participants exposed to air pollution levels below the average were designated as having low exposure, while those exposed to pollution levels above the median were identified as high exposure.
"The decrease in full-scale IQ score among the more exposed children is similar to that seen with low-level lead exposure," said lead author Frederica P. Perera, Dr.P.H., professor at Columbia's Mailman School of Public Health and director of the Columbia Center for Children's Environmental Health.
A 1999 study found that PAHs that are abundant in house dusts increase the toxicity of chlorpyrifos in vitro, particularly at low levels (i.e., 2-50 FM PAHs with 1-180 nM chlorpyrifos-oxon, a metabolite of chlorpyrifos that inhibits acetyl cholinesterase.
According to Beyond Pesticides' wood preservatives campaign research, PAHs are one of the three classes of chemicals found in coal-tar creosote that are known to cause harmful health effects. Many of the components of the creosote mixture, such as PAHs, are rapidly absorbed through the lungs, stomach and intestines. Creosote is made up of about 75-85 percent PAHs. PAHs can attach to soil particles and may move with sediments into streams or remain part of a tarlike mass, but they may also move into groundwater in sandy soils low in organic matter. The remaining PAHs are bioaccumulative and carcinogenic. According to ATSDR's Toxicological Profile on PAHs, "Studies of people show that individuals exposed by breathing or skin contact for long periods to mixtures that contain PAHs and other compounds can also develop cancer." Creosote contains several carcinogenic P AHs, including benz[a]anthracene, benzo[a]pyrene, and dibenz[a,h]anthracene. The Department of Health and Human Services has determined that these three PAHs are known animal carcinogens. The EPA and the International Agency for Research on Cancer (IARC) have determined they are probable human carcinogens.
"IQ is an important predictor of future academic performance," said Dr. Perera. "Fortunately, airborne PAH concentrations can be reduced through currently available controls, alternative energy sources and policy interventions."
This study adds to the body of scienific literature that links toxic chemical exposure to intellectual impairment in children. Joseph L. Jacobson, Ph.D., and Sandra W. Jacobson, Ph.D., in "Intellectual Impairment in Children Exposed to Polychlorinated Biphenyls in Utero" (1996), conclude that infants and young children whose mothers had eaten a diet of Great Lakes fish contaminated with polychlorinated biphenyls (PCBs) suffer adverse neurologic and intellectual function
(Beyond Pesticides, July 23, 2009) A new study published in the August 2009 issue of Environmental Toxicology and Chemistry found that insecticides used in highly populated agricultural areas of California's Central Valley affect amphibians that breed in the Sierra Nevada Mountains to the east. This study adds to the increasing evidence that pesticides impact areas and wildlife species that are miles from sources of pesticide application.
Researchers from the Cooperative Wildlife Research Laboratory, Southern Illinois University and U.S. Geological Survey (USGS) examined the chronic toxicity of two of the insecticides most commonly used in the Central Valley- chlorpyrifos and endosulfan, to larval Pacific treefrogs (Pseudacris regilla) and foothill yellow-legged frogs (Rana boylii), the amphibians with declining populations that live and breed in meadows surrounding the Sierra Nevada. The results are discussed in "Toxicity of Two Insecticides to California, USA, Anurans and Its Relevance to Declining Amphibian Populations." The study used laboratory testing to examine how the insecticides affected the two frogs at environmentally realistic concentrations. During testing, tadpoles were observed at various stages of development to see how the insecticides affected their growth and health.
The researchers found that endosulfan was more toxic than chlorpyrifos to both species, and tadpoles of both species developed abnormalities when exposed to high endosulfan concentrations. Endosulfan also affected the growth and development rates in both species. The researchers say this affects the amphibians' behavior and increases their vulnerability to predators and hydrological events such as floods and droughts. The yellow-legged frogs, which rely more on standing water during reproduction and have seen higher population declines compared with other species like the tree frog, was the more sensitive of the two.
Winds blow insecticide residues into the mountains, and they fall as rain or snow, say the researchers, Donald Sparling, PhD, of Southern Illinois University, and Garry Fellers, PhD, of the USGS' Western Ecology Research Center in Point Reyes. Here, the chemicals breakdown more slowly due to cooler temperatures. "Concentrations of insecticides in the Sierra Nevada Mountains of California may have the ability to inflict serious damage on native amphibians," Dr. Sparling and Dr. Fellers write. "The present study adds to the increasing evidence that pesticides are very harmful to amphibians living in areas that are miles from sources of pesticide application."
A previous study reported that endosulfan was 1,000-times more lethal to amphibians than other pesticides examined in the study. Declining amphibian populations have been recorded in pristine areas far downwind from areas of active pesticide use. Another USGS study found that the breakdown products of chlorpyrifos, and other pesticides are ten to 100 times more toxic to amphibians than their parent compounds, which are already highly toxic to amphibians. Endosulfan is banned in Europe and many other countries around the world due to the serious toxic effects attributed to its use. It is an organochlorine pesticide, in the same family as DDT and lindane, and like DDT and lindane, it bioaccumulates and has been found in places as far from point of use as th e arctic. It is also a suspected endocrine disruptor, affecting hormones and reproduction in aquatic and terrestrial organisms.
(Beyond Pesticides, June 25, 2009) Although it is known that infants are more susceptible than adults to the toxic effects of pesticides, this increased vulnerability may extend much longer into childhood than expected, according to a new study by researchers at the University of California, Berkeley. Among newborns, levels of paraoxonase 1 (PON1), an enzyme critical to the detoxification of organophosphate pesticides, average one-third or less than those of the babies' mothers. It was thought that PON1 enzyme activity in children approached adult levels by age two, but instead, the UC Berkeley researchers found that the enzyme level remained low in some individuals through age seven. Based upon the findings, reported in the journal Environmental Health Perspectives, the study authors recommend that the U.S. Environmental Prot ection Agency (EPA) re-evaluate the current standards for acceptable levels of pesticide exposure.
"Current EPA standards of exposure for some pesticides assume children are three to five times more susceptible than adults, and for other pesticides the standards assume no difference," said Nina Holland, Ph.D., UC Berkeley adjunct professor of environmental health sciences and senior author of the paper. "Our study is the first to show quantitatively that young children may be more susceptible to certain organophosphate pesticides up to age seven. Our results suggest that the EPA standards need to be re-examined to determine if they are adequately protecting the most vulnerable members of the population."
The study, conducted by UC Berkeley's Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS), involves 458 children from an agricultural region who were followed from birth through age seven. Cord blood samples were collected from all children to determine their PON1 genotype and to obtain baseline measures of the enzyme's activity level.
For more than 100 of the children in the study, researchers were able to obtain at least four additional measurements - at ages one, two, five and seven - of PON1 activity. Almost all the children in the study had 2 to 3 time points assessed, for a total of 1,143 measurements of three types of PON1 enzyme activity.
One's PON1 genotypic profile determines how effectively the enzyme can metabolize toxic chemicals. For example, people with two copies of the Q form of the gene - known as a QQ genotype - produce a PON1 enzyme that is less efficient at detoxifying chlorpyrifos oxon, a metabolite of chlorpyrifos, than the enzyme produced by people with two R forms of the gene. Similarly, individuals with two T forms of the PON1 gene on a different part of the chromosome generally have a lower quantity of the enzyme than do those with two C forms of the gene.
Previous research led by Dr. Holland found that some of the QQ newborns may be 50 times more susceptible to chlorpyrifos and chlorpyrifos oxon than RR newborns with high PON1 levels, and 130 to 164 times more susceptible than some of the RR adults.
Of the children in this latest study, 24 percent had the QQ genotype, and 18 percent had the TT genotype, both of which are associated with lower activity of the PON1 enzyme. Moreover, 7.5 percent of the children had both QQ and TT genotypes, which is considered an even more vulnerable profile. On average, the quantity of enzyme quadrupled between birth and age 7. The greatest rise in enzyme activity was among children with the RR and CC variants of the PON1 gene, which quickly outpaced the increase in children with the QQ and TT genotypes.
The fact that enzyme activity remained low for certain kids with vulnerable genotypes well past age 2 was surprising for the study authors. The researchers are continuing to collect data for these children as they grow older to see if the pesticide susceptibility continues.
"In addition to its involvement in the metabolism of pesticides, many studies are now finding that PON1 may play an important role in protecting against oxidative stress, which is linked to diseases from asthma to obesity and cardiovascular disease," said study lead author Karen Huen, a UC Berkeley Ph.D. student in environmental health sciences. "The children in our study whose genotypes are related to lower PON1 activity may not only be more susceptible to pesticides throughout much of their childhood, they may also be more vulnerable to other common diseases related to oxidative stress."
Notably, other studies have found that PON1 genotypes vary by race and ethnicity, with the Q variants more common among Caucasians, less common among Latinos, and least common among African Americans. The majority of the subjects in this study were Mexican-American.
"What's important about this study is that it shows that young children are potentially susceptible to certain organophosphates for a longer period of time than previously thought," said Brenda Eskenazi, Ph.D., UC Berkeley professor of epidemiology and director of CHAMACOS and the Center for Children's Environmental Health Research. "Policymakers need to consider these vulnerable populations when establishing acceptable levels of exposure to different pesticides."
(Beyond Pesticides, June 24, 2009) An analysis of the New York City Public Housing system's pest management practices finds that a combination of preventive management practices and least toxic pesticide options are more effective than conventional chemical-dependent practices.The analysis finds that integrated pest management (IPM)practices with a focus on sealing cracks and proper sanitation, coupled with boric acid controls cockroaches better than chemical approaches.
The study, entitled "Effectiveness of an Integrated Pest Management Intervention in Controlling Cockroaches, Mice and Allergens in New York City Public Housing," finds that apartments utilizing integrated pest management (IPM) measures have significantly lower counts of cockroaches at three months and greater success in reducing or sustaining low counts of cockroaches at three (75 percent decline) and six months (88 percent decline). IPM was associated with a more than 50 percent drop in cockroach allergen levels in kitchens at three months, and in beds and kitchens at six months. In contrast, the number of cockroaches in buildings receiving professional exterminator visits every three to six months increased slightly. Pesticide use was reduced in apartments using IPM relative to apartments with chemical practices in place. Residents of IPM apartments also rated building services more positively. The researchers also found that that an easily replicable single IPM visit was more effective than the regular application of pesticides alone in managing pests.
According to the researchers, the New York City Housing Authority (NYCHA) is the largest public housing owner in North America with more than 405,000 low-income residents. A successful implementation of IPM in an institution of this size is thought to offer many potential benefits such as pesticide use reduction, improved pest management and reduced pest and allergen burdens in housing populated by largely Black and Hispanic families with disproportionately high prevalence of asthma- which is mostly attributed to pest allergens.
In the study, 323 apartments were evaluated. The practices include mechanical and steam cleaning using soap on kitchen cabinets, stoves, refrigerators, floors and countertops, and bathroom floors and fixtures. Practices also include the use of latex caulk to seal cracks and crevices, gaps within kitchen cabinets and between the cabinets and wall, gaps and cracks in baseboards, plumbing joints, and other potential ports of entry for pests; and boric acid and cockroach baits were applied. Apartment residents were instructed to store open food in sealed containers, cover garbage containers with a tight-fitting lid, and dispose of garbage frequently. Residents were also provided with a covered garbage container, food storage containers and cleaning supplies, including sponges, soap, powdered cleanser, and degreasing solution. Residents were also instructed not to use aerosol/spray pesticides for the duration of the study. No repeat IPM visits were scheduled. Cockroach populati ons were monitored with pheromone glue traps, three and six months later.
This study is the first to show that a single, short, low-cost visit by housing authority workers to address the underlying source of pests can be more effective at controlling cockroaches and their allergens in buildings than repeated professional pesticide applications. However, other studies also found that IPM techniques are effective, especially in the long-term, against pests.
Source: University of California, Berkeley
By NICHOLAS D. KRISTOF
Published: June 27, 2009
The New York Times
Some of the first eerie signs of a potential health catastrophe came as bizarre deformities in water animals, often in their sexual organs.
Frogs, salamanders and other amphibians began to sprout extra legs. In heavily polluted Lake Apopka, one of the largest lakes in Florida, male alligators developed stunted genitals.
In the Potomac watershed near Washington, male smallmouth bass have rapidly transformed into “intersex fish” that display female characteristics. This was discovered only in 2003, but the latest survey found that more than 80 percent of the male smallmouth bass in the Potomac are producing eggs.
Now scientists are connecting the dots with evidence of increasing abnormalities among humans, particularly large increases in numbers of genital deformities among newborn boys. For example, up to 7 percent of boys are now born with undescended testicles, although this often self-corrects over time. And up to 1 percent of boys in the United States are now born with hypospadias, in which the urethra exits the penis improperly, such as at the base rather than the tip.
Apprehension is growing among many scientists that the cause of all this may be a class of chemicals called endocrine disruptors. They are very widely used in agriculture, industry and consumer products. Some also enter the water supply when estrogens in human urine compounded when a woman is on the pill pass through sewage systems and then through water treatment plants.
These endocrine disruptors have complex effects on the human body, particularly during fetal development of males.
“A lot of these compounds act as weak estrogen, so that’s why developing males whether smallmouth bass or humans tend to be more sensitive,” said Robert Lawrence, a professor of environmental health sciences at the Johns Hopkins Bloomberg School of Public Health. “It’s scary, very scary.”
The scientific case is still far from proven, as chemical companies emphasize, and the uncertainties for humans are vast. But there is accumulating evidence that male sperm count is dropping and that genital abnormalities in newborn boys are increasing. Some studies show correlations between these abnormalities and mothers who have greater exposure to these chemicals during pregnancy, through everything from hair spray to the water they drink.
Endocrine disruptors also affect females. It is now well established that DES, a synthetic estrogen given to many pregnant women from the 1930s to the 1970s to prevent miscarriages, caused abnormalities in the children. They seemed fine at birth, but girls born to those women have been more likely to develop misshaped sexual organs and cancer.
There is also some evidence from both humans and monkeys that endometriosis, a gynecological disorder, is linked to exposure to endocrine disruptors. Researchers also suspect that the disruptors can cause early puberty in girls.
A rush of new research has also tied endocrine disruptors to obesity, insulin resistance and diabetes, in both animals and humans. For example, mice exposed in utero even to low doses of endocrine disruptors appear normal at first but develop excess abdominal body fat as adults.
Among some scientists, there is real apprehension at the new findings nothing is more terrifying than reading The Journal of Pediatric Urology but there hasn’t been much public notice or government action.
This month, the Endocrine Society, an organization of scientists specializing in this field, issued a landmark 50-page statement. It should be a wake-up call.
“We present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology,” the society declared.
“The rise in the incidence in obesity,” it added, “matches the rise in the use and distribution of industrial chemicals that may be playing a role in generation of obesity.”
The Environmental Protection Agency is moving toward screening endocrine disrupting chemicals, but at a glacial pace. For now, these chemicals continue to be widely used in agricultural pesticides and industrial compounds. Everybody is exposed.
“We should be concerned,” said Dr. Ted Schettler of the Science and Environmental Health Network. “This can influence brain development, sperm counts or susceptibility to cancer, even where the animal at birth seems perfectly normal.”
The most notorious example of water pollution occurred in 1969, when the Cuyahoga River in Ohio caught fire and helped shock America into adopting the Clean Water Act. Since then, complacency has taken hold.
Those deformed frogs and intersex fish not to mention the growing number of deformities in newborn boys should jolt us once again.
I invite you to comment on this column on my blog, On the Ground. Please also join me on Facebook, watch my YouTube videos and follow me on Twitter.
(Beyond Pesticides, June 18, 2009) Do you ever wonder about pesticides on your food or in your drinking water, and in particular, which of those pesticides are most hazardous? On June 17, 2009, Pesticide Action Network North America (PANNA) launched its What's On My Food database, which makes the results of government tests for pesticide residues in food available online in a searchable, easy-to-use format. The database shows what pesticides are found on each food, in what amount, and – for the first time – links those residues to the health effects associated with exposure to each of the chemicals.
"This kind of public visibility around pesticides is particularly needed in the U.S., since regulators base their decisions on toxicology studies that are almost all done by industry," explains Brian Hill, PhD, senior PANNA scientist and the primary developer of the database. "Nearly 900 million pounds of pesticides [excluding wood preservatives, chlorine and specialty biocide pesticides] are used in the U.S. every year, yet regulations depend on studies that are not peer-reviewed and are kept hidden behind the veil of ‘confidential business information.'" Dr. Hill notes that the 900 million figure is long overdue for updating, as the most recent pesticide use figures from the Environmental Protection Agency (EPA) are for 2001.
In addition to highlighting the potential direct health effects of pesticide residues, What's on My Food points to the many problems associated with pesticide use before food reaches the kitchen table. Widespread use of agricultural chemicals threatens the health of workers and those in nearby communities and schools, as well as harming wildlife and contaminating ecosystems, according to the site.
In the "Take Action" section of the site, Pesticide Action Network calls on consumers not only to vote with their dollars by choosing organic foods whenever possible, but also to become involved as "food citizens" and sign a petition that asks the Obama Administration to support conversion to organic agriculture; ensure environmental justice for farmworkers communities; protect future generations from persistent pollutants; and, reduce overall exposure to pesticides.
(Beyond Pesticides, June 17, 2009) A new study finds that toxic pesticides, including those already banned, persist in homes. The study's results indicate that most floors in occupied homes in the U.S. have measurable levels of insecticides that serve as sources of exposure to home dwellers. These persistent residues continue to expose people, especially vulnerable children, to the health risks associated with these chemicals.
Published in Environmental Science and Technology, the study, entitled "American Healthy Homes Survey: A National Study of Residential Pesticides Measured from Floor Wipes," was conducted as a collaboration between the U.S. Environmental Protection Agency (EPA) and the U.S. Department of Housing and Urban Development. Five hundred randomly selected homes were sampled using alcohol wipes to collect dust from hard surface floors, mostly kitchen floor surfaces. The swipes were analyzed for 24 currently and previously use residential insecticides in the organochlorine, organophosphate, pyrethroid and phenylpyrazole classes, and the insecticide synergist piperonyl butoxide.
Researchers found that currently used pyrethroid pesticides were, not surprisingly, at the highest levels with varied concentrations. Fipronil and permethrin, both currently used, were found in 40 percent and 89 percent of homes respectively. However, the researchers found that long discontinued pesticides like DDT and chlordane were found in 42 percent and 74 percent of homes respectively, with DDE, the breakdown product of DDT, also found in 33 percent of homes. Even chemicals no longer permitted for residential use, such as chlorpyrifos and
The authors point out that the "high detection frequencies observed for chlordane, chlorpyrifos, and permethrin suggest these compounds are essentially ubiquitous in our living areas and that popular use, both past and present, has a major influence on their occurrence in homes." Children are at particular health risk given their more frequent contact with flooring, as well as hand to mouth activity. Concerning is the fact that DDT was found in a higher percentage of homes than its breakdown product, DDE. This could mean that DDT is not degraded well in homes, due to a lack of sunlight or microbes, and that residents are being exposed to current sources of DDT.
This is not the first study to document the prevalence of pesticide residues in households. In 2008, a study found significant amounts of pyrethroid pesticides in indoor dust of homes and childcare centers. Other studies throughout the years have also documented the occurrence of pesticide residues in indoor dusts and air samples, including a sampling of homes of pregnant women which found that 75% of their homes were contaminated with pesticides. A 1998 study (Gurunathan, S. et al) found that chlorpyrifos accumulated on furniture, toys and other sorbant surfaces up to two weeks after application, while another 1996 study (Nishioka, M., et al) found that the herbicide 2,4-D can be tracked from lawns into homes, leaving residues of the herbicide in carpet s.
Exposure to synthetic pyrethroids has been reported to lead to headaches, dizziness, nausea, irritation, and skin sensations. There are also serious chronic health concerns related to synthetic pyrethroids. EPA classifies permethrin as a possible human carcinogen, based on evidence of lung tumors in lab animals exposed to these chemicals. Many synthetic pyrethroids have been linked to disruption of the endocrine system, which can adversely affect reproduction and sexual development, interfere with the immune system, and increase chances of breast cancer. Children are especially sensitive to the effects of permethrin and other synthetic pyrethroids. A study found that permethrin is almost five times more toxic to eight-day-old rats than to adult rats due to incomplete development of the enzymes that break down pyrethroids in the liver.
(Beyond Pesticides, June 8, 2009) A new epidemiological study finds that Parkinson's disease patients who have been exposed to pesticides through their work show elevated rates of the disease. The researchers find that French farmworkers have nearly double the risk for the disease if exposed to pesticides, with a dose-effect for the number of years of exposure. When they looked at the three major classes of pesticides (insecticides, fungicides and herbicides), they find that the farmworkers who used insecticides had over a two-fold increase in the risk of Parkinson's disease. A slightly higher risk is found for exposure to organochlorine insecticides. According to the study, these associations are stronger in men with older onset Parkinson's disease than in those with younger onset Parkinson's.
The study, "Professional Exposure to Pesticides and Parkinson's Disease," published in Annals of Neurology, involved individuals affiliated with the French health insurance organization for agricultural workers who were frequently exposed to pesticides in the course of their work. Occupational health physicians constructed a detailed lifetime exposure history to pesticides by interviewing participants, visiting farms, and collecting a large amount of data on pesticide exposure. These included farm size, type of crops, animal breeding, which pesticides were used, time period of use, frequency and duration of exposure per year, and spraying method.
"Our findings support the hypothesis that environmental risk factors such as professional pesticide exposure may lead to neurodegeneration," notes lead study author Alexis Elbaz M.D., Ph.D., of Inserm, the national French institute for health research in Paris, and the University Pierre et Marie Curie.
The second most common neurodegenerative disease affecting more than one million people in the U.S., Parkinson's disease occurs when nerve cells in the substantia nigra region of the brain are damaged or destroyed and can no longer produce dopamine, a nerve-signaling molecule that helps control muscle movement.
In the past year several studies have been published that make the connection that Parkinson's disease is caused by a combination of environmental risk factors such as pesticide exposure and genetic susceptibility. For example, residential exposure to an agriculture application of the fungicide maneb and the herbicide paraquat significantly increases the risk of developing Parkinson's disease, according to a University of California, Berkeley study. A study by University of California, Los Angeles (UCLA) researcher s found pesticide exposure and genetic variability in the dopamine transporter (DAT), a protein that plays a central role in dopaminergic neurotransmission of the brain, interact to significantly increase the risk factor for Parkinson's disease. Another study by UCLA researchers found chronic exposure to commonly used dithiocarbamate fungicides, such as ziram, contribute to the development of Parkinson's disease. A University of Texas study found a strong correlation between Parkinson's disease patients and the use of the pesticide rotenone. In addition, Duke University and University of Miami researchers studying related individuals who share environmental and genetic backgrounds found a significant association between Parkinson's disease and use of herbicides and insecticides, such as organochlorines and organophosphates.
(Beyond Pesticides, May 28, 2009) Two commonly used herbicides, pendimethalin and EPTC, show a statistically significant exposure-response association with pancreatic cancer. The new study, "Agricultural Pesticide Use And Pancreatic Cancer Risk In The Agricultural Health Study Cohort," published earlier this month in the International Journal of Cancer, is a case-control study of pesticide applicators and their spouses in Iowa and North Carolina. After controlling for age, smoking and diabetes, the study finds a three-fold increased risk with lifetime pendimethalin use and a two-and-a-half-fold increased risk with lifetime use of EPTC when compared to those that never used the chemicals. Among the 24 pesticides examined, having ever used one of five pesticides (trifluralin, chlorimuron-ethyl, pendimethalin, EPTC or heptachlor) shows at least a 40 percent excess risk of pancreatic cancer.
According to the U.S. EPA's pesticide sales and usage statistics, pendimethalin is the third most commonly used home and garden (and other non-agricultural use) herbicide and the 7th most commonly used herbicide in agriculture, totaling 21-30 million pounds applied annually in the U.S. Pendimethalin is listed by the U.S. EPA as a Group C - Possible Human Carcinogen and is a suspected endocrine disruptor. Pendimethalin has been found to cause central nervous system depression in mice and rats. In addition, the herbicide potentiates hypnosis caused by other drugs such as pentobarbitone, barbitone or ether, and lengthened recovery from drug effects. The percentage of apoptosis increased in mouse embryos exposed to low doses of pendimethalin, suggesting that at levels considered to be safe in humans by regulatory standards pendimethalin has adv erse effects very early in development.
EPTC is also a commonly used herbicide, with more than 5-8 million pounds used annually, according to EPA. It is regularly used on feed and food crops such as alfalfa, potato, and corn as well as non-agricultural uses such as rights-of-way and landscapes. EPTC, a thiocarbamate pesticide, is a cholinesterase inhibitor and is linked to increasing the risk of developing asthma.
Pancreatic cancer is the fourth leading case of cancer-related death in the U.S. The National Cancer Institute estimates that pancreatic cancer will lead to more than 35,000 deaths in 2009 and more than 42,000 new cases will be diagnosed in 2009. There has been a slight increasing trend in pancreatic cancers since the early 1990's, with higher rates in men than woman.
Several studies published over the past 15 years have linked pesticide exposures to pancreatic cancer:
* A 2009 study analyzing pesticide sales in different parts of Brazil and cancer mortality rates a decade later found a statistically significant correlation with the mortality rates for several cancers, including cancer of the pancreas;
* A 2007 Finnish study found a more than six-fold increased risk of pancreatic cancer for male gardeners;
* A 2007 study identifying risk factors for pan
creatic cancer in Egypt found a more than two and a half increased risk for those individuals exposed to pesticides;
* A 2001 National Cancer Institute study found excess risk for occupational exposure to fungicides (odds ratio (OR) 1.5) and herbicides (OR 1.6);
* A 2000 case-control study in Spain found occupational exposure to pesticides causes a three-fold increased risk for pancreatic cancer;
* A 1999 study of aerial pesticide applicator pilots found a significantly elevated risk for pancreatic cancer;
* A 1995 case control occupational study<
/FONT> in Finland found a 1.7 increased risk for occupa
tional pesticide exposure; and,
* A 1993 case-referent study of Italian farmers found a significantly increased risk of pancreatic cancer among licensed pesticides users with greater than 10 years experience.
Last month, EPA announced that it will be moving forward with preliminary testing of 67 active and inert pesticide ingredients for possible endocrine disrupting effects. Yet, according to prominent researcher and author Theo Colborn, Ph.D., EPA's testing protocol will not detect chemicals that can alter development and function of the pancreas, and its hormone, insulin, which could lead to diabetes and obesity.
Looking for information on different pesticides? Find data on more than 80 pesticides commonly used in the U.S. in the Pesticide Gateway. Beyond Pesticides created this database tool to provide decision and policy makers, practitioners and activists with easier access to current and historical information on pesticide hazards and safe pest management, drawing on and linking to numerous sources and organizations that include information related to pesticide science, policy and activism.
(Beyond Pesticides, May 14, 2009) President Barack Obama signed an executive order on Tuesday creating a Federal Leadership Committee for the Chesapeake Bay to be chaired by the U.S. Environmental Protection Agency. The executive order calls for EPA and six other federal agencies to coordinate and expand federal tools and resources to help speed cleanup of the nation's largest estuary. At the meeting of the Chesapeake Bay Program Executive Council at Mount Vernon, Virginia, EPA Administrator Lisa P. Jackson presented the executive order, which creates the Federal Leadership Committee for the Chesapeake Bay.
The Executive Council confirmed at a 2007 meeting that the Bay Program would not meet its commitment to clean up the Bay by 2010 as per the 2000 Chesapeake Bay Agreement. At that meeting, short-term two-year deadlines were set. However, since measures to improve the Bay's heath have not been successful in the nine years since stakeholders were tasked with its clean-up, it is unclear how these milestones will be met by the two-year deadline in 2011. Chairman of the Chesapeake Executive Council, Virginia Governor Timothy Kaine, stated at the 2007 meeting that shorter term goals create the pressure to produce results. Many states are now tasked to significantly increase the pace of cleanup. For example, Maryland must increase progress to reduce nitrogen entering the Bay by 138 percent and Virginia by 86 percent.
The federal committee will be chaired by EPA and will manage new plans by a team of seven federal agencies to strengthen and bring accountability to efforts to protect and restore the bay. In addition to the executive order, Administrator Jackson announced that EPA's renewed commitment to bay restoration will include a bay-wide set of strict pollution caps backed by state action plans and federal consequences to assure progress; sharp reductions in air pollutants that impact the bay; robust use of existing authorities; key funding support, and scientific and technical assistance.
"This executive order is a strong signal of the President's commitment to restoring this national treasure, which is so vital to the environment, the local economies, and the way of life for millions of people," said Administrator Jackson. "We are bringing the full weight of this partnership to bear on this challenge, and I am extraordinarily hopeful about what we can accomplish working together."
Federal agencies will create action reports that will be integrated into a draft federal strategy within 180 days of the signing of the executive order. The federal strategy will include annual commitments and progress reports and periodic reviews by an independent evaluator. For its part, EPA's plan will identify actions to make full use of Clean Water Act tools, including strengthening existing permit programs and extending coverage where necessary. The agency also will implement a compliance and enforcement strategy to ensure that regulated entities follow the rule of law.
EPA is also set to work with its state partners to develop a bay-wide total maximum daily load (TMDL) by December 2010 that will assign strict pollution caps to meet the state's existing Chesapeake Bay water quality standards. The TMDL will identify the total pollution caps necessary to meet clean water standards and allocate pollution budgets to the states. Those allocations will be used to develop detailed state action plans that will be supported by two-year commitments and accountability provisions with federal consequences for lagging performance. According to the EPA, the TMDL process will involve strong public participation, including a first round of public meetings this summer. By meeting these and future milestones, the Bay states must put in place all pollution control measures necessary for a restored Bay no later than 2025.
"We have charted a new course for the Chesapeake Bay's recovery that will succeed because it includes the short-term goals necessary to make steady progress and is backed by federal and state leaders who share a profound conviction to protect our environment," said Governor Kaine. The Executive Order also includes: reducing water pollution from federal property; developing a Bay climate change strategy; improving agricultural conservation practices; and expanding public access to the Bay.
The widespread cosmetic use of chemicals on residential lawns and agricultural pesticide applications are significant contributors to the high loads of nitrogen and other chemical runoff to the Chesapeake Bay. A study by the U.S. Geological Survey found that "synthetic organic pesticides and their degradation products have been widely detected at low levels in the watershed, including emerging contaminants such as pharmaceuticals and hormones." Pesticides such as glyphosate (Round-up), atrazine, carbofuran, lindane and others have been detected in headwater streams that feed into the Bay. The annual report, "State of the Bay", published by the Chesapeake Bay Foundation consistently reports that the health of the Bay is declining.
Source: EPA New Release , Chesapeake Bay Program
(Beyond Pesticides, May 13, 2009) Last week, nine new hazardous chemicals were added to the list of chemicals to be banned under the 2001 Stockholm Convention on Persistent Organic Pollutants. Lindane, a pesticide commonly used in head lice treatments in the U.S. and whose use has already been banned in many countries, was added to the list for phase out. The U.S. Congress has never ratified the Stockhom Convention because of controversy associated with ratification legislation that would weaken federal pesticide law rather than adhere to more protective international standards. Meanwhile, environmental and public health groups in the U.S. have been urging U.S. officials to ban lindane due t o its toxic and bioaccumulative effects.
More than 160 governments (including those countries that have ratified the Stockholm Converntion) agreed last Saturday to include the nine pesticides and industrial chemicals to the list of 12 other persistent organic pollutants (POPS) in order to strengthen a global effort to eradicate some of the most toxic chemicals known to humankind. The nine chemicals are:
* alpha hexachlorocyclohexane - produced as an unintended byproduct of lindane;
* beta hexachlorocyclohexane -produced as an unintended byproduct of lindane;
* hexabromodiphenyl ether and heptabromodiphenyl ether- used in flame retardants;
* tetrabromodiphenyl ether and pentabromodiphenyl ether- used in flame retardants;
* chlordecone -an agricultural pesticide;
* hexabromobiphenyl, or HBB - a flame retardant;
* lindane - used in creams for treatment head lice; also has been used in other insecticides;
* pentachlorobenzene - used in PCB products, dyestuff carriers, as a fungicide, a flame retardant
* PFOS, perfluorooctane sulfonic acid, its salts and perfluorooctane sulfonyl fluoride - appears in a wide range of products from electronics components to fire-fighting foam (listed for elimination or restriction)
The Stockholm Convention, which was adopted in 2001 and entered into force 2004, requires Parties to take measures to eliminate or reduce the release of POPs into the environment.
"Just five years after this convention came into force, we will have nine new chemicals added to the list of those that the world community agrees we need to control and ultimately get rid of," said Achim Steiner, executive director of the U.N. Environment Programme (UNEP), which hosted the conference.
Donald Cooper, executive secretary of the Stockholm Convention, set out why the banned substances were exceptionally dangerous: They cross boundaries and are found everywhere, from the Tropics to Polar Regions; they persist for long periods in the atmosphere, soil and water, and take years to degrade; they accumulate in bodies; they accumulate in food chains. The chemicals can also damage reproduction, mental capacity and growth and cause cancer, Mr. Cooper said.
Countries that have ratified the treaty also enact national legislation to enforce the bans and restrictions it imposes. Participating countries have one year to say whether they will ban or restrict the chemicals or whether they will need more time or an exemption. The additions to the list make it possible for developing countries to receive international help in containing and destroying stockpiles of the chemicals which might otherwise seep into the soil and water supply.
Last month, groups in the U.S. called for the international ban of lindane and its inclusion onto the Stockholm Convention. The coalition of groups called on the Secretary of State Hillary Clinton and Acting Commissioner of the Food and Drug Administration Joshua Sharfstein M.D., to support listing of lindane under the international treaty without exemption for lotions and shampoos ("pharmaceutical uses"). It is unclear whether the listing of lindane as a POP to be banned would have any impact in the U.S. since the U.S. has not ratified the Stockholm Conventi on.
Lindane is a neurotoxic, organochlorine pesticide which has been linked to seizures, developmental disabilities and hormone disruption. It is known to be particularly hazardous to children. Lindane and associated isomers are among the most ubiquitous chemicals in the Arctic environment, contaminating traditional foods of Indigenous communities in the region. Lindane is banned in the state of California and has also been restricted in Michigan for use on head lice and scabies.
In the document, "Transforming Government's Approach to Regulating Pesticides to Protect Public Health and the Environment," which identifies what the Obama administration can/should take on under existing authority/statutory responsibility, Beyond Pesticides, Pesticide Action Network North America and other coalition groups urge Congress to ratify the Stockholm Convention on Persistent Organic Pollutants (POPs) in a way that gives the U.S. EPA the authority to take prompt action on pesticides and other chemicals identified as POPs by the international community, and to protect children from dangerous pharmaceutical pesticide products like lindane.
Source: Reuters, MSNBC World News
(Beyond Pesticides, May 4, 2009) Targeting areas frequented by children, such as playgrounds, picnic areas, baseball fields, campgrounds, beaches, and hiking trails, New York Governor David A. Paterson announced an initiative to substantially reduce pesticide use throughout the State park system. "New York has a magnificent State park system that is a tremendous resource for all New Yorkers," said Governor Paterson. "People visiting our parks, particularly children, should not be exposed to pesticides. This effort will reduce or, when possible, eliminate the use of pesticides in our State parks and historic sites."
The pesticide reduction policy is an outgrowth of Governor Paterson's Executive Order No. 4, adopted in April 2008, which established procurement specifications to minimize State pesticide use by State agencies. The State Parks policy goes further than the Executive Order requirements by eliminating pesticide use to the maximum extent possible. The goal is to keep parks pesticide-free. The approach is outlined in the Office of Parks, Recreation and Historic Preservation's Sustainability Plan, an agency-wide strategy to improve energy conservation, improve the sustainability of parks and historic sites, improve waste reduction and recycling efforts, enhance green procurement, and incorporate sustainability in education, training and interpretation efforts.
"Now that the snow has melted, people in every community across this State will begin visiting our parks, and for good reason—they are safe and affordable. The use of some pesticides can compromise that safety because nearly every time a pesticide is sprayed, something other than the target is hit," said Senate Majority Leader Malcolm Smith. "Limiting their use is a very smart move and will help us avoid any potential health concerns they may cause."
The policy asserts in the introduction that, "[T]he use of pesticides can cause potential environmental and human health risks, even when pesticides are used in compliance with regulatory requirements and manufacturer recommendations." The goal of the policy "is to eliminate pesticide uses wherever possible. In special instances where pesticide use is required, we will limit our use to least toxic alternatives." The policy covers all New York State Office of Parks, Recreation and Historic Preservation (OPRHP) agency facilities and operations, including concessions and contracted services.
The new policy requires implementation of an Integrated Pest Management (IPM) program for the design and maintenance of buildings, grounds, landscapes and water bodies under OPRHP's jurisdiction. IPM is described in the policy as a decision making process, a program for long-term pest suppression or elimination based on inspection, pest population monitoring and establishing action thresholds. The IPM program will "predominantly include structural and procedural modifications that establish physical barriers to pests, and reduce the food, water, and harborage available to them." Pests will be managed "using mechanical, sanitary, cultural, or biological means with the use of chemicals as a last resort." After non-chemical means have been exhausted, the use of allowed least toxic pesticides include those exempt from US EPA registration due to their low toxicity; rodent control in tamper-resistant bait stations or placed in areas inaccessible to children, pets, or wildlife; U.S. EPA registered biopesticides; antimicrobial pesticides; and, boric acid and disodium octaborate tetrahydrate, silica gels, diatomaceous earth, and other non-volatile insecticidal gels and baits. Specific pesticides are banned from use including: foggers; dusts or sprays in concession or food areas; and, carbamate and organophosphate insecticides.
On February 10, 2009, Executive Order 4 Turf and Ornamental Management specifications were adopted and compels OPRHP to strive to adhere to the land care specifications and practices prepared by the Northeast Organic Farmers Associations: NOFA Standards for Organic Land Care, NOFA Organic Landcare Committee, March 2008.
Policy exceptions allow the use of pesticides (with the lowest toxicity and least persistent product to be used first) for imminent health and safety threats such as human disease outbreaks, bees, wasps, deer ticks and poison ivy situations where immediate action is required. Although attempts will be made to follow IPM practices to the maximum extent possible, when pest problems cannot be controlled through non-chemical means pesticides are allowed for use on golf courses and arboretums, utility and transportation right-of-ways, and invasive species control.
"Patrons should be confident that the beaches, playgrounds, picnic areas and campgrounds where they go to relax and enjoy the great outdoors have not been treated with potentially harmful chemicals, said New York State Office of Parks, Recreation and Historic Preservation Commissioner Carol Ash. "Our efforts to significantly reduce pesticide use will help ensure the well-being of park visitors, especially young children, and will safeguard the long-term health of our parks and the plants and wildlife within them."
In addition to this State park policy, the New York State Department of Environmental Conservation recommends residents to stop using lawn chemicals, listing suggestions and resources to having a green lawn without toxic pesticides on their website. Highlighting the problem with lawn chemicals, the website states, "The chemically dependent lawn is more prone to disease and less able to handle stresses from drought, heat and insects. In addition, lawn chemicals and toxins can build up in soils, leach into our water, and pose potential hazards to people, pets and non-target species such as bees and birds."
"It is important to remember that our natural environment is not a special interest. Pollution and waste raise costs and kill jobs. Sustaining a healthy environment is central to creating jobs and rebuilding our economy for the future," said Governor Paterson at an Earth Day event announcing the pesticide reduction park policy. "Today, we should not have to fight to keep the air we breathe clean. But we do. We should not have to fight to keep the water we drink clean. But we do. We should not have to fight to preserve the integrity of our land. But we do have to. So we fight on…"
The New York State Park policy is just one of many around the country that establishes pesticide-free parks. Other examples of pesticide-free programs and policies include: Chicago City Parks; 29 communities and townships in New Jersey; at least 17 cities in the Northwest covering more than 50 parks; and, communities throughout Massachusetts,
On April 20, the National Marine Fisheries Service (NMFS) released a Biological Opinion (BiOp) finding that three additional pesticides, carbaryl, carbofuran, and methomyl, harm salmon and steelhead protected under the Endangered Species Act (ESA). The BiOp prescribes measures necessary to keep these pesticides out of salmon waters in Washington, Oregon, California, and Idaho. It is the second such plan issued in the last six months under a court settlement with fishermen and conservationists, filed by the non-profit law firm Earthjustice. The previous BiOp identified three organophosphate insecticides: chlorpyrifos, diazinon, and malathion.
"These pesticides are designed to kill insects on agricultural crops, but when they get into the water system, they also kill aquatic insects that salmon feed on." said Angela Somma, who heads the NMFS endangered species division.
From: Heather Hamlin , Environmental Health News
Published May 8, 2009 10:08 AM
Little is known conclusively about what causes brain cancer in children, but research studies are consistently finding links to prebirth pesticide exposure.
A new study finds that children who live in homes where their parents use pesticides are twice as likely to develop brain cancer versus those that live in residences in which no pesticides are used. Herbicide use appeared to cause a particularly elevated risk for a certain type of cancer.
It is well established that many pesticides cause cancer in animals.
This study highlights a new and compelling reason to avoid or limit pesticide use and take necessary precautions during exposure. It also adds to a growing body of research that finds that pesticide exposure -- especially with farm life and pesticide use -- might be contributing significantly to this deadly disease.
Brain cancer is the second most common cancer in children, yet why it develops is not clear. Genetics plays a role in some cases, but researchers believe those not due to associated genes are related to environmental factors and exposures.
The authors explain that "parental exposures may act before the child’s conception, during gestation, or after birth to increase the risk of cancer." Exposures at each time period may trigger different changes that lead to cancers, such as genetic mutations or changes in gene expression or hormone and immune function.
The study evaluated more than 800 fathers and more than 500 mothers that lived in residential areas in four Atlantic Coast states (Florida, New Jersey, New York (excluding New York City) and Pennsylvania). Researchers match and compare every person that is "exposed" to an "unexposed" person of the same age and status. In this case, more than 400 fathers and 250 mothers of exposed children were included.
By H. Hedrick Belin
Silver Spring
Sunday, April 19, 2009
After more than a quarter of a century of Clean Water Act legislation and enforcement, the Washington area's river and bay waters are nowhere near as healthy as they should be.
The main sources of the impairments are no mystery: sedimentation, agricultural runoff, rainwater running off paved surfaces. But recently, it has come to light that there is more going on in the Potomac River than meets the eye. While we have long tracked traditional pollutants, "Poisoned Waters," the documentary that will run on PBS's "Frontline" on Tuesday, highlights a new face in the lineup: chemical compounds that interact with and possibly interfere with the workings of the endocrine system. The endocrine system controls growth, metabolism and reproduction in humans and animals.
This class of pollutants is called "endocrine disruptors." These compounds are the primary suspect in the mystery of intersex fish that have been found in the Potomac and Shenandoah rivers. To date, we know that these compounds disrupt the development of many aquatic species, most notably male smallmouth bass that have developed eggs. This condition has been documented in the Potomac River watershed and beyond. It is becoming a global phenomenon.
Washington area residents get almost 90 percent of their drinking water from the river. Endocrine disruptors may enter our water in many different ways. Chemical-laden runoff from our lawns and roads flows into the river through the storm sewer system. Pharmaceuticals and personal-care products go down our toilets and drains and through the wastewater treatment plant, which does not remove them. Agricultural chemicals wash out of fields and chicken houses and into nearby streams. Drinking-water treatment plants do not treat for these chemicals before the water is delivered to our tap. In short, every place where water and chemicals combine becomes a potential source of endocrine disruptors in our drinking water.
Intersex fish in our rivers are an ominous sign of things to come. We know little about what causes this condition, and we need to know more. The Potomac Conservancy believes that it is time to answer the question of whether and how these compounds affect animal and human health, in particular, the development of our children. We call on the new administration to find -- and fund -- solutions for this important problem.
EPA Administrator Lisa Jackson spoke recently on this issue and promised a hard look at solutions. Last week, the agency announced its plan to test more than 67 chemicals contained in pesticides for possible involvement in endocrine processes. That is a promising start, but the compounds that will be studied represent only a fraction of the hundreds of thousands of chemicals in our water that could act as endocrine disruptors. These include a variety of products we all use in our daily lives, including shampoos, hand sanitizers, pharmaceuticals and lawn products.
The new pollutants don't set our rivers on fire, wash up on our shores or taint our air. As such, they are easy to overlook. We think it's high time to take a closer look at what is in our river water and our drinking water.
The writer is president of the Potomac Conservancy.
(Beyond Pesticides, March 18, 2009) The U.S. Environmental Protection Agency (EPA) has released a new online database that collects information on more than 500,000 synthetic chemicals from over 200 public sources. The Aggregated Computational Toxicology Resource (ACToR) database provides access to hundreds of data sources in one place, enabling easy access for environmental researchers, scientific journalists and the public. However, more than half of these chemicals do not have any detailed testing data.
ACToR, which is actually a collection of databases, was developed to support the ToxCast program of the EPA National Center for Computational Toxicology (NCCT). ToxCast was designed to develop faster methods to evaluate the potential toxicity for thousands of chemicals using computer modeling and advanced molecular biology techniques. More than 200 sources of publicly available data on environmental chemicals have been brought together on ACToR and made searchable by chemical name and other identifiers, and by chemical structure. Data includes chemical structure, physico-chemical values, in vitro assay data and in vivo toxicology data. Chemicals include, but are not limited to, high and medium production volume industrial chemicals, pesticides (active and inert ingredients), and potential ground and drinking water contaminants. Sources of information include EPA, U.S. Fo od and Drug Administration, U.S. National Institutes of Health, U.S. Centers for Disease Control and other federal agencies; state databases, Health and Environment Canada, the European Union, the World Health Organization and other international groups; and non-governmental organizations, private companies and universities.
ACToR was used to analyze toxicity information on almost 10,000 chemicals regulated by EPA and identify data gaps to be addressed by ToxCast, to help EPA prioritize future testing of chemicals. While acute toxicity data is available for 59 percent of the surveyed chemicals, detailed testing information is much more limited. Only 26 percent of the 10,000 chemicals have carcinogenicity testing data, 29 percent have developmental toxicity testing data, and 11 percent have complete reproductive toxicity test results.
The lack of toxicological data on more than half of the 10,000 chemicals overseen by the EPA means that there are numerous data gaps and thus, a lack of adequate safety tests which continues to undermine the integrity of EPA's risk assessment process. With little to no data on chemicals that are allowed to enter the consumer market place, the agency is failing to protect human and environmental health. A recent GAO report found that the EPA does not have sufficient chemical assessment information to determine whether it should establish controls to limit public exposure to many chemicals that may pose substantial health risks. The report went on to state that EPA has not responded to recommendations made to reduce agency shortcomings and has "not sufficiently improved the scientific information available to support critical decisions regarding whether and how to protect human health from toxic chemicals."
Source: EPA News Release
(Beyond Pesticides, March 16, 2009) Exposure to a mixture of the fungicide maneb and the herbicide paraquat significantly increases the risk of developing Parkinson's disease, according to a new University of California, Berkeley study, "Parkinson's Disease and Residential Exposure to Maneb and Paraquat from Agricultural Applications in the Central Valley of California." Published in the American Journal of Epidemiology, the study findings show that exposure to both pesticides within 500 meters of an individual's home increases the risk of developing Parkinson's by 75 percent. For individu als 60 years of age or younger at the time of diagnosis, there is a more than four-fold increase in risk of the disease when exposed to a combination of maneb and paraquat and a more than doubling of risk when exposed to either maneb or paraquat alone.
The Berkeley researchers used geographic information systems that analyzed data from California Pesticide Use Reports and land-use maps to calculate historical residential exposure to agricultural exposure to the two pesticides. From 1998 to 2007, the researchers enrolled 368 incident Parkinson's disease cases and 341 population controls from California's Central Valley and developed potential exposure estimates incurred between 1974 and 1999.
Also published this month by some of the same researchers, "Dopamine Transporter Genetic Variants and Pesticides in Parkinson's Disease," finds that certain genes and these same pesticides, maneb and paraquat, interact to increase to the risk factor for Parkinson's disease. This University of California, Los Angeles study looks at pesticide exposure and genetic variability in the dopamine transporter (DAT), a protein that plays a central role in dopaminergic neurotransmission of the brain which makes them more susceptible to Parkinson's. In this study, high residential exposure to maneb and paraquat increases risk almost 3-fold in individuals who have one DAT susceptibility allele and 4.5 fold in those with two or more susceptibility alleles.
The second most common neurodegenerative disease affecting more than one million people in the U.S., Parkinson's disease occurs when nerve cells in the substantia nigra region of the brain are damaged or destroyed and can no longer produce dopamine, a nerve-signaling molecule that helps control muscle movement.
Exposure to the herbicide paraquat has long been associated with Parkinson's disease. Several studies show an increased risk for Parkinson's with occupational exposure to and contact with paraquat. A case-control study in Taiwan found that those who had used paraquat were at greater risk of developing the disease than those that had used other pesticides. A 2007 study examined a cohort of 80,000 licensed private applicators and spouses and found that farmworkers exposed to paraquat have twice the expected risk of developing the Parkinson's. For those that were exposed to herbicides and could recall their exposure history, a Canadian population-based case-control study reported one individual using paraquat, between the ages of 26 and 31 years, and was the only herbicide-exposed case in the study whose onset of symptoms occurred before the age of 40.
Paraquat induces dopaminergic nigral apoptosis and acts through oxidative stress-mediated mechanisms. In laboratory animal studies, paraquat exposure triggers processes characteristic of early stages of dopaminergic neuron degeneration by stimulating an increase in the protein alpha-synuclein in the brain, likely due to preferential binding of the pesticides to a partially folded alpha -synuclein intermediate. The protein kills the dopamine-producing brain cells which lead to Parkinson's. In 2002, researchers from the Parkinson's Institute published that their findings "unequivocally show that selective dopaminergic degeneration, one of the pathological hallmarks of Parkinson's disease, is also a characteristic of paraquat neurotoxicity."
For researchers testing the role of oxidative stress in paraquat exposed mice, they find that the "initial exposure acts as a ‘priming' event, enhancing neuronal vulnerability to a subsequent toxic insult." Suggesting that dopaminergic cell degeneration appears to be dependent on the sequence of toxic challenges and the interaction between cell vulnerability, damaging effects and protective responses. Nigrostriatal neurons are vulnerable to oxidative processes. Depending on the paraquat exposure, oxidative stress may be reversible or lead to neurodegneration.
The synergistic effects of maneb and paraquat together have previously been linked to Parkinson's disease as well. In lab studies, University of North Dakota researchers find maneb affects rat brain mitochondria. Low levels of maneb can injure the antioxidant system in the dopamine neurons, especially with concurrent exposure to other environmentally relevant oxidative stressors, such as paraquat. University of Rochester scientists discovered that the synergistic effects of paraquat and maneb target the nigrostriatal dopamine system and indicate progressive neurotoxicity with continuing exposure. Their findings show that while there are no or only marginal effects when these chemicals are administered individually, together they produce synergistic effects when given in combination. In another study, these researchers again chronically expose mice to a low-level combination of maneb and paraquat, resulting in significant reductions in locomotor activity, levels of striat al dopamine and dopaminergic neurons in the substantia nigra, more so than when exposed individually.
A laboratory study finds that "prenatal exposure to the pesticide maneb produces selective, permanent alterations of the nigrostriatal dopaminergic system and enhances adult susceptibility to paraquat exposure." Additional studies show that exposure to maneb and paraquat during the post-natal and juvenile period causes Parkinson-like declines in dopaminergic neurons and makes the substantia nigra more susceptible to additional exposures in adulthood, "suggesting that developmental exposure to neurtoxicants may be involved in the induction of neurodegenerative disorders and/or alter the normal aging process."
(Beyond Pesticides, March 4, 2009) The Ontario government is set to announce sweeping new regulations that will prohibit the use of 85 chemical substances, found in roughly 250 lawn and garden products, from use on neighborhood lawns. Once approved, products containing these chemicals would be barred from sale and use for cosmetic purposes.
On November 7, 2008, the Ontario government released a proposed new regulation containing the specifics of the Cosmetic Pesticides Ban Act, passed last June. Then, Ontario joined Quebec in restricting the sale and cosmetic use of pesticides but environmental and public health advocates said then that the new law preempted local by-laws and actually weakens protections in some municipalities with stronger local protections. There are over 55 municipalities in Canada where the residential use, but not sale, of pesticides is banned. The prohibition of these 85 substances is the latest step in this Act. The proposal contains:
* List of pesticides (ingredients in pesticide products) to be banned for cosmetic use
* List of pesticide products to be banned for sale
* List of domestic pesticide products to be restricted for sale. Restricted sale products include those with cosmetic and non-cosmetic uses (i.e., a product that's allowed to be used inside the house but not for exterior cosmetic use), and would not be available self-serve.
The 85 chemicals to be prohibited are listed under "Proposed Class 9 Pesticides" of the Act. Among the 85 pesticides banned for cosmetic use include commonly used lawn chemicals: 2,4-D (Later's Weed-Stop Lawn Weedkiller), clopyralid, glyphosate (Roundup Lawn & Weed Control Concentrate), imidacloprid, permethrin (Later's Multi-Purpose Yard & Garden Insect Control), pyrethrins (Raid Caterpillar & Gypsy Moth Killer), and triclopyr.
However, golf courses and sports fields remain exempt. The use of pesticides for public health safety (e.g. mosquito control) is also exempt. The proposed regulation would also allow for the use of new ‘notice' signs to make the public aware when low risk alternatives to conventional pesticides are used by licensed exterminators, such as the use of corn gluten meal to suppress weed germination in lawns.
The prohibition, once passed, would likely take effect in mid-April. Stores would be forced to remove banned products from their shelves or inform customers that the use of others is restricted to certain purposes. Residents must then dispose of banned products through municipal hazardous waste collection, and use restricted products for only prescribed purposes. Errant users would first receive a warning, but fines would later be introduced. By 2011, stores will be required to limit access to the pesticides, keeping them locked behind glass or cages and ensuring that customers are aware of limitations on use before taking them home.
In light on impeding legislation to restrict pesticide use, the Canadian division of Home Depot announced on April 22, 2008 that it will stop selling traditional pesticides in its stores across Canada by the end of 2008 and will increase its selection of environmentally friendly alternatives. Other garden supply and grocery stores have already stopped selling certain pesticides in Ontario.
This proposed prohibition would have the most impact on 2,4-D, the most popular and widely used lawn chemical. 2,4-D, which kills broad leaf weeds like dandelions, is an endocrine disruptor with predicted human health risks ranging from changes in estrogen and testosterone levels, thyroid problems, prostate cancer and reproductive abnormalities. A recent petition filed with the U.S. Environmental Protection Agency and supported by Beyond Pesticides calls for the cancellation of 2,4-D, its products and its tolerances in the U.S.
Other lawn chemicals like glyphosate (Round-up) and permethrin have also been linked to serious adverse chronic effects in humans. Imidacloprid, another pesticide growing in popularity, has been implicated in bee toxicity and the recent Colony Collapse Disorder (CCD) phenomena. The health effects of the 30 most commonly used lawn pesticides show that: 14 are probable or possible carcinogens, 15 are linked with birth defects, 21 with reproductive effects, 24 with neurotoxicity, 22 with liver or kidney damage, and 27 are sensitizers and/or irritants.
Sources: The Star Ontario, The Ontario Ministry of the Environment
(Beyond Pesticides, February 23, 2009) Permethrin and lindane metabolites are found in children who use lice shampoos containing the insecticides, according to researchers affiliated with the Centers for Disease Control and Prevention. The study, "Pesticide exposure r esulting from treatment of lice infestations in school-aged children in Georgia," published in the February issue of the journal Environment International, is the first to measure children's exposure to chemical lice treatments.
The researchers collected baseline urine samples from 78 enrolled children between the ages of six to ten years of age. About one-third of those children were diagnosed with head lice and subsequently treated with at least one over-the-counter permethrin lice treatment, a prescription lindane treatment, or both. Within seven days of the insecticide application, urine samples were again collected. The permethrin exposed children had significantly higher urinary pryrethoid metabolite levels in their post-exposure urine samples. Lindane metabolites were also elevated in urine samples after treatment. Interestingly, the study states, "Exposed participants appeared to have higher pre-exposure metabolite levels – likely from multiple treatments before enrollment – than unexposed participants." Pentachlorophenol, a metabolite of lindane, was significantly higher in the urine of those children who used a lice treatment regardless of whether it was lindane-based. When looking at the children's urinary pentachlorophenol and the three permethrin metabolite levels, the study authors unexpectedly found age-related differences. The middle age group of children, between the eight and eleven years old, had lower metabolite levels than the older or younger children. In addition, "For those participants whose urine samples were collected more than one day following exposure, a larger percentage of the pesticide metabolites would have been eliminated from the body before sample collection making it more difficult to ascertain if an exposure had occurred," and thus possibly weakening the study results.
Permethrin is a possible human carcinogen and exposure is linked to possible endocrine disruption, immunotoxicity, neurotoxicity and reproductive effects. Exposure to synthetic pyrethroids such as permethrin has been reported to lead to headaches, dizziness, nausea, irritation, and skin sensations. Children are especially sensitive to the effects of permethrin and other synthetic pyrethroids. A study found that permethrin is almost five times more toxic to eight-day-old rats than to adult rats due to incomplete development of the enzymes that break down pyrethroids in the liver. Studies on newborn mice have shown that permethrin may inhibit neonatal brain development. Additionally, researchers have documented low-dose effects permethrin, doses below one-one thousandth of a lethal dose for a mouse, on those brain pathways involved in PD. The ef fects are consistent with a pre-Parkinsonsian condition, but not yet full-blown Parkinsonism.
Lindane has long been used in the treatment of head lice, yet is widely known for its neurotoxic properties, causing seizures, damage to the nervous system, and weakening of the immune system. It is also a probable carcinogen and endocrine disruptor. Lindane is particularly toxic and is also bioaccumulative. When used on people, lindane is regulated by the Food and Drug Administration (FDA). Despite the fact that it has been banned in 52 countries and restricted in over 30 more, the Food and Drug Administration (FDA) continues to allow its use in the U.S., albeit with a Public Health Advisory issued in 2003 that states, "Lindane should be used with caution in infants, children, the elderly, patients with skin conditions, and patients with low body weight (less than 110 lbs)." The last remaining agricultural uses of lindane were cancelled in 2006. It was banned in California in 2000 because of high levels of water contamination. Following the ban, water contamination dr astically declined, and an increase in head lice cases was not reported.
Head lice affect an estimated 12 million people in the U.S. each year, and are rapidly becoming resistant to over-the-counter and prescription medications. According to researchers on alternative lice treatments, one method for eliminating head lice that will not lead to resistant strains of lice is the use of hot air, which desiccates the insects and eggs, thus killing them
Written by Chipp Reid
Monday, February 09, 2009
A pair of Democratic lawmakers say they plan to grill the state Department of Environmental Protection over its efforts to restore the state's lobster industry while ignoring industry experts on the effects of pesticides lobstermen say continue to kill the animals.
Commercial fishermen claim pesticides many communities used to combat mosquitoes caused the lobster die-off in 1999 that all but wiped-out the state's $40 million lobster industry. The DEP, however, says there is not enough scientific data pointing specifically to the pesticides malathion or Altosid as the root cause of the die-off. Without that evidence, the DEP says, it cannot and will not ban the use of the chemicals.
"It's time we stop looking at Long Island Sound like it's just a recreational body of water and start looking at it like it's a job site. We lost an entire industry on the Sound," said Senate Assistant Majority Leader Bob Duff, D-Norwalk. "If we had a massive die-off on a farm in northern Connecticut, you can bet the DEP would still be conducting tests and would ban everything to find out why. I don't understand why it's different with the Sound."
Connecticut has spent $1 million trying to restore the lobster fishery and could spend another $200,000 on the program. State Rep. Richard Roy, D-Milford and chairman of he House Environment Committee, said he finds the DEP stance puzzling."They're trying to restore an industry, but they don't listen to the industry about potential problems with pesticides. That's odd," Roy said. "It doesn't make much sense to work to restore the lobster fishery if we're allowing chemicals to keep killing the lobsters."
Environmentalists agree
Fishermen and environmentalists agree with Roy. They say the restoration program little more than a waste of money if the DEP doesn't ban malathion or Altosid.
"It doesn't make a lot of sense to spend money on restoring a fishery if we're just going to allow people to keep using the pesticides that killed the lobsters in the first place," said Nick Crismale, president of the Connecticut Lobstermen's Association.
"We know. We were there. We saw what can only be the effects of pesticide poisoning. If the DEP doesn't do something about the pesticides, there's no way we can restore the lobsters."
The 1999 die-off came days after towns in Fairfield County, Westchester County and Long Island as well as New York City, sprayed malathion to kill mosquitoes carrying the West Nile virus. At the same time, the remnants of Hurricane Floyd inundated the state. Fishermen say the storm washed the pesticides into Long Island Sound, resulting in the die-off. The DEP, however, says the storm caused many other factors that led to the mass die-off.
"You had a number of effects from the storm, from hypoxia [lack of oxygen] to extremely low salinity to a major increase in water temperature," said Penny Howell, an environmental scientist with the fisheries division of the DEP. "Those had to have been bad things for the lobsters. There is simply no evidence pesticide could have covered the entire Sound to have the kind of effect that caused the die-off."
The DEP uses a series of tests Stony Brook University in New York conducted in the wake of the die-off. Those tests concluded water conditions as well as a parasite killed the lobsters rather than a particular chemical. However, the School of Pathobiology and Veterinary Medicine at the University of Connecticut, in a test it conducted in 2003, found even minute traces of malathion can have lethal effects on lobsters. According to the UConn study, 0.55 parts per billion of malathion — equivalent to a teaspoon of chemical in an Olympic-sized swimming pool — either kills lobsters outright or severely degrades its immune system.
"If a lobster's immune system is degraded, of course it's susceptible to a parasite," Crismale said.
Crismale also said attempts at the Lobster Institute of the University of Maine to infect healthy lobsters with the parasite the Stony Brook report cited failed.
"A healthy lobster killed the parasite," he said "Lobsters affected by pesticides died. You be the judge."
Roy said he believes there is more than enough circumstantial evidence for the DEP "to act on the side of caution."
"We really don't know what the killed the lobsters," he said. "But we are trying to bring them back, and we are spending money. I think the only way to find out is to begin to eliminate possible causes. We can't do much to change the water temperatures. We can do something about pesticide use. If we eliminate the pesticide, and the lobsters get better, then we know we're onto something."
The Commissioner's Office
Roy said he would take up the issue with DEP Commissioner Gina McCarthy.
The DEP itself appears divided over whether to enact even a limited ban on malathion and Altosid. Scientists in the fisheries division believe the pesticides pose a potential threat, but they also say there is not enough direct evidence linking the pesticides to the die-off.
Dennis Schain, a spokesman for McCarthy, took a much firmer tack.
"If there isn't any science to support a ban, we won't ban it," he said. "Case closed."
At least one lawmaker disapproved of that approach.
"We've banned other pesticides without hard scientific data, and I see no reason why this should be different," said Duff. "We're talking about jobs and the health of Long Island Sound. We should err on the side of caution, and if that means stopping the use of some chemicals, then we should stop."
The debate over pesticides could rise to the federal level as well. The U.S. Environmental Protection Agency tells the states which pesticides it allows. Ray Putnam, a scientists in the pesticide division of the EPA office in Boston, said it was then up to the states to decide whether to shorten that list.
U.S. Senator Joseph I. Lieberman said he believes it's time for Connecticut to adopt a shorter list.
"I will continue to fight the dumping of pesticides in Long Island Sound and will remain a staunch defender of the Sound's shorelines and its marine life," Lieberman said in a statement. "Long Island Sound is a precious natural resource, and it is essential that we remain good stewards by preserving the Sound's environmental integrity."
Roy said the state has already taken steps to ban pesticide use on playgrounds and at nursery and pre-schools.
"We want to protect children under 3 from exposure to harmful chemicals," Roy said.
The Milford Democrat also said adding malathion to a banned list would bring the state one step closer to his eventual goal.
"I would like to see the state go completely organic in pesticide and fertilizer," Roy said. "I really don't see the issue when it comes to a certain pesticide of not using it if it's a problem chemical."
© 2009 Hersam Acorn Newspapers
(Beyond Pesticides, January 23, 2009) A study by researchers at the UC Davis M.I.N.D. Institute has found that the seven- to eight-fold increase in the number children born in California with autism since 1990, a trend which shows no sign of abating, cannot be explained by either changes in how the condition is diagnosed or counted, and that environmental factors must be looked at more closely.
Published in the January 2009 issue of the journal Epidemiology, the study is entitled "The Rise in Autism and the Role of Age at Diagnosis." Results from the study suggest that research should shift from genetics to the host of chemicals and infectious microbes in the environment that are likely at the root of changes in the neurodevelopment of California's children, including pesticides and household chemicals.
"It's time to start looking for the environmental culprits responsible for the remarkable increase in the rate of autism in California," said UC Davis M.I.N.D. Institute researcher Irva Hertz-Picciotto, PhD, a professor of environmental and occupational health and epidemiology and an internationally respected autism researcher. Dr. Hertz-Picciotto said that many researchers, state officials and advocacy organizations have viewed the rise in autism's incidence in California with skepticism.
The incidence of autism by age six in California has increased from fewer than nine in 10,000 for children born in 1990 to more than 44 in 10,000 for children born in 2000. Some have argued that this change could have been due to migration into California of families with autistic children, inclusion of children with milder forms of autism in the counting and earlier ages of diagnosis as consequences of improved surveillance or greater awareness.
Dr. Hertz-Picciotto and her co-author, Lora Delwiche of the UC Davis Department of Public Health Sciences, initiated the study to address these beliefs, analyzing data collected by the state of California Department of Developmental Services (DDS) from 1990 to 2006, as well as the United States Census Bureau and state of California Department of Public Health Office of Vital Records, which compiles and maintains birth statistics.
Dr. Hertz-Picciotto and Ms. Delwiche correlated the number of cases of autism reported between 1990 and 2006 with birth records and excluded children not born in California. They used Census Bureau data to calculate the rate of incidence in the population over time and examined the age at diagnosis of all children ages two to 10 years old.
The methodology eliminated migration as a potential cause of the increase in the number of autism cases. It also revealed that no more than 56 percent of the estimated 600-to-700 percent increase, that is, less than one-tenth of the increased number of reported autism cases, could be attributed to the inclusion of milder cases of autism. Only 24 percent of the increase could be attributed to earlier age at diagnosis.
"These are fairly small percentages compared to the size of the increase that we've seen in the state," Dr. Hertz-Picciotto said. The remaining percentage must then be explained by genetics or environmental inputs. "There's genetics and there's environment. And genetics don't change in such short periods of time," she said.
Dr. Hertz-Picciotto said that the study is a clarion call to researchers and policy makers who have focused attention and money on understanding the genetic components of autism. She said that the rise in cases of autism in California cannot be attributed to the state's increasingly diverse population because the disorder affects ethnic groups at fairly similar rates.
"Right now, about 10 to 20 times more research dollars are spent on studies of the genetic causes of autism than on environmental ones. We need to even out the funding," Dr. Hertz-Picciotto said. One recent study of environmental factors linked residential proximity to pesticides and a higher incidence of autism.
Dr. Hertz-Picciotto and her colleagues at the M.I.N.D Institute are currently conducting two large studies aimed at discovering the causes of autism. Dr. Hertz-Picciotto is the principal investigator on the CHARGE (Childhood Autism Risk from Genetics and the Environment) and MARBLES (Markers of Autism Risk in Babies-Learning Early Signs) studies.
"We're looking at the possible effects of metals, pesticides and infectious agents on neurodevelopment," Dr. Hertz-Picciotto said. "If we're going to stop the rise in autism in California, we need to keep these studies going and expand them to the extent possible."
(Beyond Pesticides, January 22, 2009) A new English study has found that chemicals found in rivers and waste waters could be linked to male infertility. These chemicals, known as anti-androgens, block the action of the male sex-hormone testosterone and could impact the development of male reproductive organs in humans.
The study entitled, "Statistical Modeling Suggests That Anti-Androgens in Wastewater Treatment Works Effluents Are Contributing Causes of Widespread Sexual Disruption in Fish Living in English Rivers," and published in the journal Environmental Health and Perspectives identifies a group of river pollutants that cause testosterone to stop working. These chemicals, released from wastewater treatment operations into rivers and other surface waters are responsible for the feminization of male fish and abnormalities in male reproductive organs. Previous studies have attributed these problems in male fish to estrogenic compounds also found in surface waters.
However, this study is the first to identify anti-androgens with the feminization of male fish. It also indicates that male feminization may be the result of a rather more complicated interaction taking place between different classes of pollutants, resulting in an endocrine disrupting chemical cocktail.
"We have identified a new group of chemicals in our study on fish, but we do not know where they are coming from or what they are. We've only been able to measure their testosterone-blocking potential" said Susan Jobling, PhD, of Brunel University, one of the authors of the study.
The scientists analyzed anti-androgenic activity in samples of river water taken near 30 sewage outflows. They were able to demonstrate statistically that this activity could be linked with feminized fish found in the same rivers. Several chemicals in widely-used pharmaceuticals and pesticides are known to have anti-androgenic activity. They include several compounds found in agricultural pesticides.
Relatively high levels of anti-androgenic chemicals were detected near sewage outflows, suggesting they came from domestic sources. One possibility is that drugs excreted from the body may end up in rivers. However, the scientists also believe that the anti-androgens may also be seeping into rivers as run-off from agricultural land.
Feminization of male fish is a phenomena documented in recent decades in many rivers and surface waters in the US and Britain. Studies have long pointed to chemical contaminants such as pesticides and other endocrine disrupting chemicals, as having the potential for wreaking such hormonal chaos. Many pesticides have been implicated, including atrazine, permethrin, glyphosate (Round-Up) and 2,4-D. Other animals like polar bears, big cats, alligators and frogs have been observed with abnormalities in their reproductive organs, which have been attributed to environmental contaminants. Research has also shown that pregnant women exposed to environmental contaminants gave birth to babies with male reproductive defects.
Sources: The Independent (UK), Environmental Health Perspectives
(Beyond Pesticides, January 9, 2009) Environmental Toxicology and Chemistry has published a study (Vol. 27(12):2496–2500) entitled "Effects of Malathion on Embryonic Development and Latent Susceptibility to Trematode Parasites in Ranid Tadpoles (http://www.allenpress.com/pdf/entc_27.12_2496.pdf)." It shows that malathion used as an agricultural insecticide is responsible for interfering with the normal development of pickerel frog embryos, thus leaving them more susceptible to parasite invasion.
Malathion is present in natural water sources that have been exposed to urban and agricultural runoff. This organophosphate pesticide can be applied by planes in mosquito control program, and as esult enters water from the air.
Although direct lethal and sublethal effects of chemical contaminants have been documented, latent and long-term effects have been less well documented. Therefore, researchers sought to fill this knowledge gap and found, as suspected, that tadpole survival rates decreased and malformations and susceptibility to parasite encystment rates increased as a result of exposure to malathion concentrations mimicking those found in actual water sources.
Tadpoles are being exposed to increasing numbers of parasites in waters that are warming as a result of global climate change, and the researchers who performed this study speculate that, as a consequence, those exposed to malathion will have weakened immune systems that render them less able to defend themselves from invasion. Indeed, trematode infection was observed in tadpoles seven weeks after embryonic exposure to low concentrations of malathion.
This study shows that declines in amphibian populations are related to the agricultural application of malathion, which causes various kinds of damage to frog embryos and tadpoles that are, as a consequence, increasingly susceptible to parasite invasion. A similar study, published in October, 2008, found that some tadpole populations are being further threatened by malathion, as the chemical kills zooplankton, their primary food source. A 2007 U.S. Geological Survey study found malathion's breakdown product 10-100 times more toxic to amphibians than the parent product.
Malathion is one of a variety of agricultural and household chemicals that threaten amphibians' health and our drinking water. For more information on water contamination, visit Beyond Pesticides' brochure, Threatened Waters: Turning the Tide on Pesticide Contamination.