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HomeMy WebLinkAboutCOM 0392.113 2014-2016P/ EMC BILL 71 COMM. 392 4 PM 4: 6 How pesticides are undermining our children's health & intelligence SUBMITTED BY: JENNIFER RUGGLES V PESTICIDE ACTION NETWORK NORTH AMERICA Comm. No. Y Ref. To. 2it�1t,�- Ref. Date A11r, 0 4 M15_ Pesticide Action Network North America Pesticide Action Network North America (PAN North America) works to replace the use of hazardous pesti- cides with ecologically sound and socially just alternatives. As one of five PAN Regional Centers worldwide, we link local and international consumer, labor, health, environment and agriculture groups into an international citizens' action network. This network challenges the global proliferation of pesticides, defends basic rights to health and environmental quality, and works to ensure the transition to a just and viable society. Acknowledgements This 2013 printing is made possible by a grant from the Ceres Trust. To learn more about to how to protect children from pesticides, please contact PAN at healthykids@panna.org or 415-625-9026. This report and related information can also be downloaded at www.panna.org/kids. If you are interested in receiving a ship- ment of 10 or more reports, please contact the Ceres Trust at haddad@cerestrust.org. This report would not have been possible without the dedicated and careful work of hundreds of scientists at academic institutions in the U.S. and around the world. The contribution of these researchers to our collective understanding of the links between pesticide exposure and children's health is truly invaluable. A Generation in Jeopardy also reflects the efforts and expertise of many individuals both within Pesticide Action Network and among our partner organizations and institutions. Susan Kegley, Heather Pilatic, Linda Wells and Kathryn Gi1je provided useful comments and direction as the report was being developed and finalized. Several academic reviewers representing expertise in neurodevelopmental and carcinogenic impacts of pes- ticides on children's health provided substantive comments. Laura Cossette, Kristen Parks and Maria Reyna provided valuable research assistance. Thanks also go to Brenda J. Willoughby who formatted the report for publication, Sara Knight who tracked down images, created figures and otherwise assisted immeasurably with production, Mateo Rutherford and Roy Rojas of Berkeley Interpretation, Translation and Transcription Services (BITTS) who translated the Exec- utive Summary into Spanish, and Janet Stephens and Kathryn Gilje for final proofing and copy editing. Funding for this report was provided by The A&A Fund, the Arntz Family Foundation, the Bellwether Foun- dation Inc., The California Endowment, the Cedar Tree Foundation, the Ceres Foundation, the Ceres Trust, the David B. Gold Foundation, the Fred Gellert Family Foundation, the Kresge Foundation, the McKnight Foundation, the Roy A. Hunt Foundation and the Wallace Genetic Foundation, as well as PAN's supporting members. The authors bear responsibility for any factual errors. Recommendations and views expressed are those of Pesti- cide Action Network North America, and do not necessarily represent the views of our funders and supporters. CPRSpecial thanks to our colleagues at Californians for Pesticide Reform (CPR), Tracey Brieger and Sarah Aird, for strategic thinking and input as the report was being conceived and drafted, as well as assistance with the report's release and dissemination. PAN North America is a member of CPR, and is releasing this report in partnership with the coalition. The CPR coa- lition includes over 185 public interest organizations committed to improving and protecting public health, sustainable agriculture, and environmental quality by building a movement across California to change statewide pesticide policies and practices. See www.PesticideReform.org or call 510-788-9025 for more information about CPR's statewide work. 1611 Telegraph Ave, Suite 1200 Oakland (A 94612-2130 Tel 510.788.9020 • Fax 415.981.1991 www.panna.org • www.pesti(ideinfo.org © 2012 by Pesticide Action Network North America, second printing 2013. Permission is granted to reproduce portions of this report, provided the title and publishing organization is acknowledged. Printed on recycled paper. A Generation in Jeopardy How pesticides are undermining our children's health & intelligence Kristin S. Schafer, MA Emily C. Marquez, PhD with Medha Chandra, PhD Kendra Hutchens, PhD Candidate Margaret Reeves, PhD Meriel Watts, PhD, PAN Asia-Pacific 2013 Pesticide Action Network North America Table of Contents Executive Summary 1. Brainpower at Risk: Studies find pesticides can compromise intelligence 5 • AND rates continue to rise • Autism rates jump 250% in one decade • Derailed brain development means falling IQs 2.Cancer, Birth Defects & Early Puberty: Latest science links many health harms to pesticides 10 • Some childhood cancers linked to pesticides • Birth defects rise with seasonal or occupational exposures • Changes in puberty timing linked to low-level exposures 3. Emerging Science: Obesity, diabetes & asthma 14 • Childhood obesity, diabetes & disrupted metabolism • Asthma epidemic affects more than 7 million children 4. Critical Junctures: Prenatal & early childhood exposures most harmful 18 • Fetal exposure can have lifelong effects • Pesticide exposures common at home, daycare & school • Pesticide residues, from breastmilk to the school lunch tray • Children's developing minds & bodies particularly vulnerable 5. Case Studies: Communities win protections for children 22 • Pesticide use now 1.1 billion pounds yearly • Safer pest control in daycare & at school • Pesticide -free school lunches • Parks & playgrounds without pesticides 6. Investing in Healthy Futures: A solid start for children must be a national priority 26 • Pesticide industry well served by current policies • Prioritizing children's health requires real change • Effective policies urgently needed: Our recommendations Appendix A: More Science: Key study descriptions 33 Appendix B: Top Pesticides Used in Agriculture & at Home 38 Appendix C: Online Resources & Tools 39 A Generation in Jeopardy Executive Summary Children today are sicker than they were a generation ago. From childhood cancers to autism, birth defects and asthma, a wide range of childhood diseases and disorders are on the rise. Our assessment of the latest science leaves little room for doubt: pesticides are one key driver of this sobering trend. As the recent President's Cancer Panel reports, we have been "grossly underestimating" the contribution of envi- ronmental contamination to disease, and the policies meant to protect us have fallen far short. Nearly 20 years ago, scientists at the National Research Council called for swift action to protect young and growing bodies from pesticides.' Yet today, U.S. children continue to be exposed to pesticides that are known to be harmful in places they live, learn and play. This report reviews dozens of recent studies that exam- ine the impact of pesticides on children's health. Our analysis reveals the following: Compelling evidence now links pesticide exposures with harms to the structure and functioning of the brain and nervous system. Neurotoxic pesticides are clearly implicated as contributors to the rising rates of attention deficit/ hyperactivity disorder, autism, widespread declines in IQ and other measures of cognitive function. • Pesticide exposure contributes to a number of increasingly common health outcomes for children, including cancer, birth defects and early puberty. Evidence of links to certain childhood cancers is particularly strong. • Emerging science suggests that pesticides may be important contributors to the current epidemic of childhood asthma, obesity and diabetes. • Extremely low levels of pesticide exposure can cause significant health harms, particularly during pregnancy and early childhood. Children's developing bodies are particularly vulnerable to the health harms of pesticides. Prioritizing children's health requires real change As a nation, we value the wellbeing of our children. In addition to our natural urge to protect what we love, we know that at a societal level their successful development is key to a vibrant, secure future. Poll after poll shows more than 80 percent of Americans consider healthy children a top priority. We must line up our practice and policies with these values. Many communities across the country have stepped up to create local or state policies to protect children from pesticide exposure. From pesticide -free schools, parks and playgrounds to protective buffer zones in agricul- tural areas, locally -driven actions are leading the way to healthier childhood environments. But to ensure protection of all children from the harms of pesticides, we must dramatically reduce the use of these chemicals nationwide. An estimated 1.1 billion A Generation in Jeopardy • Pesticide Action Network North America pounds of pesticides are used in the U.S. every year, with more than 20,000 products on the market. This volume of use is undermining the health of the next generation and, as the science demonstrates, derailing development of our children's potential. Scientists have understood for decades that children are particularly vulnerable to the harms of pesticide exposure. Quickly growing bodies take in more of everything, they eat, breathe and drink more, pound for pound, than adults. As physiological systems undergo rapid changes from the womb through adolescence, interference from pesticides and industrial chemicals— even at very low levels—can derail the process in ways that lead to significant health harms. Reducing overall pesticide use would not only limit children's exposure during their most vulnerable years, it would also lower pesticide levels in the bodies of men and women of childbearing age—protecting current and future generations in one fell swoop. Those pesti- cides most harmful to children should be first on the list. Figure 1: Children's Health Harms on the Rise, 1975-2011* While we must each do what we can with food choices and decisions about home pest control, we cannot accomplish this goal at an individual household level. Policy change is required. Effective policies urgently needed To protect children from the health harms of pesti- cides, policymakers need much more effective tools. We believe change is most urgently needed in the way decisions are made about these three questions: • Which pesticides are used in agriculture? • Which pesticides are used in places children live, learn and play? • How are farmers supported as they reduce reliance on pesticides? 1997 DEVELOPMENTAL DISABILITIES 2008 17% increase overall, ages 3-17 1997 ADHD3% increase every year, ages 6-17 2006 2002 AUTISM 2008 78% increase, age 8 1975 ja CHILDHOOD CANCERS 2004 25% increased incidence, ages 0-19 1990 DIABETES 2011 53% increase, ages 0-19 OBESITY 1980 2004 171% increase, ages 6-11 1975 2011 Statistics show steady increases in many childhood diseases and disorders over the past 30 years. Those highlighted here are just some of the health harms on the rise. Sources: see endnotes 4, 13,24, 52 and 94. * With the exception of cancer, all other data are prevalence data, i.e., representing the U.S. population or based on data at several sites within the U.S. Prevalence is total number of cases in a population at a given time, while incidence is a measure of the number of new cases per year. The autism data are from 14 sites in the Autism and Developmental Disabilities Monitoring Network and are not considered fully representative of the U.S. population. The 1990 diabetes data are for type 1 only (type 2 being extremely rare among children at that time), while 2011 data include both type 1 and 2. Prevalence of type 2 diabetes among children is difficult to determine for various reasons, including difficulty of diagnosis. A Generation in Jeopardy • Pesticide Action Network North America We recommend the following policy changes in each of these arenas: 1. Prevent the pesticide industry from selling agricultural products that can harm children's health Take swift action on existing pesticides: If studies find a pesticide to be a neurodevelopmental or reproductive toxicant, endocrine disruptor or human carcinogen—and it has been measured in humans, in schools or homes, or as residues on food or in drinking water—EPA should target the pesticide for rapid phaseout, triggering USDA resources to assist rapid farmer transitions to safer pest control methods. Block harmful new pesticides: EPA should not approve any new pesticide that scientific studies suggest is a neurodevelopmental or reproductive toxicant, endocrine disruptor or human carcino- gen—including short-term "conditional" registra- tions. Table 1: Pesticides & Childhood Health Harms Herbicides 441 million lbs' e.g., atraane, gb* 1,4-D Insecticides 65 million lbs 40 e.g., chlorpyrifos, .� malathion, permethri Fungicides CG) 44 million lbs e.g., mancozeb, chlorothalonil Fumigants 108 million lbs e.g., metam sodium, i bromide, chloropicrin Prevent harmful low-level exposures: EPA should act on existing evidence that exposures to endocrine disrupting pesticides pose a particular danger to developing children; the long-delayed endocrine disruptor screening program (EDSP) should be swiftly implemented. 2. Protect children where they live, learn & play Kid -safe homes, daycares ea' schools: EPA should withdraw approval of existing pesticide products and not approve new pesticides for use in homes, daycare centers or schools when scientific evidence indicates the chemicals are possible neurodevelop- ment or reproductive toxicants, endocrine disrup- tors or human carcinogens. • Safer parks & playgrounds: State and local officials should enact policies requiring that all public playgrounds, playing fields and parks be managed without using pesticides that studies show are harmful to children's health. Researchers have linked exposure to various pesticides with a range of childhood health harms. A ✓ indicates that links to the health harm are particularly well supported by scientific evidence. See Appendix A and www.pesticideinfo.org t 2007 use estimates, refers to "active ingredient" From Pesticide Industry Sales & Usage, 2006 and 1007 Market Estimates, U.S. EPA, Washington, DC, Feb 1011. See www.epa.gov/ opp00001/pestsales/07pestsales/market_estimates2007.pdf. Table 3.4. A Generation in Jeopardy • Pesticide Action Network North America Childhood Health Harms" Birth Brain& nervous system - childhood Metabolic Reproductive& effects Immune developmental (e.g., obesity, disorders, Impacts cancers defects harms diabetes) asthma Y Y Y 'n Y Y Y Y Y nethyl v Researchers have linked exposure to various pesticides with a range of childhood health harms. A ✓ indicates that links to the health harm are particularly well supported by scientific evidence. See Appendix A and www.pesticideinfo.org t 2007 use estimates, refers to "active ingredient" From Pesticide Industry Sales & Usage, 2006 and 1007 Market Estimates, U.S. EPA, Washington, DC, Feb 1011. See www.epa.gov/ opp00001/pestsales/07pestsales/market_estimates2007.pdf. Table 3.4. A Generation in Jeopardy • Pesticide Action Network North America 3. Invest in farmers stepping off the pesticide treadmill • Corral resources for farmers. Federal and state officials should mobilize and coordinate exist- ing resources to help farmers adopt well-known, effective pest management strategies that reduce reliance on pesticides. • Increase investment in innovative farming: Congress should authorize significant funding for programs supporting farmers' adoption of sustainable prac- tices that reduce use of harmful pesticides. • Set use reduction goals: EPA and USDA should set specific and aggressive national pesticide use reduc- tion goals, focusing first on pesticides that studies show to be harmful to children. To track progress toward this goal, farmers should work with appli- cators and pest control advisors to report their pesticide use to a nationally searchable database. • Source for children's health: Food distributors should require that their suppliers limit use of pesticides that harm children's health. These proposals are all common-sense measures in the face of clear evidence that our children's wellbeing is at risk. It's time to muster the political will to prioritize the health of our children, grandchildren and future gener- ations. Even at very low levels, pesticide exposure can derail development and undermine the ability to learn. A Generation in Jeopardy • Pesticide Action Network North America Brainpower at Risk New studies find pesticides can compromise intelligence Knowledge of environmental causes of neurodevelopmental disorders is critically important because they are potentially preventable. — Dr. Philip Landrigan The process of establishing the architecture of the human brain begins in the womb and continues into early adulthood. During this long window of development, many complex processes take place, involving tens of billions of nerve cells Mechanisms of Harm Misfiring neurons & altered brain architecture Pesticides can interfere with brain function and development in several ways; we describe three of the most common and best understood mechanisms of harm here: Neurotransmitter control.• Organophosphate pesticides can block the normal functioning of acetylcholinesterase, an enzyme that degrades— and thus controls—a neurotransmitter called acetylcholine. When the functioning of the enzyme is blocked, acetylcholine is not degraded and neurons continue firing instead of shutting down after they've accomplished their mission. This can cause serious problems in the normal functioning of the nervous system. Developing brain cells: To date, EPA assessments have relied on acetylcholinesterase levels as a marker of organophosphate exposure risk, yet studies now show adverse effects can occur at much lower doses than those that block acetylcholinesterase. For example, chlorpyrifos has been shown to interfere with neural cell replication, differentiation and survival. As the brain structure is developing—particularly at key stages in utero—chlorpyrifos can disrupt the process in ways that permanently alter the architecture of the brain.' Sodium flow into nerve cells. Pyrethroid insecticides act on neurons by perturbing voltage -sensitive sodium channels. These sodium "gates" are what allow sodium to flow into a nerve cell, controlling how a neuron fires and transmits signals along a nerve. Pyrethroids cause these gates to open and close more slowly, changing how the nerve cell normally responds—either inducing repetitive firing or causing the nerve cell not to fire at all.' " Rauh, V. A., F. P. Perera, M. K. Horton, R. M. Whyatt, R. Bansal, X. Hao, et al. "Brain Anomalies in Children Exposed Prenatally to a Common Organophosphate Pesticide! Proceedings of the National Academy of Sciences. May 2012109 (20): 7871-6. See http:// www.pnas.org/cgi/doi/10.1073/pnas.12033%109. f Shafer T.1., D.A. Meyer and K.M. Crofton. "Developmental neurotoxicity of pyrethroid insecticides: critical review and future research needs " Environ Health Persp. Feb 2005 113(2):113-36. See http://www.ncbi.nlm.nih.gov/pubmed/15687048. making trillions of connections. Cells migrate from one section of the brain to another, and nerve tracts are laid as the final structure of the brain is created. Many of the processes that occur during brain development are vulnerable to disruption from pesticides. Exposure to neurotoxic pesticides during critical moments of fetal devel- opment, even at very low levels, has been shown to f inda- mentally alter brain architecture.' Pesticides that disrupt the hormone system—and particular those affecting the func- tioning of the thyroid, which plays a key role in brain devel- opment—can cause lasting damage. The impacts of exposures are often irreversible because unlike other organs, the brain cannot repair damaged cells (see sidebar). Children whose brain infrastructure or nervous system fails to develop normally may be disabled for the rest of their lives. Developmental disabilities include autism spectrum disorders, attention deficit disorders, hearing loss, intellectual impair- ment and vision loss. People with developmental disabilities are often challenged by everyday life activities such as lan- guage, mobility, learning and independent living. Reduced cognitive abilities can also lead to behavioral problems, from aggression and social alienation to increased risk of drug abuse.' A "Silent Pandemic" Some 15 percent of all U.S. children have one or more devel- opmental disabilities—representing a 17 percent increase in the past decade. For some disorders, the numbers are rising even more rapidly." Overall, researchers estimate that between Pesticides can interfere with brain function in several ways, from altering architecture during fetal development to interfering with neurostransmitter control. Gaetan Lee A Generation in Jeopardy • Pesticide Action Network North America Figure 2: AND Prevalence among Children Ages 3 to 17, from 1997-2008 010 0 a L 3 s a 0 0 c 6 a 0 Cn m 2 d 1997-1999 2000-2002 2003-2005 2006-2008 Year ■Boys infancy and childhood may contribute significantly to decline in the cogni- tive abilities of our children. A recent comprehensive review of the science on health effects of pesticides by the Ontario College of Family Physicians found exposure to pesticides in the womb to be "consistently associated with measurable deficits in child neurodevelopment. 1112 ■ Girls We look here at three areas where the evidence is particularly strong: ADHD, autism and falling IQs. A few of the key studies are highlighted below, and more detailed descriptions—along with additional studies—are provided in Appendix A. The number of children diagnosed with AND increased an average of 3 percent every ye f 1997 to 2008. Boys are much more likely to be affected. source: C. Boyle et al., "Trends in the Prevalence of Disabilities in U.S. Children, 1997- 2008.° 400,000 and 600,000 of the four million U.S. children born each year are affected by a neurodevelopmental disorder.' Public health experts from Harvard and Mt. Sinai Hospital have called the damage that chemicals are causing children's developing minds a "silent pandemic, "6 and scientists now point to a combination of genetic and environmental fac- tors to explain this rapid rise of developmental, learning and behavioral disabilities .7 Some children, for example, may have a genetic susceptibility to attention deficit/hyperactivity disorder (ADHD) or autism, but it may only develop if the child is exposed to a trigger- ing chemical during a certain period of development. Other children may be genetically programmed to produce less of a common detoxifying enzyme, rendering their brain and ner- vous system more susceptible to lasting harm when they are exposed to neurotoxic pesticides (see sidebar, p. 25).$ Genetic mutations that occur in parents (both men and women) in response to chemical exposures over the course of their lifetime can also, according to recent research, raise the risk of neurodevelopmental disorders for their children.','o The National Academy of Sciences now estimates that about one third of all neurobehavioral disorders (such as autism and ADHD) are caused either directly by pesticides and other chemicals or by interaction between environmental exposures and genetics." Some experts say this estimate is likely to be low, as the health profession is just beginning to fully rec- ognize the contributions of environmental factors to disease formation.' Whatever the mechanism of harm, recent studies leave little doubt that exposures to pesticides during fetal development, * See for example the 2010 President's Cancer Panel report "Reducing Environmental Cancer Risk: What we can do now" http://deainfo.nci.nih.gov/advisory/pcp/annualReports/index.htm. AND rates continue to rise ar rom ADHD is quite clearly on the rise, and Developmental though changes in diagnosis play a role, this cannot fully explain the trend. The number of children diagnosed with ADHD increased an average of three percent every year from 1997 to 2006, and an average 5.5 percent per year from 2003 to 2007 (see Figure 2).13• t The Centers for Disease Control and Prevention (CDC) estimates that ADHD now affects three to seven percent of all school children in the U.S.; one independent study puts the figure at 14 percent.14 Boys are much more likely to be diagnosed with ADHD, although the American Psychological Association notes that girls are more likely to suffer from the "attention deficit" part of the disorder, and their symptoms are often overlooked.]' A variety of brain functions are compromised in children exhibiting ADHD. Learning is often impaired, and those with the disorder may exhibit impulsive behavior and hyper- activity, and lack the ability to sustain attention. As with other neurodevelopmental disorders, the social impacts can be immense. Parents report that children with ADHD have almost three times as many problems interact- ing with peers as children without. Diagnosed children are almost 10 times as likely to have difficulties that interfere with friendships, including experiencing exclusion from peer groups. 16 The Science Researchers estimate that from 20 to 40 percent of ADHD cases are caused by something other than genetics. 17 Studies have found links to a variety of environmental contaminants, including exposure to organophosphate and pyrethroid insec- ticides during pregnancy and throughout childhood. t The CDC outlines diagnostic criteria here: hitp://www.cdc.gov/ncbddd/adhd/diagnosis.htmi, specifying that children must display at least six characteristic behaviors within six months, and that some symptoms must be present before the age of seven. CDC explains shifts in diagnostic criteria here: http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5810al.htm. A Generation in Jeopardy • Pesticide Action Network North America Children with higher levels of organo- phosphate breakdown products in their urine were more likely to have ADHD. Researchers found that 94 percent of the 1000+ children tested by CDC had detectable levels of these metabolites, and those with levels above the median were twice as likely to be diagnosed with ADHD as those with no metabolites found.18 Organophosphate metabolites at levels commonly found in the bodies of U.S. children are linked to increased likeli- hood of ADHD. Every 10 -fold increase in levels of organophosphate metabolites in the urine of children aged eight to 15 years was associated with a 55 to 72 percent increased likelihood of the disor- der.' Prenatal organophosphate exposure has been linked to attention problems. Each ten -fold increase in a pregnant mother's urinary concentration of organophos- phate metabolites led to a five -fold increased risk that her child would be diagnosed with ADHD by age five .21 Figure 3: Autism Prevalence among Children Ages 3 to 17, from 1997-2008 E 1.2 0.9 01 CL 3 1997-1999 2000-2002 2003-2005 2006-2008 Year Boys Girls Rates of autism have risen dramatically in the past decade. While overall prevalence is higher among boys, the rate of increase is higher among girls. source: C. Boyle et al, 'Trends in the Prevalence of Developmental Disabilities in U.S. Children, 1997-2008.' • Children with low birth -weight are more likely to have ADHD '21 and there is considerable evidence linking re- duced birth -weight with prenatal exposure to organophos- phate pesticides .21 • Mouse pups were hyperactive after being exposed to the pyrethroid insecticides pyrethrin or cypermethrin, and adult mice injected with permethrin or deltamethrin had long-term elevation of the dopamine transporter, a marker that has been linked to ADHD .21 Table 2: Chemicals Contributing to Autism • Lead • Methylmercury • Polychlorinated biphenyls • Organophosphate pesticides Organochlorine pesticides • Endocrine disruptors • Automotive exhaust • Polycyclic aromatic hydrocarbons • Brominated flame retardants • Perfluorinated compounds This list from public health experts includes both commonly used organophosphate pesticides and long lasting organochlorine pesticides, as well as other chemicals commonly found in consumer products. source: Landrigan, et al., 2011 Autism rates jump 250% in one decade The autism spectrum includes classic autism, Asperger's Syn- drome and atypical autism. Incidence rates have risen rapidly in recent years; in its 2012 report, CDC estimated—based on 2008 data on eight -year-olds from 14 states—that 1.1 percent of U.S. children, or one in every 88, are now on the autism spectrum. Boys are more likely to have the disorder, with one in 54 affected. Data from the National Health Interview Surveys reveal a dramatic rate of increase. Between 1997 and 2008, autism prevalence among boys ages three to 17 years increased 261%. Prevalence among girls, while much lower than boys overall, rose even more quickly, showing an increase of more than 385% over the same period (see Figure 3).24 In California, the number of children with autism who are enrolled in statewide programs rose from 3,864 in 1987 to 11,995 in 1998, an increase of more than 210 percent in 11 years.15 Other states saw similar rates of increase between 2002 and 2006.26 Though shifts in diagnosis account for some of this dramatic rise, public health experts have deter- mined that diagnostic changes do not fully explain the trend. Researchers believe autism spectrum disorders reflect changes in brain structure occurring during critical windows of devel- opment in the womb. These shifts in brain architecture may be caused by genetics, environmental insults such as chemical exposure, or an interaction between the two. 27, 28 In 2012, a group of researchers led by Dr. Philip Landrigan of Mt. Sinai Medical Center released a list of ten types of chem- icals most likely to be linked to the development of autism (see Table 2), and laid out an urgent strategy for research into the role of these contaminants and how children can be better protected from them. The list includes both commonly used organophosphate pesticides and longlasting organochlorine A Generation in Jeopardy • Pesticide Action Network North America pesticides, as well as other chemicals commonly found in consumer products.29 The Science Studies examining the links between pesticide exposure and autism suggest prenatal exposures are particularly damaging. • One study in California's Central Valley found that when mothers were exposed early in pregnancy to the organo- chlorine pesticides endosulfan and dicofol, the risk of autism among their children increased sharply. Children whose mothers lived within 500 feet of fields being sprayed were six times more likely to be on the autism spectrum." • Mothers in Californias central coast region who had higher levels of organophosphate metabolites in their urine during pregnancy were much more likely to have children with pervasive developmental disorder—which can include or be an indicator of autism. The risk more than doubled each time metabolite concentrations went up by a factor of 10.31 • A study in New York City found that infants most exposed to chlorpyrifos in utero were significantly more likely to have pervasive developmental disorders—including au- tism—by the time they were three years old." • A trio of U.S. studies examined links between environmen- tal exposures among parents (including, but not limited to, pesticides) and incidence of autism among their chil- dren.33 Among other findings, the scientists reported that older fathers are more likely to transmit tiny, spontaneous gene mutations—that occur over a lifetime in response to environmental stressors—to their offspring, that in turn increase the risk of autism. Recent research in Iceland con- firmed these findings." • Minnesota researchers explored the interaction of exposure to organophosphate pesticides, gene expression and dietary factors as potential contributors to autism.35 Among other things, they found that mineral deficiencies linked to high fructose corn syrup consumption' make developing minds more susceptible to the neurotoxic effects of pesticides. These various recent studies show how complex the path to our current autism epidemic has been. But evidence suggests that pesticide exposure—particularly during pregnancy—is implicated in a number of ways. Derailed brain development means failing IQs The societal implications of reduced cognitive abilities across an entire generation are nothing short of staggering and have been a concern among public health specialists since the IQ effects of lead exposure became clear in the 1970s. As Dr. Ted Schettler observed back in 2000: A loss of five _points in IQ is of minimal significance in a person with an average IQ. However a shift of five IQ points in the average IQ of a population of 260 million increases the number of functionally disabled by over 50 percent (from 6.0 to 9.4 million), and decreases the number of gifted by over 50 percent (from 6.0 to 2.6 million).46 * High fructose corn syrup is found in a wide range of processed foods and beverages. Twelve years later, Dr. David Bellinger echoed this observa- tion. He pointed out that cognitive effects, often dismissed as "clinically unimportant" at the individual level, become very significant across a whole society in terms of declining intellectual capacity, lost economic productivity and increased costs for education and health care. Bellinger reviewed published data linking organophosphates and cognitive effects, and concluded that overall, exposure to organophosphate insecticides may be responsible for lowering U.S. children's IQ levels by 17 million points—not much less than the 23 million point loss attributed to lead poisoning.37 Bellinger argues that because the potential impacts of organo- phosphates are so widespread and significant to society, "a risk assessment that focuses solely on individual risk, and fails to consider the problem in a public health context" is mislead- ing and will not lead policymakers to sound and protective decisions. The Science Pesticide exposure during pregnancy can have dramatic effects on cognitive development. From a wide range of animal research to studies tracking the intellectual development of children over time, the evidence points squarely at prenatal pesticide exposures as significantly harming the development and functioning of the brain. These harms can then lead to both lower IQ levels and neurodevelopmental delays. A particularly compelling study used Magnetic Resonance Imaging (MRI) technology to observe the developing brains of infants who had been exposed to chlorpyrifos during pregnancy. Researchers observed significant structural changes, including abnormal areas of thinning and enlarge- ment. Areas of the brain related to attention, language, reward systems, emotions and control were affected .38 Three cohort studies# released in 2011 document cognitive impairment caused by exposure to organophosphates in the womb.4 The first study found that higher metabolite levels in a mothers' urine late in pregnancy increased the likeli- hood of reduced cognitive development in their children .31 The second study linked prenatal exposure to a seven -point reduction in IQ by age seven.40 The third study found that even very low levels of chlorpyrifos residues in cord blood resulted in lower IQ and reduced working memory.41 • Pregnant mothers exposed to chlorpyrifos through house- hold use (before this use was withdrawn)' had infants with lower birth weight and reduced head circumference, both indicators of impaired cognitive ability later in childhood .42 t The accuracy of Intelligence Quotient (IQ) testing to measure intellectual capacity has long been a source of contention, but IQ is currently the best index for measuring cognitive abilities across a population. f See sidebar in Appendix A for a description of the various types of scientific studies highlighted in this report. § See this editorial in Environmental Health Perspectives for a discussion of the importance of these three studies: "Strength in Numbers: Three Separate Studies Link in Utero Organophosphate Pesticide Exposure and Cognitive Development," available online at: http://ehp03.niehs.nih.gov/ article/fetchArticle.action?articleURI=info%3Adoi%2F1O.1289%2Fehp.1104137 1 Chlorpyrifos was withdrawn from home use in 2001, but remains widely used in agricultural settings where farm, farmworker and rural community mothers and children still face exposure. Children also continue to be exposed from residue on fruits and vegetables. A Generation in Jeopardy • Pesticide Action Network North America • Exposure to the organophosphate pesticides diazinon and parathion during early childhood may reduce cognitive function, according to results from animal studies. Low- dose exposures caused changes in the developing brains of rats known to correspond to reduced ability to learn." Other animal studies indicate that in utero and neonatal exposure to organophosphates increases the risk of develop- mental delays. • Children at three months of age who were most highly exposed to the pyrethroid pesticide synergist piperonyl butoxide,' as assessed by personal air monitors, scored 3.9 points lower on the Bayley Mental Developmental Index. These scores are predictive of school readiness, and the authors described their results as modest, yet "worrisome."45 • Prenatal exposure to the DDTt breakdown product DDE is also associated with neurodevelopmental delays in children, especially the "psychomotor" skills linkinmovement or muscular activity with mental processes. And exposure in utero to DDT itself has been associated with reduced cognitive functioning, memory and verbal skills among preschoolers. 47 Strong emerging evidence links childhood pesticide exposure to other, adult-onset neurological effects such as Parkinson's and Alzheimer's diseases; these studies are not examined here .41 The combined, society -wide impact of the various syndromes, disorders and deficits resulting from damage to children's brains and nervous systems early in life is immense. Health professionals and educators across the country have indicated concern that our current policies don't adequately protect our children as their nervous systems develop49 Something must be done to address this gap, as the results of such exposures have profound consequences for individuals, families and society as a whole. * Piperonyl butoxide, or 1`60, is commonly included in formulations of pyrethroid pesticide products to increase the potency of the active ingredient. t Agricultural uses of DDT were banned in the U.S. in 1972, but because of its persistence, DDT and its breakdown products continue to appear in human blood samples. DDT use continues in some countries for malaria control programs. Exposure of a developing fetus, infant or child to neurotoxic pesticides can lead to greater risk of learning disabilities and significant drops in IQ. A Generation in Jeopardy • Pesticide Action Network North America 2 Cancer, Birth Defects & Early Puberty Latest science links many childhood health harms to pesticide exposure If we are going to live so intimately with these chemicals—eating and drinking them, taking them into the very marrow of our bones—we had better know something about their nature and their power. —Rachel Carson Our children face a range of health challenges that were not encountered by past generations. Public health experts are concerned, and are increasingly focusing on the contributing role of environmental factors such as pesticides and other chemicals. The President's Cancer Panel's 2010 report, for example, concluded that the role environmental contaminants play in contributing to cancer has been "grossly underestimated" and called for urgent action to reduce the current widespread exposure to carcinogens. The Panel's chair, Dr. LaSalle Leffall, urged preventative measures to protect public health—even in the face of some uncertainty.' The increasing number of known or suspected environmental carcinogens compels us to action, even though we may currently lack irrefutable proof of harm." Meanwhile, evidence continues to mount linking chemical exposure to a range of children's health harms. Below we present a summary of some of the growing body of recent findings on pesticides and childhood cancer, birth defects and early puberty. More detailed descriptions and additional studies are included in Appendix A. Some childhood cancers linked to pesticides Cancer is the second most common cause of death among U.S. children one to 14 years old.' Over the past 30 years, the number of children diagnosed with all forms of invasive cancer has increased 29 percent, from 11.5 cases to 14.8 cases per 100,000 children per year (see Figure 4).51 There are many types of childhood cancer, and incidence rates vary widely. Leukemia and childhood brain cancers are now the most common cancers among children, with rates for these two cancers rising 40 to 50 percent since 1975: leuke- mia from 3.3 to 4.9 per 100,000 children, and brain cancers from 2.3 to 3.2 (see Table 3).52 Survival rates have also risen. Improved cancer treatments have led to dramatic increases in survival of all types of childhood cancer, particularly leukemia (from 50 percent survival in 1975 to more than 80 percent in 2004) and non -Hodgkins lymphoma (from 43 to 87 percent survival over the same time period.) For all types of childhood cancers, * This call for action in the face of some uncertainty is an example of the "Precautionary Principle," an approach to decision making that has been adopted by many local governments in the U.S. and in countries around the world. For a definition and more information, see the Science and Environmental Health Network's FAQ: http://www.sehn.org/ppfags.html t Lethal accidents are the most common cause of death. Figure 4: Incidence of Cancer among Children, 1975 & 2004 Ages 0-14 - Ages 0-19 1975 2004 Over the past 30 years, the number of children diagnosed with all forms of cancer has increased from 11.5 to 14.8 cases per 100,000 children per year. Source: SEER, 2004 Table 3: Top 5 Childhood Cancers • Leukemia • Brain and other nervous system tumors • Neuroblastoma • Wilms'tumor • Lymphoma The types of cancers that occur most often in children are different from those seen in adults. Source: American Cancer Society African-American children have a lower survival rate than do white children (73 vs. 81 percent).53 For some cancers, genetics is a powerful predictor. But as outlined by the President's Cancer Panel, cancers can have multiple and often interacting causes. In some cases genetic factors make an individual more susceptible, and exposure to environmental carcinogens may trigger cancer development. The Science A large number of recent studies link pesticide exposure to childhood leukemia, brain tumors and neuroblastoma. Some evidence suggests pesticide exposure may also be associated with other types of children's cancer, such as non-Hodgkin's lymphoma, Wilms' tumor and Ewing's sarcoma. Many studies 10 A Generation in Jeopardy • Pesticide Action Network North America find in utero exposure during key windows of fetal develop- ment or parental exposure before conception to be particu- larly important. • Home insecticide use during pregnancy can increase risk of childhood leukemia, according to a review of 15 studies over the past two decades. Timing of exposure appears to be particularly important.54 The risk of a child developing acute lymphocytic leuke- mia—the most common type of childhood leukemia—is higher when the mother is exposed to home insecticides during pregnancy. Risk increased with the frequency of the mother's exposure; the highest risk was associated with use of household insecticides more than five times over the course of gestation." • Mothers who have a particular genetic variant of an enzyme involved with the metabolic processing of wastes and toxins (including carcinogens)' are more likely to have a child with leukemia when they use pesticide products during preg- nanry.56 • Several case -control studies link exposure to herbicides and household insecticides during pregnancy to an increased risk of childhood brain cancer. 17 • Higher risk of neuroblastoma, the most common cancer among infants, was observed in children whose parents reported garden and home pesticide use.5' An older case - control study of U.S. and Canadian children indicated in- creased risk of neuroblastoma among children whose fathers were landscapers and groundskeepers.51 • In a national case -control study in Australia, increased risk of Ewing's sarcoma tumors among children was linked to occupational exposures of mothers and fathers who worked on farms around the time of conception.60 • Children who lived in areas of high agricultural activity in the U.S from birth to age 15 experienced significantly in- creased risk of childhood cancers.61 And a study in Norway of agricultural census data found that of 323,359 children under 14, those who grew up on a farm—combined with a high level of pesticides purchased by the family—were nearly twice as likely have brain tumors.61 A number of studies—not reviewed here—explore potential links between prenatal or childhood pesticide exposures and incidence of cancers later in life. For example, according to the President's Cancer Panel, girls who were exposed to DDT before they reach puberty are five times more likely to develop breast cancer in middle age.63 In general, the association between pesticide exposures and childhood cancer outcomes may be underestimated, as data are somewhat limited and studies focus on certain cancers more than others. In addition, common methodological problems—such as occupational exposures being identi- fied only through self -reporting or job title, considerations of other routes of exposure, small sample sizes, and relying on recall to estimate exposures—may contribute to skewed findings.G4 * The CYP1A1 gene codes for the expression and activity level of an enzyme that helps clear the body of potentially harmful compounds. Birth defects rise with seasonal or occupational exposures Birth defects are the leading cause of infant mortality in the U.S., accounting for 19 percent of the 29,138 infant deaths in 2007. And the overall incidence of birth defects is ris- ing.65 According to CDC data, about one in every 33 babies born today has some kind of birth defect. 16 Birth defects can affect almost any part of the body; some are mild and impact appearance only, others affect the functioning of organs and can be life threatening, although overall survival rates have increased significantly since 1979.67 Incidence trends vary by specific birth defect. Cleft lip/palate is the most common birth defect reported, and incidence has declined slightly over the last decade. Rates of Down Syndrome, gastroschisis (an abdominal wall defect resulting in protrusion of the intestines) and anencephaly (absence of portions of the brain, skull and scalp) have all increased since 1999.61 Like many children's health outcomes, a combination of genetic and environmental factors is often at play. CDCs research on environmental factors has focused primarily on smoking, alcohol intake, obesity and diabetes." Other scien- tists, however, have examined the role of parental exposure to pesticides and other chemicals before conception, and of mothers' exposure to environmental contaminants during pregnancy (see sidebar, p. 17). The Science Parents exposed to pesticides occupationally, from exposures in their community or by in-home pesticide use may increase the risk of birth defects in their newborn. Studies indicate that. exposure of both mothers and fathers, particularly during the period of conception, can influence birth defect outcomes. Several studies in agricultural areas have correlated conception during peak pesticide spray season with increased birth defect risk. A mother's exposure during pregnancy can also play a key role, with specific timing once again emerging as a critically important variable. Children whose mothers were exposed to herbicides and household insecticides during pregnancy have an increased risk of developing brain cancer. A Generation in Jeopardy • Pesticide Action Network North America Farmworker Families & Pesticides As a community organizer and health educator in North Carolina, Ana Duncan Pardo works with many communities directly affected by pesticides. When we spoke with Ana about her experience working with farmworkers, she described a particular instance—when she was setting up for a presentation to farmworker parents—that awoke her tp the health harms faced by many of these families: Within five minutes I had noted multiple cleft palates and several children with apparent Down Syndrome.... It was shocking and disturbing to walk into a room with a group of parents and children that easily represented three to four times the national average for birth defects. Farmworkers and their families face unique risks, as the harmful chemicals applied in the field follow workers home on their skin, shoes and clothing, and may also drift into their homes from the nearby fields. And, like all families, the food they eat every day may contain pesticide residues. Ana Duncan Pardo is the farmworker organizer & communications coordinator for Toxic Free North Carolina, and a member of PAN's board. A multi-year, national review of USGS water data and CDC birth defect records found a strong seasonal associa- tion between birth defects and the presence of the herbicide atrazine in surface water. Infants conceived between April and July, when elevated concentrations of the herbicide are found, have a significantly higher birth defect risk (see Figure 5).70 • In Washington state, a seasonal analysis of the risk of the abdominal wall defect gastroschisis showed prevalence peaking when conception occurred between March and May. The birth defect occurred most frequently among infants whose mothers lived within 50 kilometers of a site with high surface water concentration of atrazine .71 • Male pesticide applicators in Minnesota had a significantly higher number of children with birth defects, in a study examining 4,935 births to pesticide applicator fathers over three years. The birth defects were more common among boy offspring than girls .7' Egyptian fathers exposed to pesti- cides at work also had a greater risk of having children with congenital malformations .71 • Increased risk of boys' urogenital malformations such as hy- pospadia, micropenis and cryptorchidism' has been linked in many studies to prenatal exposure to environmental con- taminants. One recent meta-analysis of studies from seven countries (Canada, Denmark, Italy, Netherlands, Norway, Spain and the U.S.) indicated a 36 percent increased risk of hypospadia when mothers were exposed to pesticides at work, and a 19 percent increased risk with fathers' occupa- tional exposure to pesticides .74 * Hypospadia is a defect in which the urethral opening develops in the wrong location along the shaft of the penis. Micropenis is a defect where boys have severely reduced penile size, and cryptorchidism is a defect where the testes descend improperly, or not at all. Figure 5: Atrazine Seasonal Exposure & Birth Defects 1.4 1.2 1.0 0.9 S 0.6 0.4 0.2 Birth Defects vs Atrazine 1996-2002 U.S. 1640 1620 1600 1590 1560 1540 1520 0.0 11M 1500 Jan Feb Mar Apr May Jun Jul Au0 Sep Od Nov Dec Month Seasonal exposure to pesticides during pregnancy has been linked to increased risk of birth defects. Source: Winchester, P.D., J. Huskins and J. Ying. 'Agrichemicals in surface water and birth defects in the United States! Acta Paediatrica. 2009 98: 664-669. • The risk of having a child with neural tube defects, which are birth defects of the brain and spinal cord, has also been linked to pesticide exposure. Studies indicate a higher risk of this birth defect if insecticide bombs or foggers are used in the home during the period of conception. Risk is also higher if women live within a quarter mile of a cultivated field where pesticides are sprayed .71 • Mothers exposed to pesticides at work during a particular period of pregnancy have a significantly greater risk of having a child with anencephaly (a rare defect involving ab- sence of a large part of the brain and skull).71 A meta-anal- ysis of studies examining fathers' exposure to Agent Orange (containing the herbicides 2,4-D and 2,4,5-T) found the risk of having offspring with spina bifida, a "split spine" defect caused by incomplete formation of the neural tube, was twice as high among those fathers who were exposed. 77 t Many epidemiological studies over the years have found no association between pesticide exposure and birth defects. It must be considered, however, that these studies may not have taken timing of exposure into account, a variable that is proving to be a critical factor in birth defect outcomes. And as with cancer studies, results may be skewed by use of inap- propriate surrogates for pesticide exposure (e.g. job title) or inaccurate subject recall. Changes in puberty timing linked to low-level exposures Young girls in the U.S. are moving from childhood to ado- lescence at an ever -younger age. Changes in the timing of sexual development over the past two decades have been so widespread that the age of "normal" puberty onset has been redefined by health professionals .71 t Agent Orange was widely used as a defoliant during the Vietnam War and was often contaminated with dioxins which have also been linked to birth defects. One of the herbicide ingredients, 2,4-D, is still in use in the U.S., and a proposal is currently under consideration for a genetically engineered variety of corn designed to allow increased 2,4-D application. 12 A Generation in Jeopardy • Pesticide Action Network North America Dr. Herman -Giddens and her colleagues first documented this acceleration in 1996, in a study finding that the number of girls having some sign of puberty onset before the age of eight was "substantially higher" than previously found .79 These initial findings of early puberty were corroborated in 2010 by researchers who found that by age seven, 10 percent of white girls, 23 percent of black non -Hispanic girls, and 15 percent of Hispanic girls had begun the process of breast development, also known as thelarche.80 Some changes in pubertal development in boys have also been documented. Changes in puberty timing are concerning for several reasons. For both boys and girls, self-esteem and body image issues can sometimes lead to self-destructive behaviors and poor perfor- mance in school. Additionally for girls, both early puberty and obesity (a contributing factor for early puberty) have been linked to health impacts later in life, increasing the risk for breast cancer and later reproductive health issues such as polycystic ovary syndrome.81, 82 These changes cannot be fully explained by ethnic, geo- graphic, or socioeconomic factors, and thus a growing body of research has turned to examining the role of endocrine -dis- rupting chemicals in accelerating puberty in children.83 The Science Although the number of studies is relatively small, researchers have found some associations between pesticide exposure— either during fetal development or early childhood—and effects on puberty. Most studies focus on in utero exposures to pesticides with endocrine -disrupting effects that can interfere with the healthy development of the reproductive system—par- ticularly if exposure occurs at certain times in the process (see sidebar) .14 The majority of studies focus on precocious puberty in girls, but a few studies have also found links between pesticide exposure and changes in the timing of puberty among boys. Much of the research to date examines impacts of long-lasting organochlorine pesticides. Some of these are chemicals that have already been banned in the U.S. (e.g., DDT, hex- achlorobenzene); others are in the process of being phased out (e.g., lindane, endosulfan); but all are still present in our food supply, environment, and in our bodies.85,' Though few stud- ies have yet examined the connections, pesticides currently in use are also implicated in some studies. • Prenatal exposure to the herbicide atrazine was linked to delayed pubertal development in both male and female rats in a recently released animal study." • Danish greenhouse workers exposed to a range of pesticides during pregnancy were more likely to have daughters show- ing breast development from 6-11 years old. 17 Increased likelihood of early puberty in girls in Jerusalem was found to coincide with seasons of intensified pesticide usage.88 * CDC sampling from 1999-2000, for example, found DDT's breakdown product in blood samples of 99 percent of U.S. population. See http://www,cdc.gov/exposurereport/. Mechanisms of Harm Endocrine disruption = development derailed The term "endocrine" refers to systems in the body that are controlled by hormones, such as brain development, growth, reproduction and puberty. Hormones are chemicals synthesized in the body that bind to receptors to trigger actions at the cellular level resulting in physiological changes. Once their job is done they are released and free to act again. Some pesticides act as "endocrine disruptors" that mimic hormones and can interfere with systems normally controlled by hormonal action. If such disruption occurs at times during development known as "windows of vulnerability,"—such as when the reproductive system is coalescing, brain or nervous systems are developing, immune system is forming or puberty is getting underway—the process can be derailed in significant ways, sometimes with life-long effects. Because hormones themselves act at extremely low levels, biological processes controlled by hormones are tremendously sensitive. This means there often is no "threshold" or "safe" dose when it comes to endocrine disrupting compounds.' * Zoeller, R.T., T. R. Brown, L. L. Doan, A. C. Gore, N. E. Skakkebaek, A. M. Sotp et al. "Endocrine -Disrupting Chemicals and Public Health Protection: A Statement of Principles from The Endocrine Society." Endocrinology June 2012. See http://endo. endojournals.org/content/early/2012/06/21/en.2012-1422.abstract. Vandenberg, L., T. Colborn, T. Hayes, J. Heindel, D. Jacobs, D.H. Lee, et al. "Hormones and Endocrine -Disrupting Chemicals: Low -Dose Effects and Nonmonotonic Responses" Endocrine Reviews. March 2012 33(3): 378-455. • Daughters in Michigan were more likely to reach puberty at a younger age if their mothers had higher blood levels of the DDT breakdown product, DDE. Participants in this study included women who regularly consumed fish from the Great Lakes, which for years have been heavily contami- nated with industrial pollutants such as PCBs and DDT.89 • Higher blood levels of hexachlorobenzene and DDE were associated with early puberty among Flemish boys.90 Two recent studies of boys in India and Russia linked exposure to the pesticide endosulfan and the industrial by-product dioxin to delayed puberty among boys.91 • The pyrethroid insecticide esfenvaleratet has shown endo- crine -disrupting effects related to puberty timing in female rats. Rats exposed to low levels (half of EPA's "no observable effect" level) for seven days showed significant delays in onset of puberty. 12 As evidence mounts that developmental exposures to pesti- cides can have an effect on puberty timing, additional studies are now focusing on such endocrine -disrupting effects of pesticides currently in use. t Esfenvalerate is listed for Tier 1 screening under EPA's Endocrine Disruptor Screening Program. See http://www.regulations.gov/#IdocumentDetail;D=EPA-HO-OPP-2009-0634-0001. A Generation in Jeopardy • Pesticide Action Network North America 13 14 3 Emerging Science Obesity, diabetes & asthma Chemicals that disrupt hormone messages have the power to rob us of rich possibilities that have been the legacy of our species and, indeed, the essence of our humanity. —Theo Colburn Many of the health challenges facing children today have strong genetic and/or behavioral components. The rise in childhood obesity, for example, in part reflects the increasingly sed- entary habits of many U.S. children.' But it's becoming increasingly clear that personal lifestyle choices do not tell the whole story. The speed and scope of the society -wide rise in childhood health problems suggest a complex interaction of genetic, behavioral and environ- mental variables. Researchers are beginning to tease apart these interactions to more fully under- stand how exposure to environmental contami- nants are involved. We examine here the rapidly emerging science exploring how pesticides may contribute to the recent rise in childhood obesity, diabetes and asthma. Additional studies are included and described in Appendix A. Childhood obesity, diabetes & disrupted metabolism The recent dramatic rise in childhood obesity in the U.S. has the focused attention of health specialists and the public. The number of clini- cally obese children has more than tripled in the past 30 years, with obese children ages six to 11 jumping from seven percent of the total in 1980 to nearly 20 percent in 2008. The percentage of obese adolescents (12-19 years old) increased from five to 18 percent over the same period (see Figure 6).93, t Figure 6: Prevalence of Obesity among Children Ages 2 to 19 between 1976-2008 Ages 2-5 Ages 6-11 Ages 12-19 20 Y AL 16 t 12 0 1 1976-1980 1988-1994 1999-2000 2001-2002 2003-2004 Selected Years Between 1976-2008 Prevalence of obese U.S. children ages 6 -11 jumped from 7 percent in 1980 to 20 percent in 2008, while the percentage of obese adolescents increased from 5 to 18 percent. source: Center for Disease Control, "Prevalence of Obesity Among Children and Adolescents: United States, Trends 1963-1965 Through 2007-2008" Obesity is closely linked to childhood diabetes, which is also on the rise. According to the National Institutes of Health, about 215,000 Americans under the age of 20 had diabetes in 2010—up from roughly 123,000 in 1990.94 91 In addition to increasing related health risks, both obesity and diabetes can have a negative effect on quality of life in terms of ability to engage in physical activities, societal acceptance and self-image. * CDC points to estimates that U.S. children spend an average 4.5 hours a day watching television and 7.5 hours using entertainment media (TV, computers, video games, cell phones and movies) as a contributing factor to childhood obesity. See http://www.cdc.gov/obesity/childhood/problem. html t See CDC's "History of State Obesity Prevalence" showing trends in adult obesity by state from 2000-2010, at the bottom of this page: http://www.cdc.gov/obesity/data/adult.html The Science So much new science exists around the links between obesity and environmental contaminants that a new term, "obesogen" (like carcinogen) has emerged in the literature.# Findings increasingly suggest that exposures to pesticides and other chemicals play a role by altering developmental programming in ways that raise the likelihood of obesity and related meta- bolic effects such as diabetes .16 In 2002, Baillie -Hamilton reviewed data suggesting that the obesity epidemic coincided with the marked increase in usage of industrial chemicals, including pesticides, over the past 40 years (see Figure 7). The author suggested that pesticides and other industrial chemicals potentially cause weight gain by affecting the hormones that control weight, altering sensitivity # See Wendy Holtcamp's review article, "Obesogens: An Environmental Link to Obesity" (Environmental Health Perspectives, Feb. 2012) for an overview of the current literature. Available online at http://ehp03.niehs.nih.gov/article/info%3Adoi%2FlO.l289%2Fehp.120-a62#rl3. A Generation in Jeopardy • Pesticide Action Network North America to neurotransmitters, or altering the activity of the sympathetic nervous system. 97 In the 10 years since this review, many studies have linked exposure to endocrine -disrupting chemicals with increased incidence of obesity and diabetes.9' The National Institutes of Health is offering grants to study "the role of environmental chemical expo- sures in the development of obesity, type 2 diabetes and metabolic syndrome,"99 and the National Children's Study, an ongoing 21 -year prospective study of 100,000 U.S. children, is now exploring the hypothesis that prenatal exposures to endocrine disruptors are linked to obesity.'oo • In one animal study, rats exposed to low-level doses of the organophosphate pesticide chlorpy- rifos early in life developed metabolic dysfunc- tion resembling pre-diabetes.101 • In Denmark, children exposed prenatally to pesticides through their mothers' work in green- houses had significantly higher BMI (body mass index) scores than greenhouse worker mothers who were not occupationally exposed, with highly exposed children also having larger skin folds and higher body fat percentages.102 • Exposure to the pesticide lindane" during childhood has been linked with increased abdominal fat, increased waist circumference, higher BMI and fat mass percent- age in adults.10' • Organochlorine pesticide exposure' can be a predictor of developing type 2 diabetes later in life, particularly among obese individuals. Serum concentrations of organochlorines were strongly associated with type 2 diabetes, and the association was stronger among obese persons than non -obese persons.104 • Obese children are more likely to have higher concentra- tions of 2,5-DCP in their urine, a metabolite of the pes- ticide found in mothballs (p -dichlorobenzene). This cor- relation was observed in data from the National Health and Nutrition Examination Survey (NHANES).'os A number of specific genes have been identified as con- tributing to obesity, with several thought to specifically contribute to obesity in children. Such genes may play a role in regulating metabolic hormones.106 Scientists are now investigating the role of environmental factors (such as exposure to pesticides) in influencing the expression of such genes. Such "epigenetic" changes can include the expression of genes that are typically "silent," or inactivation of a gene that is normally active. Research- ers are finding that some of these changes can be passed from one generation to the next (see sidebar).117 * Lindane, an organochlorine insecticide, is slated for global phaseout under the Stockholm Convention on Persistent Organic Pollutants. Agricultural uses were phased out in the U.S. in 2006, pharmaceutical uses (lice shampoos and scabies treatments) were phased out in California in 2001, but are still allowed in other states. t Most organochlorine pesticides are now banned in the U.S., and many have been targeted for international phaseout under the Stockholm Convention. Rapid implementation of this treaty will reduce further exposure to these long lasting chemicals that continue to travel the globe on air and water currents. Figure 7. Chemical Production & the Percentage of Overweight Adults in the U.S. 160 Chemical production 70 65 140 s % Overweight adults, survey points 60 120 ------ % Overweight adults, interpolated . 55 0 100 50 0 80 45 d � � 60 40 a a a 35 0 40 " r 30 c 20 _-- 25 0111 20 1930 1940 1950 1960 1970 1980 1990 2000 Years Researchers note that the obesity epidemic coincides with the increase in use of industrial chemicals, including pesticides, over the past 40 years. source: Baillie -Hamilton, P.F. 'Chemical toxins: a hypothesis to explain the global obesity epidemic.' l Altern Complement Med. 2002 8:185-192. Mechanisms of Harm Changing gene signals Many environmental pollutants can strip or add chemical tags to DNA, locking the expression of genes on or off and changing how they function. These changes are called "epigenetic tags," and have been linked to various health effects including early puberty, disrupted ovarian function, death of sperm -forming cells and changes in metabolic rate. Recent studies suggest that some chemicals can even override the genetic "reset button" that usually protects a developing fetus from such changes being passed from one generation to the next. A Generation in Jeopardy • Pesticide Action Network North America 15 Today, more than seven million children have asthma, up from just over two million 30 years ago. Asthma epidemic affects more than seven million children Asthma is a chronic disease of the pulmonary system that causes wheezing, breathlessness, chest tightness and coughing. The number of U.S. children with asthma today is much higher than it was 30 years ago, rising from 2.1 million in 1980 to 7.1 million in 2009.108 Today, it is the most common chronic childhood disease in the U.S. (see Figure 8). Asthma is the leading cause of hospital admission among urban children, with over 200,000 hospitalizations every year. Asthma is also the top cause of days lost from school, with more than 10.1 million school days missed every year. "9 Missed school days in turn negatively impact academic performance, such that children with Figure 8• severe asthma symptoms are more likely to suffer academically than children with milder symptoms."' to 1 Asthma disproportionately affects people of color. Data from 2009 show that roughly one in six (17 percent) non -Hispanic black children had asthma in 2009, the highest rate among any racial/ethnic group. Overall, boys are more likely than girls to suffer from asthma (11.3 vs 7.9 percent) from birth through adolescence. As adults, women are more likely to be asthmatic than men.111, The Science 9 a irritants" in the home environment to triggering the onset of asthma, including cockroaches, dust mites, molds and air pol- lutants. Many pesticides are considered respiratory irritants,t and studies suggest that pesticide exposures may play a role in triggering asthma attacks, exacerbating symptoms, or height- ening the overall risk of developing asthma. 112 Pesticides may also play a role in increasing asthma inci- dence by affecting the body's immune system, triggering either hypersensitivity or suppression of the body's immune response. Allergic responses, for example, are a hyper- sensitivity of the immune system to an allergen in the environment."' Numerous studies have documented the association of pesticides and asthma incidence for adults, and more recent studies have examined potential links to both asthma inci- dence and triggering or exacerbation of wheezing episodes among children. • In a study of over 4,000 children from 12 southern Califor- nia communities, exposure to pesticides in the first year of life significantly increased the risk of being diagnosed with asthma by age five.14 • A cross-sectional study of 3,291 Lebanese school children found a potential association between childhood asthma and parental occupational exposure to a range of current use pesticides."' • In Spain, children diagnosed with asthma at age six had higher levels of cord serum DDE at birth than children without asthma. And in a study of 343 German children aged 7-10 years who had the DDT breakdown product Asthma Prevalence by Age and Sex in U.S., 2001-2009 rye, ry�ti lf° 1P" ti°°� 1p" ti°°1 o, 4P Percentages are age-adjusted. Children All Females Total Adults All Males Many studies have explored the relative Source Centers for Disease Control and Prevention, Vital Signs: Asthma in the U.S. See http://www.cdc.gov/VitalSigns/Asthma/ importance of common "respiratory index.html, viewed May 2012. * In May 2012, the President's Task Force on Environmental Health and Safety Risks to Children released the Coordinated Federal Action Plan to Reduce Racial and Ethnic Asthma Disparities. The effort lays out a plan to address this crucial public health challenge during the next three to five years. See http://www.epa.gov/asthma/childrenstaskforce, t Seethe Recognition and Management of Pesticide Poisonings page of EPA's National Pesticide Information Center site: http://npic.orst.edu/health/Child.html 16 A Generation in Jeopardy • Pesticide Action Network North America Rethinking "Safe" Why the dose does not make the poison Traditional toxicology relied for years on the mantra "the dose makes the poison." We now know that this statement is, in many cases, simply inaccurate. It assumes that the level of harm always increases as the level of exposure goes up (i.e., that every "dose response curve" follows a linear pattern). Assuming a higher dose is always more dangerous, policymakers often base regulations on a level below which no health risks is expected—a "safe" threshold. The reality, as scientists now understand, is quite different. For some pesticides, the linkage between exposure and effect actually follows a U-shaped curve. In this scenario, a very low dose elicits a high level of "response" or health harm. At a higher dose that is along the bottom of the U, this same chemical elicits little or no response. Then at the highest doses, the effects increase again. For other pesticides, an inverted U–shaped curve can occur, where intermediate doses cause the greatest response, and testing at high doses can completely miss the effect. Given these complex dose -response patterns, picking a threshold dose—below which exposure can always be considered "safe"—is simply not possible. Throw into the mix the dramatic differences in how sensitive individuals DDE present in their blood, the risk of having asthma was significantly higher."', • Childhood exposure to organophosphate, carbamate and pyrethroid insecticides may trigger or exacerbate asthma symptoms among children by promoting bronchial constriction."' Recognizing the rising prevalence of asthma among U.S. children, Dr. David Schwartz recently called on fellow researchers to focus more attention on the potential links between exposure to air pollutants and environmental contaminants like pesticides and child- hood asthma.1' * These measurements were taken from blood serum and were thought to represent early life or prenatal exposures, but the actual route of exposure was not known. may be to chemical exposures, plus the vulnerabilities of children at particular times during development, and it quickly becomes clear that it is much more than the "dose" that determines how much harm a pesticide will cause.' High Low Low High Dose • Vandenberg, L., T. Colborn, T. Hayes, J. Heindel, D. Jacobs, D.H. Lee, et al. "Hormones and Endocrine -Disrupting Chemicals: Low -Dose Effects and Nonmonotonic Responses." Endocrine Reviews. March 2012 33(3): 378-455. A Generation in Jeopardy • Pesticide Action Network North America 17 18 4 Critical Junctures Children exposed just as they are most vulnerable Children cannot make choices about their environment; it is up to adults to make the right decisions to ensure that they are protected. — Dr. Lynn R. Goldman Environments we would like to consider "safe" often bring children into contact with pesticides and other chemicals that have been linked to health harms. Many chemicals pass across the placenta into the womb, where they become part of the first environment of a developing fetus. In the months after birth, infants begin to explore their new world, often testing new sights and smells by touching and bringing objects to their mouths. When harmful chemicals are present, they are often taken in. The environments of toddlers and school-age children expand to include daycare centers, classrooms, playing fields and parks, all of which may offer risk of pesticide exposure. Resi- dues on and in food—from breastmilk to the highchair to the school lunch tray—are also an important source of pesticides throughout childhood. Many pesticides can pass across the placenta into the womb, where they become part of the first environment of a developing fetus. Physiological systems undergo rapid development at various stages of childhood, in finely tuned processes often triggered and orchestrated by hormones. During this same period, children take in more food, water and air than adults pound - for -pound, and their biological systems are less able to process harmful contaminants than adults. In short, the multiple pathways of pesticide exposure mean that in a given day, a child may absorb a wide range of poten- tially harmful chemicals just as their young bodies are at their most vulnerable. Fetal pesticide exposures can have life-long effects Exposure to pesticides has been clearly documented dur- ing one of a human organism's most vulnerable stages: fetal development. Pesticides that have accumulated for years in an expectant mother's body—stored in blood and fatty tissues—can be mobilized during pregnancy and cross the placental barrier. A mother's exposures to pesticides during pregnancy add to this chemical mixture in the womb.' 19 Many studies have documented the pesticide load newborns bring with them into the world. Researchers in New York documented pesticides and their breakdown products in umbilical cord blood of more than 80 percent of newborn infants tested."o One 2001 study found metabolites of organophosphate pesticides in 100 percent of the cord blood samples taken. 121 A pilot study of amniotic fluid also found organophosphate metabolites, providing further evidence of fetal exposure. 122 Pesticide residues from the food mothers eat during preg- nancy have also been found in infants. A recent Canadian study showed that when pregnant women consumed soy- beans, corn and potatoes that had been genetically modified for use with particular herbicides, metabolites of one of the herbicides showed up in cord blood of 100 percent of their babies. 1 I Fetal development is almost entirely controlled by the expec- tant mother's hormones, acting at very low levels to trigger and control growth of the various systems of the body. Some chemicals—including many pesticides—mimic hormones and so interfere with natural developmental processes. This disruption of hormone function can lead to irreversible life- long effects including birth defects or learning disabilities in childhood, or adult onset cancer or infertility later in life (see sidebar, P. 17).124 Pesticide exposures common at home, daycare & school Pesticides tend to be especially persistent in the indoor environment where sunlight, rain, soil microorganisms and high temperatures cannot degrade them, which means longer windows of exposure. At home & in daycare facilities Infants and toddlers have busy hands that often reach their mouths, and they commonly play on or near the floor—so * The women in the study were in urban environments, and had no contact with the herbicides beyond residues on or in their food. A Generation in Jeopardy • Pesticide Action Network North America Children as Farmworkers Some children are exposed to pesticides as they work in agricultural fields. Specific rules vary from state to state, but federal law allows children under 12 to do field work outside of school hours on farms where their parents are employed.' Age restrictions for hazardous work such as applying pesticides are more lenient in the agriculture sector, and age restrictions simply do not apply for children working on farms owned or operated by a parent or guardian. Documenting the exact number of child workers in U.S. agriculture is difficult, and estimates vary widely. A Human Rights Watch report published in 2000 put the number somewhere between 300,000 and 800,000! The nonprofit group Toxic Free North Carolina recently documented the experience and voices of young farmworkers facing pesticide exposure in the field; the stories can be viewed at www.panna. org/youngfarmworkers. U.S. Dept. of labor. "Child Labor Requirements in Agricultural Occupations Under the Fair Labor Standards Act " lune 2007 See http://www.dol.gov/whd/regs/compliance/ childlabor102.htm. t Human Rights Watch. Fingers to the Bone: United States failure to Protect Child Farmworkers. Washington: Human Rights Watch, 2000. National Center for Farmworker Health. Child Labor. Buda, Texas. 2009. See www.ncfh. org/docs/fs-Child%20Labof.pdf Davis, S. and J.B. Leonard, The Ones the Law Forgot: Children Working in Agriculture, Farmworker Justice, Washington DC. 2000. when pesticides are used in homes or daycare facilities, exposure is a near certainty. Inhaling spray droplets, vapors or pesticide -contaminated dust from indoor use of pesticide products is one of the primary routes of exposure for many U.S. children. Pesticides used to control ticks and fleas on pets are another important source of children's exposure.1 ' One Massachusetts study found residues of DDT in house dust many decades after use of the chemical had been discon- tinued.126 Even pesticides that are relatively short-lived in the environment are more persistent indoors; one study found the semi -volatile insecticide chlorpyrifos to be longer lasting than expected in closed apartments, detectable for more than two weeks on rugs, furniture, soft toys and pillows. 127 Pesticide vapors often settle after application indoors, so levels tend to be highest in the infant breathing zone."' Exposure from home lawns and gardens or outdoor play areas at daycare centers can also be significant. Children often roll and play on lawns and sit or lie on bare soil, and toddlers are known to put dirt directly into their mouths. 129 If pesticides have been used in these areas, the likelihood of ingestion or inhalation is high. In rural communities, the risk may be compounded by drift from nearby agricultural fields. A study conducted in Wash- ington State found residues of several agricultural pesticides— including chlorpyrifos and ethyl parathion—in outdoor play areas.130 Air monitoring studies using PAN's Drift Catcher in Evidence shows that when pesticides are used at home, on pets or in daycare centers, children's exposure is a near certainty. California and Minnesota have documented a range of agri- cultural pesticides in backyards and play areas as well. 131.132 Rural infants and toddlers also face potential exposure from drift directly into their homes, and from pesticide contami- nation of water supplies. Water sampling results from Illi- nois, Nebraska, Iowa and Minnesota detected the common herbicide atrazine at levels above those linked to low birth weight. 133 Young children in farmworker families face addi- tional exposure from residues carried into the home on the bodies and work clothes of working family members."" At school & on playgrounds Pesticides used in school buildings can settle on desks, books, counters and walls. When children touch contaminated surfaces, they may absorb chemical residues that can remain in the school environment for days. Herbicides used to keep playing fields free of weeds may be picked up on children's hands, bodies, clothes and tennis shoes, or drift into class- rooms after application. According to one recent national review, of the 40 pesticides most commonly used in schools, 28 are probable or possi- ble carcinogens, 26 have been shown to cause reproductive effects, 26 damage the nervous system, and 13 have been linked to birth defects. 135 In rural areas, pesticides often drift into schoolyards during and after spraying on nearby fields. Community air monitor- ing studies across the country using the Drift Catcher device have documented pesticides in or near school grounds in agri- cultural communities, 136 and incidents of pesticide poisonings in schools are not uncommon. For example: • In Florida, high school students used a Drift Catcher to measure the pesticides endosulfan, diazinon and trifluraliri drifting into the school from nearby cabbage fields. 137 * Endosulfan is currently being phased out in the U.S., and also globally under the Stockholm Convention on Persistent Organic Pollutants. See http://www.epa.gov/oppsrrdl/reregistration/ endosulfan/endosulfan-cancl-fs.html. A Generation in Jeopardy • Pesticide Action Network North America 19 3 20 • Schoolchildren in Strathmore, CA were exposed to pes- ticides sprayed in a neighboring field, feeling dizzy and falling sick in November, 2007.138 • Seven children were hospitalized and a total of 11 people sickened in Kahuku, Hawaii, in 2007, when fumes from an organophosphate insecticide drifted over the school from a nearby sod farm.13' Pesticide use on playing fields has raised concerns among families and environmental health advocates nationwide. The National Coalition for Pesticide -Free Lawns notes that "the common, everyday practices used to maintain our children's playing fields are unintentionally and unnecessarily exposing them to carcinogens, asthmagens, and developmental toxins," and calls for a shift to organic turf management on playing fields across the country. 140 Pesticide residues, from breastmilk to the school lunch tray Pesticide residues in food and drink are a key source of con- stant, low-level exposure to mixtures of pesticides throughout childhood. Nature's Finest, Compromised Pesticides in breastmilk Human breastmilk is without doubt the best source of nutrition for infants, offering the perfect combination of fats, carbohydrates and proteins for developing babies. It also offers protection from infection, increases resistance to chronic disease and contributes to the emotional wellbeing of both infant and mother. But decades of breastmilk sampling also leaves no doubt that around the world, nature's perfect food for infants is compromised by pesticides and other toxic chemicals. Today there is no corner of the planet where human breastmilk remains pure. The chemicals found in a mother's milk represent a combination of long-lasting pesticides and industrial pollutants that have accumulated over a lifetime (many of which the body tends to store in fatty tissues), and shorter - lived chemicals that a woman is exposed to during pregnancy and breastfeeding. This chemical burden is transferred to nursing infants just as their bodies are most vulnerable to chemical harms. The good news is that analysis of decades of banked breastmilk in Sweden shows that bans on specific chemicals can result in rapid and dramatic decreases in the levels of some of those compounds in human milk.' Noren K., D. MeironytO. "Certain organochlorine and organobromine contaminants in Swedish human milk in perspective of past 20-30 years' Chemosphere. May -Jun 2000;40(9-11):1111-23. See http://www.ncbi.nlm.nih.gov/pubmed/10139053. Natural Resources Defense Council. "Healthy Milk, Healthy Baby: Chemical Pollution and Mothers Milk' See www.nrdc.org/breastmilk. Children take in more food, water and air than adults pound -for -pound, just as their bodies are less able to process harmful contaminants. Studies from around the world have documented pesticides in human breastmilk, though experts agree it remains the best source of nutrition for infants (see sidebar). Baby foods and fruit juices consumed by infants and toddlers tend to be highly processed, which can sometimes concentrate pesticide residues existing on the fresh produce. 141 U.S. researchers measuring pesticides in baby foods found low-level residues of many pesticides, including eight known to be toxic to the nervous system, five that disrupt hormones and eight that are potential carcinogens."' Food consumed by school-age children can also contain pesticide residues. Researchers examining the diets of urban children found that 14 percent of the foods sampled con- tained at least one organophosphate pesticide. In total, 11 dif- ferent organophosphates and three pyrethroids were found. 141 USDA residue sampling of produce commonly eaten by children—such as carrots, apples and peaches—found metabolites of dozens of different pesticides in each of these foods over the course of their testing (26 found in carrots, 42 in apples and 62 in peaches).' Pesticides directly measured in children's bodies also tell a story about the importance of dietary exposure. Researchers compared levels of organophosphate metabolites in the urine of children who were eating organic fruit, vegetables and juice with children eating conventionally farmed produce. They found that those with more organic diets had metabolite levels six times lower than those with conventional diets. 114 Other studies show that when families switched to organic fruits and vegetables, metabolites of the insecticides chlorpyri- fos and malathion fell quickly to undetectable levels. 141 The widespread presence of pesticide metabolites in children's bodies, 146 combined with studies showing that changes in these levels are linked to changes in dietary exposure, make a very clear case that pesticide residues in food are a consistent source of children's daily intake of a mixture of pesticides. * These numbers do not necessarily reflect residues on a single sample. See USDA data at www. whatsonmyfood.org. A Generation in Jeopardy • Pesticide Action Network North America Why children are particularly vulnerable So what do all of these well-documented pesticide exposure pathways mean for children's health? In their first six months of life, children take in roughly 15 times more water than the average adult per pound of body weight. 147 Children also inhale more air. Up to around age 12, a child's breathing rate is roughly twice that of an adult, which means a child will inhale roughly double the dose of a pesticide in the air from spray drift or household Use. 141 Exposure to pesticides occurs largely through touching, inhal- ing or ingesting. For each of these routes, children are much more likely to absorb what they come into contact with than adults. The skin of infants and young children, for example, is particularly permeable, and the skin surface area relative to body weight is much greater in children than adults. 14' The lung surface area relative to rate of breathing is also higher among children, 150 and absorption levels in the gastrointes- tinal tract are also greater (especially for alkaline pesticides), as adult levels of gastric acid are not reached until a child is about two years old. 151 As noted above, the brain and nervous system are especially vulnerable during fetal development and for the first six months of life. During this period the blood -brain barrier,' which provides the adult nervous system some protection from toxic substances, is not yet fully developed. I" Finally, young bodies are less equipped to process and excrete harmful chemicals as the liver and kidneys—the body's primary detoxifying organs—are not yet fully developed. Lev- els of enzymes that help the body process chemicals are also not yet at full strength (see sidebar). Genetic variations lead to tremendous range in the production of these protective enzymes—with some newborns as much as 164 times more vulnerable to chlorpyrifos than less sensitive adults."' According to researchers, this finding alone means that most, if not all infants and toddlers—as well as a subpopulation of adults—are much more likely to have adverse health effects from organophosphate exposure. Policies that don't account for this variability fail to protect the most vulnerable, leaving many children in harm's way. " The blood -brain barrier is made up of high-density cells that protect the brain from potentially harmful substances circulating in the bloodstream. Mechanisms of Harm When enzymes don't detoxify Enzymes are proteins that catalyze reactions on a molecular level, and there are many that occur naturally in the human body. Without enzymes to catalyze reactions, some of the chemical reactions that make up the normal functioning of our body could take much longer, or not happen at all. One key human enzyme, known as paraoxonase 1 (or "PON 1 "), catalyzes the metabolic process that renders organophosphate pesticides and other compounds less harmful to our systems. Researchers say infants have very low levels of this enzyme up to age two, and children don't reach adult PON1 levels until about age seven.' This suggests that children are less protected from harmful contaminants by enzyme activity, and newborns may be especially vulnerable. There is also tremendous natural variability in the level and effectiveness of the PON 1 enzyme, which means some individuals are much more susceptible to health harms of organophosphate pesticides and other contaminants! Huen K., K. Harley, A. Bradman, B. Eskenazi, N. Holland. `Longitudinal changes in PONT enzymatic activities in Mexican -American mothers and children with different genotypes and haplotypes," Toxicol Appl Pharmocol. 2010.244(2):181-9. See http:// www.n(bi.nlm.nih.gov/pmc/articles/PM(2846980/?tool=pubmed t Holland, N., C. Furlong, M. Bastaki, R. Richer, A. Bradman, K. Huen, et al. "Paraoxonase Polymorphisms, Haplotypes, and Enzyme Activity in Latino Mothers and Newborns." Environ Health Persp. July 2006114 (1): 985-991. See http://www.ncbi.nlm.nih.gov/ pmc/articles/PMC1513322/. The human body undergoes rapid growth and development throughout childhood, with many processes vulnerable to disruption from pesticides and other chemicals. A Generation in Jeopardy " Pesticide Action Network North America 21 5 Case Studies Communities win protections for children What we love we must protect. — Sandra Steingraber Since the middle of the last century, the overall increase in pesticide use in this country has been steady and dramatic. As documented above, these pesticides are a critical contributor to many of the chronic diseases and disorders now affecting our children. To address the unique vulnerability of children, concerned communities, public health officials and advocates are begin- ning to put policies in place at the state and local level that reduce the use of harmful pesticides. In this chapter we pro- vide a brief overview of U.S. pesticide use patterns and trends, and highlight on -the -ground stories of successful efforts to protect children from exposure in their early environments. Pesticide use now 1.1 billion pounds yearly Since 1945, use of herbicides, insecticides and other pesticides has grown from less than 200 million to more than 1.1 billion pounds per year, with well over 1,000 chemicals registered Figure 9e Pesticide Use on Major Crops, 1964-2004 700 - i ■ Other 600 ■ Insecticides Soo 100 Source: "Land and Farm Resources: ARE], 2006 Edition;' USDA Economic Research Service and formulated into more than 20,000 pesticide products (see Figure 9). This does not include pesticides used as wood preservatives or specialty biocides (in plastics and paints, for example). If these products are included, the number jumps to more than five billion pounds annually. 114,155,156 Pesticide use in agriculture The majority of pesticides are used in agricultural fields, with weed -killing herbicides being the highest by volume. Soil fumigants, which are injected as a gas into soil before planting to kill weeds, insects and fungi, are used at particularly high volumes and have a tendency to drift after application. Use of organophosphate insecticides, which gained widespread use in the 1980s as replacement chemicals for long-lasting organo- chlorine pesticides (such as DDT, chlordane and aldrin) has gradually declined in recent years. In part to address growing concerns about organophosphate toxicity, a group of insecticides called pyrethroids were marketed as "safer" and gained widespread use in the 1990s, and use has grown rapidly. According to the American Chemical Society, use of pyrethroids in California (agricultural, structural and landscape maintenance applications) almost tripled from 1992 to 2006.157 Recent research suggests that pyrethroids may be more harmful to humans than originally believed, acting as developmental neurotoxicants, endocrine disruptors and carcinogens. 151, + Another class of pesticides now in widespread and rap- idly rising use is neonicotinoids. Most neonicotinoids show much lower toxicity in mammals than insects, but emerging science demonstrates that many may also have neurodevelopmental effects, and some are con- sidered likely carcinogens by EPA. 151 These pesticides are considered systemic,' which means they are often applied at the root (as seed coating or drench) and are then taken up through the plant's vascular system. Systemic pesticides on food cannot be washed off. Neonicotinoid pesticides have been linked with honey bee colony collapse disorder and bee kills, and several products have been banned in European countries for this reason. One neonicotinoid, imidacloprid, is now one of the most widely used insecticides in the world. 160 " Ten years' worth of adverse -reaction reports (filed by manufacturers) show that pyrethrins and pyrethroids together accounted for more than 26 percent of all fatal, 'major," and 'moderate' human pesticide poisoning incidents in the U.S. in 2007, up from 15 percent in 1998. See http:// apps.cdpr.ca.gov/calpiq/calpiq_input.cfm to see the primary data; for data analysis, see http:// www.iwatchnews.org/environment/health-and-safety/perils-new-pesticides. 22 A Generation in Jeopardy • Pesticide Action Network North America Pesticide use at home While 80 percent of all pesticides are applied in agricultural fields, use in homes, gardens, playgrounds, schools, hospitals and other buildings is also significant—and as noted above, such uses pose a particular risk to children's health. In 2007, an estimated 78 million pounds of pesticides (measured by active ingredient) were applied in homes and gardens across the country, with the herbicides 2,4-D and glyphosate (RoundUp) topping the list. 16' The household pesticide product industry has an estimated annual net worth of $1.4 billion; according to EPA, more than 78 million households—roughly 74 percent of all households in the U.S.—report using pesticides at home (see Table 5).162 Many home -use insecticides contain pyrethroids, and the chemicals are used extensively in homes where the potential for exposure to children is very high. Researchers from Emory University and the CDC found that even children fed an exclusively organic diet had pyrethroid metabolites in their systems after their parents had used pyrethroid insecticides in their homes. 161 Neonicotinoid products are widely used in pet products to control fleas and ticks—another use which poses particularly high exposure risks for children.t64 Safer pest control at schools & daycare centers More than 3,000 pesticide products are currently approved for use in schools; 165 yet current national pesticide rules do not address the use of pesticides in and around schools or daycare centers. The federal School Environmental Protec- tion Act (SEPA) was first introduced in November 1999 in an attempt to address this oversight—and it continues to be debated in Congress today. In the non-profit sector, the national Children's Environmen- tal Health Network (CEHN) moved to fill this gap by creat- ing the Eco -Healthy Child Care (EHCC) program to provide Table 4: Pesticide Usage in All Market Sectors, 2007 Pesticide Class Active Ingredient Herbicides 531 million lbs Insecticides 93 million lbs Fungicides 70 million lbs Fumigants/Nematicides 133 million lbs Other 30 million lbs Total 857 million lbs Herbicides are the most commonly used type of pesticide in the U.S., with 531 million pounds of active ingredient applied in 2007. Source: Pesticide industrySoles & Usage, 2006 and 2007 Marker Estimates, U.S. EPA, Washington, DC Feb 2011. See www.epa.gov/opp00001/pestsales/07pestsales/market_ estimates2007.pdf. To protect children's health, several states have put policies in place prohibiting the use of pesticides on playing fields and playgrounds. tools that facilities need to create environmentally healthy spaces for children. Today, the program endorses over 1600 "Eco -Healthy" daycare facilities across the country and pro- vides this list to parents online.' Meanwhile, several states are moving forward with policies designed to protect children from pesticides in these early environments. • In 2005 Connecticut lawmakers prohibited use of pesti- cides on K-8 lawns and playing fields; in 2009, the law was extended to daycare center grounds. Through this policy, schools have successfully implemented organic turf pro- grams in various municipalities. 166 • New York followed suit in 2010, signing the Child Safe Playing Fields Act into law to ban the cosmetic use of pesti- cides on playgrounds and sports fields at schools (including high schools) and daycare centers. 167 Table S: Households Using Pesticides Pesticide Type # Households Insecticides 59 million Fungicides 14 million Herbicides 41 million Repellents 53 million Disinfectants 59 million Any pesticides 78 million According to EPA, more than 78 million households— roughly 74 percent of all households in the U.S.—use pesticides at home. Source: EPA estimates based on the 1992 EPA National Home and Garden Survey and 2000 U.S. Census Bureau population estimates (www.quickfacts.census.gov/qfd/states). * See http://www.cehn.org/ehcc for more information about this program. A Generation in Jeopardy • Pesticide Action Network North America 23 At What Cost? Economic impacts of health harms The impact on families of caring for—and sometimes losing—a child in ill health cannot be reflected in monetary terms. Nor can the incalculable costs of lowered IQ, lost opportunities and social alienation that can accompany developmental effects. But actual costs of providing medical care for a child with a chronic condition or illness can be calculated, and according to public health officials, health care costs for childhood diseases are significant. Here are some examples: ADHD: Researchers estimate annual ADHD health care costs in the U.S. to be between $36 and $52 billion (in 2005 dollars).' Autism: One analyst at the Harvard School of Public Health estimates that it costs $3.2 million to care for an autistic person over their lifetime! Cancer.• The total costs per case of childhood cancer— from treatment, to laboratory costs to lost parental wages—is an estimated $623,000 per year.t This translates into a society -wide cost of roughly $6.5 billion annually for the 10,400 newly diagnosed cases each year. Asthma: Families nationwide pay a combined total of $14.7 billion dollars a year on medical care costs of asthma.4, ' The combined direct and indirect costs of asthma to the U.S. economy were an estimated $19.7 billion in 2007.' Society -wide costs also include higher educational costs for public school systems to meet the needs of children with neurodevelopmental disorders, missed school days (and thus less well-educated students) caused by asthma, and the general productivity losses due to time parents and caregivers take off from work to care for an ill child. The numbers above do not take into consideration the loss to individuals, families and society as a whole of children not reaching their full physical or intellectual potential. The overall impact of lost creativity, productivity, problem - solving skills and civic engagement, along with higher rates of social alienation and disruption, cannot be overstated. Pelham W., E.M. Foster and 1.A Robb. 'The Economic Impact of Attention Deficit/Hyperactivity Disorder in Children and Adolescents" Journal of Pediatric Psychology. 2001. See http://jpepsy. oxfordjournals.org/content/32/6/111.full.pdf+html. Centers for Disease Control and Prevention. Attention-Deficity/Hyperactivity Disorder (ADHD): Data and Statistics in the United States. See htip://www.(dc.gov/ncbddd/adhd/data.html. t Ganz, Michael "The Costs of Autism,' in Understanding Autism: From Basic Neuroscience to Treatment (CR( Press, 2006). See http://www.hsph.harvard.edu/news/press-releases/2006- releases/press04252006.htmi t Landrigan, P. J., C.B. Schechter,l.M. Lipton, M.C. Fahs and J. Schwartz. "Environmental pollutants and disease in American children: estimates of morbidity, mortality, and costs for lead poisoning, asthma, cancer, and developmental disabilities." Environ. Health Perspea 2002;110, 721-728. § EPA, Children's Heath Protection. "Fast Facts on Children's Health." See http://yosemite.epa.gov/ ochp/ochpweb.nsf/content/fastfacts.htm. Viewed June 2012. 1 Centers for Disease Control and Prevention. Vital Signs: Asthma in the U.S. See http://www.cdc. goy/VitalSigns/Asthma/index.html. Viewed May 2012. ** EPA, Children's Heath Protection. "Fast Facts on Children's Health." See htip://yosemite.epa.gov/ ochp/ochpweb.nsf/content/fastfacts.htm. Viewed lune 2011. • Many school districts in California have significantly reduced pesticide use after a 2000 state law required pesticide reporting and provided incentives for adoption of IPM. School districts in Los Angeles, San Francisco, Santa Barbara and Palo Alto have made particular progress.168 • In 2001, California legislators passed a law (AB 947) allowing county agricultural commissioners to restrict pesticide spraying near sensitive sites, including schools and daycare facilities. Under this provision, communities in Tulare County won new rules in 2008 requiring a quarter mile buffer zone banning the aerial application of restricted -use pesticides around schools when they are in session or due to be in session within 24 hours, occupied farm labor camps and residential areas. 169 Kern, Stanislaus, Merced and Fresno counties enacted similar rules in subsequent years. Pesticide -free school lunches Currently, neither state nor national policies are in place to reduce pesticide residues in school lunches. But many communities across the country are leading the way to provide children with nutritious school lunches including fresh (sometimes locally produced) fruits and vegetables free from pesticides. • In Washington state, the Olympia School District has implemented an Organic Choices Salad Bar (25 percent of the produce is purchased directly from local farms and 50 percent of the salad bar is organic), and the Orcas Island Farm -to -Cafeteria Program integrates produce from local, organic farmers and a school garden, and hosts student chef competitions. • In Minnesota, the White Earth Land Recovery Project added a farm -to -school component in the 2007-2008 school year to their Mino-miijim (Good Food) Pro- gram to help reach their goal of food sovereignty on the reservation and promote access to fresh, local and organic ingredients. 170 • Berkeley, California's Edible Schoolyard (ESY) Project began as a one -acre "interactive classroom" providing primarily organic, fresh fruits and vegetables for stu- dent's meals at King Middle School. It has grown into an online initiative building and sharing a food curric- ulum, and it has inspired similar programs across the country. 171 Many of these programs are part of the National Farm to School Network (NFSN), which connects K-12 schools across the country with local farms in an attempt to serve healthy meals at school lunch tables while support- ing local, often organic, farmers. 172 Parks & playgrounds without pesticides Communities across the country are choosing to manage public parks and playgrounds without harmful pesti- cides. In the Pacific Northwest, 17 cities are phasing out pesticide use with the creation of 85 pesticide -free parks and playgrounds, building momentum for strong policies at the local level despite legislative hurdles (see sidebar on following page).17' 24 A Generation in Jeopardy • Pesticide Action Network North America Farm -to -school programs across the country are providing children with fresh, pesticide -free fruits and vegetables in school cafeterias. Seattle in particular has emerged as a pioneer of pesticide -free cities, dramatically reducing its pesticide use in parks by an estimated 80 percent since the 1970s. In 1999, they adopted a pesticide reduction strategy for all city departments and designated 14 pesticide -free parks. 17' The program is now expanding to 22 parks and 50 acres distributed throughout the city. 175 On the other side of the country, New Jersey legislators unan- imously voted in 2011 to pass "The Child Safe Playing Field Act" prohibiting pesticide use on all municipal, county and state playgrounds and playing fields, as well as daycare and school grounds. 171 Many other communities across the country are following this trend. From a pilot program in Lawrence, Kansas to innova- tive communities throughout Oregon, California and Colo- rado, cities are creating pesticide -free parks and playgrounds for children to safely enjoy. The Pre-emption Law Hurdle & Canada's Local Pesticide Bans As of 2010, 40 states had pre-emption laws specifically prohibiting municipalities from passing local pesticide ordinances that are stricter than state policy. These laws, which are strongly supported by the pesticide industry, limit the ability of city or county governments to ban or restrict pesticide use. Such pre-emption laws do not exist in Canada. Over the past 20 years, dozens of Canadian cities have used their local authority to outlaw the application of home and garden pesticides for "cosmetic" purposes such as lawn care. In 1991, the municipal council of Hudson, Canada, enacted the first ban on cosmetic uses. Similar local bans were adopted across the country, and today more than 170 Canadian cities and towns have passed full or partial bans on pesticide use, and the provinces of Quebec, Nova Scotia and Ontario have enacted comprehensive cosmetic pesticide bans. According to Canadian community activists, more than 22 million Canadians (65% of the population) are now protected from exposure to cosmetic pesticides.' " Pesticide free B.C. "Pesticide Bylaw Communities Across Canada" See http://www.pesti(idefreebc.org/index.php?option=com_ content&view=category&layout=biog&id=53&Itemid=72. Viewed July 2012, A Generation in Jeopardy • Pesticide Action Network North America 25 M 26 6 Investing in a Healthier Future A solid start for our children must be a national priority Those who argue that societies cannot afford to make immediate investments in reducing environmental pollution fail to appreciate that there are some forms of harm that cannot be repaired. — Deborah Axelrod, Devra Lee Davis & Lovell A. Jones As a nation, we value the wellbeing of our children. In addi- tion to our natural urge to protect what we love, we know that at a societal level their success is key to a vibrant, secure future. Poll after poll shows more than 80 percent of Ameri- cans consider healthy children a top priority."' We must line up our practice and policies with these values. Our current use of over a billion pounds of pesticides every year puts their wellbeing at risk and, as the science demon- strates, can derail brain and body development and rob them of their full potential. If there were no other way to control pests, it would be one kind of choice: weighing one set of needed benefits against known and evolving harms. But given the fact that there are many proven ways to control pests without use of harmful U.S. Pesticide Rules Overdue for overhaul? A little over 100 years ago, Congress enacted our first national pesticide law. The 1910 Insecticide Act put labeling guidelines in place to protect farmers from "hucksters" selling ineffective, misbranded or adulterated pesticide products. To this day, we control pesticides through a system of registration and labeling. The Federal Insecticide, Fungicide and Rodenticide Act (FIFRA), passed by Congress in 1947, is our primary national pesticide law. It has been updated several times in the last 65 years as the health and environmental effects of pesticides came into light, most significantly in 1972 and again in 1996. It remains, however, a system of registration and labeling, and as such has significant shortcomings. Our current pesticide rules: • Do not allow for quick response to emerging science; • Do not assess risk based on real-world exposures; • Rely heavily on corporate safety data that is not peer- reviewed; and • Do not encourage the safest form of pest control. In addition, enforcement of any guidelines or restrictions specified on product labels is relegated to state governments that rarely have adequate resources for the job. Overall, our current rules do not provide adequate tools to protect children from the harms of pesticide exposure. chemicals, the choice is quite clear. It is tide to have policies in place that better protect our children (see sidebar). The National Research Council recommended swift action to protect children from pesticides nearly 20 years ago, and it has been 50 years since Rachel Carson sounded the initial alarm about the health harms pesticides can cause. What is standing in the way? Pesticide industry well served by current policies Our current system of industrial agriculture and pest control relies on chemical inputs sold by a handful of corporations. These multinational corporations wield tremendous control over the system, from setting research agendas 171 to financing, crop selection and inputs throughout the production and distribution chain. Not surprisingly, these same corporations also hold significant sway in the policy arena, investing millions of dollars every year to influence voters, lawmakers and regulators at both the state and federal level to protect the market for pesticides.1' The result is agriculture, food and pest control systems that serve the interests of these corporations well. It does not, however, serve farmers, who have lost day-to-day control of their operations and are putting themselves and their families in harm's way. Farmworker interests are not served, as workers are continuously exposed to chemicals known to harm human health. And the health of children across the country is compromised by exposure to pesticides used to control pests in agriculture and where they live, learn and play. In short, the system is broken. Prioritizing children's health requires real change The best way to protect children from the harms of pesticides is to dramatically reduce the volume used nationwide. This would not only limit childreds exposure during their most vulnerable years, it would also lower pesticide levels in the bodies of men and women of childbearing age—protecting current and future generations in one fell swoop. Those pesti- cides most harmful to children should be first on the list. This is not a small change, and not a recommendation made lightly. Yet the science tells us the problem is serious and urgent, and that viable and safer alternatives are available. If we stay on our current path, our children will not reach their full potential as we continue to compromise their health. A Generation in Jeopardy • Pesticide Action Network North America Informed household food choices can help protect fami- lies and grow the market for food that is produced without harmful pesticides—encouraging more farmers to make this shift. And reducing household use of pesticides can provide immediate and long lasting benefits to children's health.` But the burden of protecting children from dangerous chemicals cannot rest solely with individual families. Policy change is required. Recommendations: Effective policies urgently needed To protect our children from the health harms of pesticides, policymakers must have much more effective tools. We believe such tools are most urgently needed as decisions are made about these three questions: • Which pesticides are used in agriculture? • Which pesticides are used in places children live, learn and play? • How are farmers supported as they reduce reliance on pesticides? We recommend the following policy changes in these three arenas: 1. Prevent the pesticide industry from selling agricultural products that can harm children's health Given the wide-ranging susceptibility of children to pesti- cide exposures, plus the potential impacts on children from extremely low doses of toxic chemicals, the current approach to assessing and controlling risks of agricultural pesticides does not adequately protect our children. Decisionmakers must have tools to remove an agricultural pesticide from the market quickly or deny a newly proposed pesticide market access when science suggests it can harm children's developing minds or bodies and there is evidence that children are likely to be exposed. Specifically, we recom- mend that rulemakers should: Take swift action on existing pesticides: If studies find a pesti- cide to be a neurodevelopmental or reproductive toxicant, endocrine disruptor or human carcinogen—and it has been measured in humans, in schools or homes, or as residues on food or in drinking water—EPA should target the pesticide for rapid phaseout, triggering USDA resources to assist rapid farmer transitions to safer pest control methods. t • Block harmful new pesticides: EPA should not approve any new pesticide that scientific studies suggest is a neurodevel- opmental or reproductive toxicant, endocrine disruptor or human carcinogen—including short-term "conditional" registrations. • Prevent harmful low-level exposures: EPA should act on existing evidence that exposures to endocrine disrupting pesticides pose a particular danger to developing children; * In addition to choosing non-toxic approaches to pest control (see PAN's Homes, Pets & Gardens online resource at http://www.panna.org/your-health/home-pets-garden), see also the National Pesticide Information.Center's page on Pesticides and Children for suggestions on reducing children's exposure in the home: http://npic.orst.edu/health/Child.htmi. t See, for example, criteria and process for developing the "chemicals of high concern" list in Maine. http://www.maine.gov/dep/safechem/highconcern/Chemicals.htm The best way to protect children from the harms of pesticides is to dramatically reduce the volume used nationwide. the long-delayed endocrine disruptor screening program (EDSP) should be swiftly implemented. At the current rate, it will be 2017 before the first set of only 58 chemicals are screened. The insecticide chlorpyrifos provides a clear example of the startling flaws in our regulatory system. Over 10 mil- lion pounds of the pesticide are still applied in agricultural When Is There Enough Evidence to Act? Scientific studies often identify a "link" or "association" between exposure to a particular pesticide and a specific health harm—but individual studies rarely demonstrate definitive causation. Epidemiological studies often lack statistical power, and case control and animal studies may miss key variables such as exposure timing. A "weight of the evidence" approach recognizes that a body of scientific work will contain conflicting studies, but holds that when a number of well designed, robust studies come to similar conclusions, the findings should be considered valid.' When such findings involve widespread, significant and irreversible health harms to our children, the bar for taking action should not be high. When credible evidence of harm emerges, a pesticide product should immediately be taken off the market until its manufacturer can prove its safety. Put simply, it is time the burden of proof shifted to the pesticide corporations, rather than regulators—and the public—as it currently stands. * Basketter, D., B. Nicholas, S. Gagen, J. Carrillo, H. Certa, D. Eigler et al. "Application of a Weight of Evidence Approach to Assessing Discordant Sensitisation Datasets: Implications for REACH! Regulatory Toxicology and Pharmacology 55, no. 1. Oct 2009; 90-96. Hill, A B. "The Environment and Disease: Association or Causation?' Proceedings of the Royal Society of Medicine 58. May 1%5; 295-300. Vandenberg, l., T. Colborn, T. Hayes, J. Heindel, D. Jacobs, D.H. Lee, et al. "Hormones and Endocrine -Disrupting Chemicals: Low -Dose Effects and Nonmonotonic Responses." Endocrine Reviews. March 2012 33(3): 378-455. A Generation in Jeopardy • Pesticide Action Network North America 27 Investing in farmers who grow food without relying on chemicals that harm children's health must be a national priority. fields every year, more than a decade after household uses were withdrawn because of clear dangers to children's devel- oping brains.' Yet children across the country continue to be exposed—in rural schools and communities, and by eating foods that have been treated with the neurotoxic chemical. 2. Protect children where they live, learn & play Policymakers need strong tools to protect children from exposure to pesticides where they live, learn and play. Such protections will help keep developing bodies and minds healthy during the years they are most vulnerable to harm from chemical exposures. We recommend rapid implementation of the following measures: • Kid -safe homes, daycares & schools: EPA should withdraw approval of existing pesticide products and not approve new pesticides for use in homes, daycare centers or schools when scientific evidence indicates the chemicals are possible neurodevelopment or reproductive toxicants, endocrine disruptors or human carcinogens. • Saferparks 6 -playgrounds: State and local officials should enact policies requiring that all public playgrounds, playing fields and parks be managed without using pesticides that studies show are harmful to children's health. • Protective buffer zones: State legislators should establish—or give local governments authority to establish—protective pesticide -free buffer zones around schools, daycare centers and residential neighborhoods in agricultural areas. • Healthier school lunches: Local school districts, state agen- cies and USDA's Farm -to -school program should provide schools with incentives to procure fresh, local fruits and vegetables that have been grown without pesticides that studies show are harmful to children's health. * Chlorpyrifos was phased out for household use after studies clearly indicated that exposed children had smaller head circumference, a known indicator of reduced cognitive function. 3. Invest in farmers stepping off the pesticide treadmill Investing in farmers who grow food without relying on chem- icals that harm children's health must be a national priority. Specifically: Corral resources for farmers: Federal and state officials should mobilize and coordinate existing resources to help farmers adopt well-known, effective pest management strategies that reduce reliance on pesticides. USDA, EPA and many state agencies and universities have important programs— research, outreach and education—with this stated aim that could be ramped up in complementary ways. • Increase investment in innovativefarming. Congress should authorize significant funding for programs supporting farmers' adoption of sustainable practices that reduce use of harmful pesticides. Existing programs receive a small frac- tion of the funding supplied to programs serving conven- tional growers. • Set use reduction goals: EPA and USDA should set specific and aggressive national pesticide use reduction goals, focus- ing first on pesticides studies show to be harmful to chil- dren. t To track progress toward this goal, farmers should work with applicators and pest control advisors to report their pesticide use to a nationally searchable database. t • Source for children's health. Food distributors should require that their suppliers limit use of pesticides that harm chil- dren's health. Effective agroecological methods exist for production of all major crops—but these approaches are often knowledge -in- tensive, requiring significant training as well as real changes in farm operation.4 Growers need direct support to make the shift away from pesticide reliance, including provision of hands-on field training and technical advice from indepen- dent experts as well as incentives to invest in agroecological practices. These proposals are all commonsense measures in the face of clear evidence that our children's wellbeing is at risk. It's time to muster the political will and prioritize the health of our children, grandchildren and future generations. t See Appendix B. t Pesticide use reporting is already in place in California; lessons learned from implementation of this program (established in 1990) should inform and enable rapid adoption of a federal use reporting system. § Agroecological practices are based on the application of intricate place -based knowledge of soil/ plant/animal interactions designed to prevent or minimize pest problems. Farmers are successfully using such practices in virtually every crop now grown in the U.S. 28 A Generation in Jeopardy • Pesticide Action Network North America Notes 1 National Research Council. Pesticides in the Diets of Infants and Children. Washington, DC. National Academy Press.1993. See http://www.nap.edu/openbook.php?isbn=0309048753. 2 Selevan, S.G., C.A. Kimmel and P. Mendola. "Identifying critical windows of exposure for children's health." 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October 2002 21(5): 403-418. 149 Ibid. 150 Bennett, W.D and K.L. Zeman. "Effect of Body Size on Breathing Pattern and Fine -particle Deposition in Children" Journal of Applied Physiology. Sept 2004 97(3): 821-826. 151 Louis, G.B., United Nations Environment Programme, International Labour Organisation, World Health Organization, Inter -Organization Programme for the Sound Management of Chemicals, and International Program on Chemical Safety. "Principles for evaluating health risks in children associated with exposure to chemicals." 2006. See http://site.ebrary.com/ id/10214527. 152 Schwenk, M., U. Gundert-Remy, G. Heinemeyer, K. Olejniczak, R. Stahlmann, W. Kaufmann, et al. "Children as a Sensitive Subgroup and Their Role in Regulatory Toxicology: DGPT Workshop Report." Archives of Toxicology. Jan 2003 77(1): 2-6. Louis et al. 2006, op. cit 153 Furlong, CE, N. Holland, R. Richter, A. Bradman, A. Ho and B. Eskenazi. "PON1 Status of Farmworker Mothers and Children as a Predictor of Organophosphate Sensitivity." Pharmacogenetics and Genomics. March 200616(3):183-190. 154 Pesticide Industry Sales & Usage, 2006 and 2007 Market Estimates, US EPA, Washington, DC Feb 2011. See www.epa.gov/ opp00001/pestsales/07pestsales/market_estimates2007.pdf. 155 "Pesticide Usage in the United States: Trends in the 20th Century." (IPM Technical Bulletin. 2003 156 Goldman, L and S. Koduru. Chemicals in the Environment and Developmental Toxicity to Children: A Public Health and Policy Perspective. School of Hygiene and Public Health, Johns Hopkins University, Baltimore, MD. June 2000. 157 Gan, J., et al. Synthetic Pyrethroids; ACS Symposium Series; American Chemical Society: Washington, DC, 2008. See http:// pubs.acs.org/doi/abs/10.1021/bk-2008-0991.ch001. 158 Shafer, T.1., D.A. Meyer, and K.M. Crofton. "Developmental Neurotoxicity of Pyrethroid Insecticides: Critical Review and Future Research Needs." Environ Health Persp 113, no. 2. Oct 2004:123-136. See also Permethrin: Technical Summary, The Endocrine Disruption Exchange, http://www.endocrinedisruption.com/ pesticides.permethrin.summary.php. 159 For an overview of health effects with multiple references provided, see PAN AP Fact Sheet "Highly Hazardous Pesticides: Neonicotinoids", PAN Asia Pacific, 2012. See http://www.panap. net/en/p/page/pesticides-campaigns-hhps/185. Chao, S.L. and J.E. Casida.. "Interaction of Imidacloprid Metabolites and Analogs with the Nicotinic Acetylcholine Receptor of Mouse Brain in Relation to Toxicity". Pesticide Biochemistry and Physiology. 1997 58: 77-88. D01:10.1006/ pest.1997.2284. See http://www.sciencedirect.com/science/ article/pii/50048357597922847. Imidacloprid - Human Health and Ecological Risk Assessment - Final Report. USDA Forest Service. December 2005. 160 Yamamoto, I. "Nicotine to Nicotinoids:1962 to 1997", in Nicotinoid Insecticides and the Nicotinic Acetylcholine Receptor, eds. Yamamoto, I. and Casida, J. Springer -Verlag, Tokyo, 1999 pp. 3-27. 161 Pesticide Use Trends in the U.S.: Pesticides for Home and Garden Uses. Univ of Florida Extension, EDIS - "This document is PI -140, one of a series of the Pesticide Information Office, Florida Cooperative Extension Service, Institute of Food and Agricultural Sciences, University of Florida. Published January 2007. Revised February 2011. See http://edis.ifas.ufl.edu/pil77. 162 Pesticide Industry Sales & Usage, 2006 and 2007 Morket Estimates, U.S. EPA, Washington, DC Feb 2011. See www.epa. gov/opp00001/pestsales/07pestsales/market_estimates2007. pdf. 163 Lu C., D.B. Barr, M. Pearson, S. Bartell and R. Bravo. "A Longitudinal Approach to Assessing Urban and Suburban Children's Exposure to Pyrethroid Pesticides." Environ Health Perspect. 2006114:1419-1423. 164 See Pest Management and Pesticide use in California Child Care Centers, UC Berkeley, 2012. Available at http://(erch.org/ information-for/childcare-providers/. 165 Use, Effects and Alternatives to Pesticides in Schools, Report to the Ranking Minority Member, Committee on Governmental Affairs, U.S. Senate. United States General Accounting Office 1999. See www.gao.gov/new.items/rc00017.pdf. 166 Owens, K. "Schooling of State Pesticide Laws 2010 Update." Pesticides and You. Fall 2009 29(3): 9-20. 167 "Child Safe Playing Field Act Signed into Law by New York Governor" Beyond Pesticides Daily News Blog, May 2010. See http://www.beyondpesticides.org/dailynewsblog/?p=3637. 168 Green Schools Within Reach: Moving Beyond the Healthy Schools Act of 2000. Californians for Pesticide Reform. See http:// pesticidereform.org/article.php?id=385. 169 "Tulare County Residents Win Greater Protection from Dangerous Pesticides: New rules announced for pesticide applications around schools, homes and labor camps," Press Release, Californians for Pesticide Reform. Feb 2008. See www.panna. org/sites/default/files/imported/files/CPR20080220.pdf. 170 White Earth Land Recovery Project, Farm to School Program. See http://nativeharvest.com/node/255 , viewed July 2012. 171 Rauzon, S., M. Wang, N. Studer and P. Crawford. An Evaluation of the School Lunch Initiative. A report by the Dr. Robert C and Veronica Atkins Center for Weight and Health, University of California at Berkeley, Sept 2010. See edibleschoolyard.org/sites/ default/files/file/Final%20Report_9-22-1 Ov4_LoRes.pdf. 172 The Olympia School Districts' Organic Choices Program, National Farm to School Network. See http://www.farmtoschool.org/ state-programs.php?action=detail&id=8&pid=58, viewed June 2012. 173 Action Alert: Help protect Ashland Parks, Schools and Waters from Pesticides. Klamath Siskiyou Wildlands Center. See http:// kswild.org/get-involved/ActionAlerts/help-reduce-or-eliminate- pesticides-at-ashland-parks-and-schools, viewed June 2012. 174 Pesticide -free parks: It's time! Northwest Coalition for Alternatives to Pesticides, Eugene OR. 2005. See www.pesticide.org/get- the-facts/ncap-publications-and-reports/pesticide-free-parks/ pfptime.pdf. 175 "Horticulture: Pesticide reduction" Seattle Parks and Recreation. See http://www.seattle.gov/parks/horticulture/pesticide.htm, viewed June 2012. 176 NJ Senate Environment Committee Passes Nation's Strongest Pesticide Bill, Press Release, Clean Water Action, Jan 2011. See http://www.cleanwater.org/press/nj-senate-environment- committee-passes-nation%E2%80%99s-strongest-pesticide- bill. 177 New Polling Data Indicates Overwhelming Public Support 32 A Generation in Jeopardy • Pesticide Action Network for Chemicals Regulation. Safer Chemicals Healthy Families: Resources. Sept 2010. See http://www.saferchemicals.org/ resources/opinion-2010.html 178 Philpott, T. "How Your College Is Selling Out to Big Ag," Motherlones, May 2012. See http://www.motherjones.com/ tom-philpott/2012/05/how-agribusiness-dominates-public-ag- research 179 Agribusiness. OpenSecrets.org, Center for Responsive Politics. See http://www.opensecrets.org/industries/indus.php?ind=A, viewed August 2012. See also Undue Influence, Pesticide Action Network at http://www.panna.org/issues/pesticides-profit/ undue -influence. Appendix A More Science: Key study descriptions Our intention in undertaking this review was not to conduct a comprehensive evaluation of the evidence. The body of scientific literature exploring how pesticides affect children's health is wide, deep and decades long. Our goal is to provide a snapshot of recent findings, coming fast and furious in the just the past few years, that—taken together— provide compelling reason for concern about the impact of pesticides on our childrerds health. In the report itself we highlight a few of the key findings for each health effect, focusing on studies that were particularly compel- ling, and/or represented other studies we reviewed with similar findings. We simplified descriptions of each study to provide a basic sense of how the research was conducted and what researchers found. Here in Appendix A we provide a bit more detail on some of the key studies described above, as well as additional studies. Study descriptions are organized by health effect, and alphabetically by author within each category. Brain & nervous system harms (reduced cognitive function, autism, ADHD) Bouchard M.F., D.C. Bellinger, R.O. Wright and M.G. Weisskopf."Attention-deficit/ hyperactivity disorder and urinary metabolites of organophosphate pesticides." Pediatrics 2010.125(6): e1270 -e1277. This study examines the association between urinary con- centrations of organophosphate metabolites and ADHD in children eight to 15 years of age. Researchers analyzed cross-sectional data from the National Health and Nutrition Examination Survey for 1139 children representative of the U.S. population. Urinary DMAP metabolite levels (which are an indicator of exposure to OP pesticides), an ADHD assess- ment, and household surveys were used in the analysis. The data support the hypothesis that organophosphate exposure, at levels common among U.S. children, may contribute to ADHD prevalence. Eskenazi B., K. Huen, A. Marks, K.G.Hadey, A. Bradman, D.B. Bar, et al. "PON1 and Neurodevelopment in Children from the CHAMACOS Study Exposed to Organophosphate Pesticides in Utero." Environ Health Perspect Aug 2010118: 17751781. See httpJ/dx.doi.org/10.1289/ehpJO02234. The enzyme paraoxonase 1 (PON I) detoxifies metabolites of some organophosphate (OP) pesticides, andPONI genetic polymorphisms influence enzyme activity and quantity. The study authors investigated whether PON1 genotypes and enzyme activity levels in mothers and their children were linked to neurodevelopmental changes, and whether PON1 levels and genotypes had an effect on the association of in utero exposure to OP pesticides (as assessed by maternal urinary concentrations of dialkyl phosphate metabolites, a marker of OP pesticide exposure) and neurodevelopment and behavior. The researchers found that of the 353 two- year -olds assessed, children with a certain variation of PON 1 (the PON1-108Tallele) scored more poorly on the Mental Development Index and somewhat lower on the Psychomotor Development Index. The authors concluded that while the variations of PON1 were associated with outcomes in child neurobehavioral development, additional research is needed to confirm whether it modifies the relation with in utero expo- sure to OP pesticides. Pessah I.N., P.J. Lein. "Evidence for environmental susceptibility in autism" in: Autism, (Zimmerman AW, ed). Totowa, NJ: Humana Press 2008409-428. The authors aim to illustrate how research into the patho- physiology and genetics of autism may inform the identifi- cation of environmental susceptibility factors that promote adverse outcomes in brain development. They highlight three examples of gene -environment interactions that are likely to contribute to autism risk, including: (1) pesticides that inter- fere with the neurotransmitter acetylcholine; (2) pesticides that interfere with y-aminobutyric acid (GABA) neurotrans- mission; and (3) persistent organic pollutants that directly A Study by Any Other Name... Epidemiological study: A study of distribution or patterns in health trends or characteristics and their causes or influences in specific populations. Includes both case -control and all types of cohort studies. Case -control study. Compares a "case" group (e.g., U.S. children ages 0-14 with cancer) with a group serving as a control (e.g., cancer -free U.S. children ages 0-14). Cohort study: Profiles a specific population where shared exposure may be assumed, such as occupational exposure to pesticides among farmworkers. Prospective cohort study: Follows a group that is slightly different in some respects. (i.e., studying a cohort of pesticide applicators who use varying protective methods while working with pesticides.) Longitudinal cohort study: Tracks a specific group over time. For example, a UC Berkeley study on the central California coast has followed a specific group of children from conception through adolescence. Meta-analysis: Pulls together several studies on the same topic and does further statistical analysis on the basic findings. Review: Examines the "state of the science" and often provides evaluation of conflicting pieces of data. Review authors give their view on what is currently happening in the field. A Generation in Jeopardy • Pesticide Action Network North America 33 alter calcium ion (Ca2+) signaling pathways and Ca2'-depen- dent effectors. If both genetic factors and environmental ones converge to interrupt the same neurotransmitter or signaling systems at critical times during development, adverse effects can be amplified. Rauh V.A., F.P. Perera, M.K. Horton, R.M. Whyatt, R. Barisal, X. Hao X, et al. "Brain anomalies in children exposed prenatallyto a common organophosphate pesticide: Proc Natl Acad Sci 2012109(20):7871-6. This study investigated associations between prenatal expo- sure to chlorpyrifos and brain morphology (examining brain structure). With a sample of 40 children—who experienced low prenatal exposure to tobacco smoke and polycyclic aromatic hydrocarbons -20 subjects with high chlorpyri- fos exposure were compared to 20 low -exposure subjects. The data revealed a significant association between prenatal exposure to chlorpyrifos, at standard use levels, and structural changes in the developing human brain. High exposure was associated with the enlargement of several areas of the brain and in preliminary analyses, the reversal of sex differences or a lack of expected sex differences. Shafer, T.1., D.A. Meyer and K.M. Crofton. "Developmental Neurotoxicity of Pyrethroid Insecticides: Critical Review and Future Research Needs." Environmental Health Perspectives 113, no. 2 Oct 2004:123-136. A review of pyrethroid insecticides and the data related to potential developmental neurotoxic effects of pyrethroids, with recommendations for improving study design and statistical analyses. The review discusses the various effects on voltage -sensitive sodium channels, which are a primary target of pyrethroids. Childhood cancers Carozza S.E., B. Li, K. Elgethun and R. Whitworth." Risk of childhood cancers associated with residence in agriculturally intense areas in the United States." Environ Health Persp 2008116(4): 559-565. Researchers from the U.S. evaluated whether children under the age of 15 who live in a county associated with greater agriculture production—and hence, exposure to pesticide drift—experienced different risk rates for developing cancer. Using incidence data for U.S. children provided by the North American Association of Central Cancer Registries, research- ers were able to compare county -level, sex- and age-specific rates of childhood cancer with agricultural census data con- taining county acreage, percent cropland, and percent acres for specific crops. The data revealed statistically significant increase in risk for many types of childhood cancers for resi- dents living in those counties with a moderate to high level of agricultural activity. Risk for different cancers varied by type of crop; for example, there was increased risk of non-Hodgkin lymphoma and thyroid cancer associated with residence at diagnosis in counties that produced corn or oats. Infante -Rivard C, S. Weichenthal. Pesticides and childhood cancer: an update of Zahm and Ward's 1998 review. J ToxicolEnviron Health RCritRev 200710(1): 81-99. Infante -Rivard and Weichenthal reviewed the epidemiological and ecological studies published since the 1998 Zahm and Ward review. The authors found that 15 case -control studies, four cohort studies, and two ecological studies have been pub- lished since this review, and 15 of these 21 studies reported a statistically significant increase in risk of childhood cancer among children whose parents were experienced occupational pesticide exposure. These studies found that the risk of all childhood cancers increased with the frequency of maternal exposure to herbicides and plant insecticides. Furthermore, maternal and paternal exposure to insecticides and herbicides up to five years before having a child increased risk of all childhood brain tumors, astroglial tumors, non-Hodgkin's lymphoma, primitive neuroectodermal tumors, and other glial tumors. Parental occupation in agriculture is also associ- ated with an increased risk of Ewing's sarcoma. The authors conclude that evidence supports an association between at least some pesticide exposure and childhood cancer. Kristensen, P., A. Andersen, L.M. Irgens, A.S. Bye and L. Sundheim. "Cancer in Offspring of Parents Engaged in Agricultural Activities in Norway: Incidence and Risk Factors in the Farm Environment." Internationallournal ofCancer. Journal International Du Cancer. Jan 1996 65 (1):39-50. A cohort study in Norway of 323,359 children born between 1952-1991 reported that children 0-14 years had a nearly doubled risk for brain tumors and a more than tripled risk for neuroepithelial tumors except for astrocytomas associated with pesticide purchase. These associations were stronger when sub -groups, such as growing up on the farm, were considered. Offspring born April -June showed a clustering of neuroepithelial brain tumors, suggesting that paternal expo- sure during periods of increased pesticide application, from 0-3 months before conception, may have been a factor. Meinert, R., J. Schuz, U. Kaletsch and J. Michaelis. "Leukemia and Non -Hodgkins Lymphona in Childhood and Exposure to Pesticides: Results of Register -based Case -Control Study in Germany."Amlournal ofEpidemiology 2000.151(7): 639-646. A case -control study conducted in Germany from 1993- 1997 found parental occupational exposure to be related to childhood cancer regardless of period of exposure and type of cancer, which the authors point out might be due to different recall of past exposures between parents of cases and parents of controls. Residential insecticide use was associated with childhood lymphoma, both professional exterminator and parental usage were significantly associated with increased risk. Nielsen S.S., R. McKean-Cowdin, F.M. Farin, E.A. Holly, S. Preston -Martin and B.A. Mueller. "Childhood brain tumors, residential insecticide exposure, and pesticide metabolism genes." Environ Health Persp 2009118(1):144-149. Researchers in California and Washington found evidence of increased risk of childhood brain tumors (CBT) associ- ated with certain genetic polymorphisms when kids were exposed to insecticides. Strong interactions between genotype and insecticide exposure during childhood was observed. Among exposed children, CBT risk increased per PON1-108T allele, whereas among children never exposed, CBT was not increased. Nielsen et al. concluded childhood exposure to organophosphorus pesticides coupled with a reduced ability to detoxify these pesticides, may be associated with CBT. 34 A Generation in Jeopardy • Pesticide Action Network North America van Wijngaarden E, P.A. Stewart, A.F.Olshan, D.A. Savitz and G.R. Bunin. "Parental occupational exposure to pesticides and childhood brain cancer."Aml Epidemiol2003.157(11): 989-997. Researchers from the U.S. evaluated parental exposure to pesticides at home or on the job in relation to the occurrence of brain cancer in children. The sample consisted of children diagnosed with cancer and matching controls from four U.S. states. Interviews were performed with the biological mothers of the subjects to assess the residential and occupational expo- sure to pesticides in the two years before the child was born. The data revealed a significant risk of astrocytoma associated with residential use and exposure to herbicides. Combining parental exposures to herbicides form both residential and occupational sources, the elevated risk remained significant. Birth defects Brender,l.D., M. Felkner, L. Suarez, M.A. Canfield and J.P. Henry. "Maternal Pesticide Exposure and Neural Tube Defects in Mexican Americans." Annals of Epidemiology. 2010 20(1):16-22. Researchers investigated the relationship between mater- nal pesticide exposures and neural tube defects (NTDs) in offspring comparing to groups of Mexican American women (184 in case group, 225 for comparison). After adjusting for differences in maternal education levels, smoking, and folate intake during pregnancy, women who reported using pesticides in their homes or yards were twice as likely to have children with NTDs than women not reporting exposures (95% confidence interval [CI], 1.2-3.1) Case -women were also more likely to live within 1/4 mile of agricultural fields. As possible sources of pesticide exposure increased, risk of NTDs also increased. Associations were stronger for risk of anen- cephaly than for spina bifida. Garry V.F., M.E. Harkins, L.L. Erickson, L.K. Long -Simpson, S.E. Holland and B.L. Burroughs. "Birth defects, season of conception, and sex of children born to pesticide applicators living in the Red River Valley of Minnesota, USA." Environ Heahh Persp 2002.110(3):441-449. A cross-sectional study performed in the Red River Valley of Minnesota examined the reproductive health outcomes in 695 farm families (analyzed data from 1,532 children) from parent -reported birth defects. Researchers determined con- ceptions in the spring time led to significantly more children born with birth defects, compared to children conceived in any other season. Their data suggests environmental agents present in the spring, like herbicides, have an adverse effect on the birth defect rate. Furthermore, the data revealed an asso- ciation between fungicide exposure and the determination of child sex—affecting the survival rate of the male fetus (female to male birth ration is 1.25 to 0. Gaspari L., F. Paris, C. Jandel, N. Kalfa, M. Orsini,l.P. Daures and C. Sultan. "Prenatal environmental risk factors for genital malformations in a population of 1442 french male newborns: a nested case -control study." Hum Reprod 2011. 26(11):3155-3162. Researchers from France analyzed a physician's examinations and parental interviews for 1442 full-term newborn males in southern France to identify risk factors for male external genital malformations, with a focus on parental occupational exposure to endocrine disrupting chemicals, such as organo- chlorine pesticides. Infants were examined for cryptochidism, hypospadias, and micropenis, while a.questionnaire asked parents about the pregnancy, personal characteristics, lifestyle, and occupational exposure to EDCs. In total, 39 cases of genital malformation were reported (2.70%). A significant relationship was observed between newborn cryptochidisni, hypospadias or micropenis and parental occupational expo- sure to pesticides with the odds of genital malformation increasing 4.41 -fold. These data supports the hypothesis that prenatal contamination by pesticides may be a potential risk factor for newborn male external genital malformation. Rocheleau, C.M, P.A. Romitti and L.K. Dennis. "Pesticides and Hypospadias: a Meta -anal ysis."lournal ofPediatric Urology. Feb 2009 5(1):17-24. A meta-analysis of studies done in 7 different countries (Canada, Denmark, Italy, Netherlands, Norway, Spain, US) indicated a 36% increased risk of hypospadia with maternal occupational exposure and a 19% increased risk of hypo- spadias with paternal occupational exposure. Winchester PD, HuskinsJ, Ying 1.2009. Agrichemicals in surface waterand birth defects in the United States. ActaPaediatr98(4 ): 664-669. Researchers from Indiana and Ohio compared water data from the USGS National Water Quality Assessment (NAWQA)—measuring the levels of nitrates, atrazine, and other pesticides in surface water—and Centers for Disease Control data detailing monthly pregnancy and birth out- come outcomes. The data reveal that between 1996 and 2002 women in the US were significantly more likely to give birth to a child with birth defects if conception had occurred in the months of April through July. NAWQA surface water samples indicate that concentrations of atrazine, nitrates, and other pesticides were also higher in the months of April through July. This correlation was statistically significant, demonstrat- ing elevated concentrations of agrichemicals in surface water coincided with a higher risk of birth defects among live births for children conceived between April and July. Early puberty Aksglaede L., K. Sorensen, J.H. Petersen, N.E. Skakkebaek and A. Juul. "Recent decline in age at breast development: the Copenhagen puberty study." Pediatrics 2009.123(5): e932-939. Researchers from Denmark collected data from 2095 females aged 5.6 to 20 years in two Copenhagen cohorts (1991-1993 and 2006-2008) to examine differences in breast develop- ment. Using the most accurate method of palpation, Aks- glaede et al. found the onset of puberty—defined as the mean estimated age at the attainment of glandular breast tissue— occurred significantly earlier in the 2006 cohort. The ages at which menarche and pubic hair development occurred also slightly decreased in the 2006 cohort. As a result of these tim- ing changes in early and later markers of puberty, the length of puberty appears to have increased. The authors interpreted these observations as indicative of gonadotropin -independent estrogenic actions at the level of breast development, rather than an earlier activation of the pituitary -gonadal axis. These changes in timing could not be explained by alterations in reproductive hormones and BMI, suggesting other factors involved need to be explored. A Generation in Jeopardy • Pesticide Action Network North America 35 Gladen B., N. Ragan and W. Rogan. "Pubertal growth and development and prenatal and lactational exposure to polychlorinated biphenyls and Dichlorodiphenyl Dichloroethene." Pediatrics 2000.136(4):490-496. Researchers from the National Institute of Environmental Health Sciences explored the relationship between prenatal and early -life exposure to PCBs and DDE on children. This is one of a very few studies examining environmental con- taminants and male puberty onset. Using 594 children from the North Carolina Infant Feeding Study cohort, they found no effect on the ages at which puberty began. However, the height and weight (adjusted for height) of boys at puberty increased with transplacental exposure to DDE. Massart F., P. Seppia, D. Pardi, S. Lucchesi, C. Meossi, L. Gagliardi et al. "High incidence of central precocious puberty in a bounded geographic area of northwest Tuscany: an estrogen disrupter epidemic?" 6ynecol Endocrino12005. 20(2):92-98. Researchers in Italy preformed an analysis of central pre- cocious puberty (CPP) distribution in northwest Tuscany (NWT). The overall incidence rate of sexual precocity is estimated at 10-20 per 100, a rate similar to that found in four of the cities in the NWT sample; however 47 percent of the CPP cases found in NWT were in the Viareggio area, a rate of 161 per 100,000. This area hosts a high density of navy yards and greenhouses—consequently it is at higher risk of chemical estrogen pollution. As this population represented only 13.73 percent of the total population of NWT, living in this area significantly increased the risk of CPP. The definite geographic distribution of CPP in this suggests that environ- mental involvement/pollution may be a major determinant of CPP development. Nebesio T and 0. Hirsh Pescovitz. " Historical perspectives." Endocrinologist 2005. 15(1):44-48. Nebesio and Pescovitz reviewed reports alleging endocrine dis- ruptors blamed for altering the age of normal puberty, includ- ing an examination of studies implicating pesticides and accidental environmental exposures. Studies reviewed include two seminal studies on early puberty in girls: Vasiliu et al.'s (2004) examination of the Michigan anglers cohort daughters and Krzstevska-Konstantinova et al.'s (200 1) examination of precocious puberty in native and non-native Belgian girls. Nebesio and Hirsch Pescovitz (2005) also review Boneh et al. (1989), who examined cases of girls with precocious sexual development from Jerusalem over a 10 -year time period and found strong evidence for a seasonal increase in incidences of early sex development observed (from April -June). Seasonal pesticide usage was a potential cause, but the reasons for this were unknown. Steingraber S. 2007. The falling age of pubertyin U.S. girls: what we know, what we need toknow. The Breast Cancer Fund. In this report Steingraber suggests that pubertal onset and menarche are two sexual maturation processes that appear to be becoming uncoupled, therefore increasing the length of puberty in girls. The author cites environmental contami- nants as the cause in light of recent evidence suggesting even minimal exposure to an endocrine disruptor on sex hormones can have a profound consequence in childhood. Obesity & diabetes Baillie -Hamilton, P.F. "Chemical toxins: a hypothesis to explain the global obesity epidemic"JAltern Complement Med 2002 8(2):185-192. Hamilton puts forth a new hypothesis to explain the global obesity epidemic: chemical toxins. Overeating and inactivity do not fully explain the current trend in obesity. Baillie -Ham- ilton calls for an examination of environmental causes rather than genetic factors. The sympathetic nervous system is perhaps the key weight -controlling system, and is targeted by many of the commonest synthetic chemicals. Numerous widely used synthetic chemicals induce weight gain, includ- ing pesticides (specifically organochlorines and organophos- phates). They do so by disrupting major weight controlling hormones, altering levels and sensitivity to neurotransmitters, interfering with metabolic processes, and causing widespread damage to body tissues. These interferences change appetite, food efficiency, and the metabolism of fats, proteins, and carbohydrates. Janesick, A. and B. Blumberg. "Endocrine Disrupting Chemicals and the Developmental Programming of Adipogenesis and Obesity.' Birth Defects Research Part C. Embryo Today: Reviews 2011.93, no. 1: 34-50. This review article explores possible explanations for the varia- tion in individual propensity to gain weight and accrue body mass, even at identical levels of caloric input. The authors review evidence from clinical, epidemiological, and biological studies showing that obesity is largely programmed early in life, including prenatally. They examine the environmental obesogen hypothesis, which holds that "prenatal or early life exposure to certain endocrine disrupting chemicals can pre- dispose exposed individuals to increased fat mass and obesity. Obesogen exposure can alter the epigenome of multipotent stromal stem cells, biasing them toward the adipocyte lineage at the expense of bone." Individuals exposed to obesogens early in life or prenatally might thus experience changes in their stem cell compartment, which in turn influences adipo- genic fate Lee D.H., I.K. Lee, K. Song, M. Steffes, W. Toscano, B.A. Baker and D.R. Jacobs."A strong dose -response relation between serum concentrations of persistent organic pollutants and diabetes: results from the National Health and Examination Survey 1999-2002." Diabetes Care 2006 29(7):1638-1644. Researchers performed a cross-sectional examination of the association between serum concentrations of six POPS (selected because they were detectable in greater than 80 percent of participants) and diabetes prevalence. Aker adjustments were made for confounding variables (age, sex, race and ethnicity, poverty income ratio, BMI and waist circumference) diabetes prevalence was strongly positively associated with lipid adjustment serum concentrations of all six POPs tested for in the sample of 2,016 adult participants from the National Health and Nutrition Examination Survey 1999-2002. Furthermore, the association between POPS and diabetes was much stronger among obese subjects compared to lean subjects. Lee, D.H., M.W. Steffes, A. Sj6din, R.S. Jones, L.L. Needham, D.R. Jacobs. "Low dose organochlorine pesticides and polychlorinated biphenyls predict obesity, 36 A Generation in Jeopardy • Pesticide Action Network North America dyslipidemia, and insulin resistance among people free of diabetes." PLoSOne 201160): e15977. In a follow up study to their 2010 study of low-dose persis- tent organic pollutant (POP) exposure and prediction of type 2 diabetes, Lee et al. conducted a nested case -control study to explore the relationship between serum concentrations of POPS and adiposity, dyslipidemia, and insulin resistance among people confirmed to be diabetes free (assessing study subjects on 5 occasions over 20 years). Researchers concluded that simultaneous exposure to various OC pesticides and PCBs in the general population may contribute to the devel- opment of obesity, dyslipidemia, and insulin resistance— common precursors of type 2 diabetes and cardiovascular diseases—among those without diabetes. POPs exposure may also contribute to excess adiposity and other dysmetabolic conditions. Ten POPS were found to predict future higher triglycerides and 14 POPs predicted lower HDL-cholesterol. Among organochorine pesticides, p,p'-DDE most consistently predicted higher BMI, triglycerides and HOMA-IR, as well as a lower HDL-cholesterol at year 20. Newbold R.R., E. Padilla -Banks, R.J. Snyder, T.M. Phillips and W.M. Jefferson. "Developmental exposure to endocrine disruptors and the obesity epidemic." Reprod Toxicol 2007.23(3): 290-296. Research from the US has shown an association between exposure to environmental endocrine disrupting chemi- cals with the development of obesity. Researchers utilize an animal model of developmental exposure to diethylstilbe- strol (DES)—a potent perinatal endocrine disruptor with estrogenic activity—to study the mechanisms involved in programming an organism for obesity. Their data supports the idea that brief exposure early in life to environmental endocrine disrupting chemicals, especially those with estro- genic activity, like DES. These chemicals may contribute to overweight and obesity as well as other obesity -associated diseases (type 2 diabetes and cardiovascular disease). This research complicates the current understanding of obesity and necessitates a consideration of more complex factors, includ- ing environmental chemicals. Asthma Hernandez A.F., T. Parr6n and R. Alarc6n. "Pesticides and asthma." CurrOpin Allergy (lin lmmuno12011 11(2):90-96. Herndndez et al. performed a review of clinical and epi- demiological studies that link exposure to pesticides, asthma attacks, and an increased risk of developing asthma. These authors concluded that while many pesticides are sensitizers or irritants, their potential to sensitize is limited. However, more importantly, pesticides may increase the risk of devel- oping asthma, exacerbate a previous asthmatic condition or even trigger asthma attacks by increasing bronchial hyper -responsiveness. Salam MT, Y.F. Li, B. Langholz, F.D. Gilliland."Eady-Iffe environmental risk factors for asthma: findings from the Children's Health Study." Environ Health Perspect 2003112(6):760-765. Researchers from the University of Southern California selected 4,244 subjects from the Children's Health Study con- ducted in 12 southern California communities to measure the relationship between childhood environmental exposures ,and asthma risk. Matching those subjects diagnosed with asthma before age five with asthma -free counterparts that acted as controls (matched for age, sex, community of residence, and in utero exposure to maternal smoking), the authors con- cluded that environmental exposures during the first year of life are associated with an increase in the risk for early-onset persistent asthma, a subtype of asthma associated with long- term morbidity. Compared to never -exposed children, chil- dren exposed to herbicides within the first year of life had a 4.6 -fold increased risk of asthma and children exposed to pes- ticides had a 2.4 -fold increase in risk—considered together children exposed to any pesticide or herbicide in the first year of life experience a 2.53 -fold higher risk of asthma compared to children who were never exposed to either of those. Salameh P.R., I. Baldim, P. Brochard, C. Raherison, B.A. Saleh and R. Salamon. "Respiratory symptoms in children and exposure to pesticides." EurRespirJ2003 22(3):507-512. Public health researchers from Lebanese University in Leb- anon and Victor Segalen Bordeaux II University in France conducted a cross-sectional study to evaluate if exposure to pesticides resulted in chronic effects on the respiratory health of Lebanese children. From 19 public schools, 3,291 randomly selected school children—aged five to 16 years— revealed exposure (residential, paraoccupational, and domes- tic) to pesticides was significantly associated with respiratory disease (1.82 -fold higher) and chronic respiratory symptoms such as chronic phlegm, chronic wheezing, and wheezing at any point (the only exception was chronic cough). Twelve per- cent of the sample reported a chronic respiratory disease and of those, 84 reported a medically confirmed asthma diagnosis (2.6 percent of the sample). SunyerJ, M. Torrent, R. Garcia -Esteban, N. Ribas-Fit6, D. Carrizo, I. Romieu et al. "Early exposure to Dichlorodiphenyldichloroethylene, breastfeeding and asthma at age six." Clin Exp Allergy 2006 36(10):1236-1241. Researchers from Spain and the United Kingdom conducted a longitudinal study from a sample of 468 Minorcan children (Balearic Island in the northwest Mediterranean sea with no local pollution sources) to examine the association between prenatal exposure to DDE and other organochlorine com- pounds and asthma. Asthma was defined as the presence of a wheeze, persistent wheezing, or parental report of doc- tor -diagnosed asthma at age four. All children were born with quantifiable levels of DDE and PCB compounds. Wheezing at age four was reported for 11.6 percent of all children. Wheezing at four years of age increased with DDE concentra- tion, particularly at the highest quartile, which was also found for persistent wheezing. This association was maintained even after adjusting for potential confounding variables. These results corroborated the association established between DDE and asthma in German school children conducted by Kar- maus et al. in 2001. A Generation in Jeopardy • Pesticide Action Network North America 37 Key Appendix B.- Top Pesticides Used in Agriculture & at Home ?— Insufficientdata ND — No data available I — Insecticide Table B-1: Most Commonly Used Pesticide Active Ingredients - Agriculture Listed by volume of use H — Herbicide F — Fungicide Pesticide & use level range (millions of lbs active ingredient) PAN HHP' Type High' acute toxicity Carcin- ogen Acute neuro- toxicant (ChE inhibitor) Devel. or reprod. toxicant Endocrine disruptor Primary crops PGR — Plant growth regulator FUM — Fumigant - — Food residues' Glyphosate (180-185) possible H ? suspected Glyphosate (5-8) ? ? Hay/pasture, soybeans, corn NO Atrazine (73-78) Y H Carbaryl (4-6) Y I ? suspected Corn, sugarcane Spinach, wheat, onions, lettuce, water Metam-sodium (50-55) Y FUM Y Y possible Y suspected Potatoes, carrots, tomatoes, onions, peanuts NO Metolachlor, (S) (30-35) Y H possible possible 7 ? suspected Tomatoes, beans, corn, cotton Oats, celery, water, corn Acetochlor (28-33) Y H Y Y Malathion (2-4) ? suspected Corn, popcorn Water Dichlorpropene (27-32) Y FUM Y Y H ? ? Strawberries, sweet potatoes, tree nuts Y 2,4-D (25-29) Y H I possible possible ? suspected Grasses, wheat, citrus fruits, tree nuts Potatoes, water Methyl bromide (11-15) Y FUM Y ? Y suspected Tomatoes, strawberries, almonds, peppers, watermelon, cucumbers NO Chloropicrin (9-11) Y FUM Y ? ? ? Tobacco, tomatoes, strawberries, bell peppers NO Pendimethalin (7-9) Y H possible ? suspected Soybeans, corn, cotton, peanuts Carrots, collard greens, kale Ethephori (7-9) PGR Y ? ? Cotton, walnuts, grapes, tomatoes NO Chlorothalonil (7-9) Y F Y Y ? ? Tomatoes, watermelons, onions Cranberries, celery, green beans Metam Potassium (7-9) FUM Y Y Y ? Lettuce, potatoes NO Chlorpyrifos (7-9) Y I Y ? suspected Tree nuts, apples, alfalfa, broccoli, citrus, grapes, sweet corn Apples, bell peppers, cranberries, kale, grapes, peaches Copper Hydroxide (6-8) F ? ? Tree nuts, grapes, peaches NO Simazine (5-7) Y H Y suspected Corn, citrus, grapes, tree nuts Blueberries, kale, water, oranges Trifluralin (5-7) Y H possible ? suspected Soybeans, cotton, green beans, broccoli, tomatoes Carrots, spinach, wheat, soybeans, brocco Propanil (4-6) Y H possible ? suspected Rice, oats, barley, wheat Wheat Mancozeb (4-6) Y F Y Y suspected Apples, tomatoes, onions, watermelon NO Acephate (2-4) Y I possible Y ? suspected Cotton, tobacco, cranberries, mint Green beans, bell peppers Diurons (2-4) Y H Y Y suspected Oranges Asparagus, oranges, water, potatoes MCPA (2-4) Y H Y possible ? ? Flax, barley, wheat, rice water Paraquat (2-4) Y H Y ? suspected Corn, soybeans, cotton, apples NO Dimethenamid (2-4) Y H possible 7 ? Corn, soybeans, sugarbeets Soybeans, water Tahlp R-2- Most [ommoniv lkpd Ppsticide Active Innredipnts — Home & Garden Listed by volume of use Pesticide & use level range (millions of lbs active ingredient) PAN HHP Type High acute toxicity Carcinogen Acute neurotoxicant (ChE inhibitor) Devel. or reprod. toxicant Endocrine disruptor 2,4-D (8-11) Y H possible ? suspected Glyphosate (5-8) H ? ? Carbaryl (4-6) Y I Y Y Y suspected Mecoprop-P (MCPP) (4-6) Y H possible ? ? Pendimethalin (3-5) Y H possible 7 suspected Pyrethroids' (2-4) Y I Y Y Y suspected Malathion (2-4) Y I Y possible Y Y suspected Dicamba (1-3) H Y ? Malathion (2-4) Y I Y possible Y Y suspected Trifluralin (1-3) Y H possible ? suspected Pelargonic Acid (< 1) H/F ? ? ? A Generation in Jeopardy • Pesticide Action Network North America Notes 1 See Table 3.6 and 3.7 in Pesticide Industry Sales & Usage, 100 and 1007 Market Estimates, U.S. EPA, Washington, DC Feb 2011. See www.epa.gov/opp00001/pestsales/07pestsales/ market—estimates2007.pdf. Aldicarb was removed from the list as registration was withdrawn in 2010. 2 PAN International has compiled and published a list of Highly Hazardous Pesticides (HNPs) that are harmful to human health and the environment, and targeted for global reduction and elimination. See www.panna.org/issues/ publication/pan-international-list-highly-hazardous- pesticides. 3 PAN's online pesticide database provides an explanation of these categories and additional toxicity, use and regulatory information for these and other pesticides. See www. pesticideinfo.org. 4 Based on USDA's Pesticide Data Program, as listed on www. whatsonmyfood.org. 5 Noted health effects not applicable for products with < 7% diuron, and applied to foliage. 6 Health hazards of specific pyrethroids vary, the effects indicated here represent those with most hazardous potentia effects. Appendix C Online Resources & Tools This compilation highlights a number of key online resources available through government agencies and public interest groups. It is not intended to be comprehensive. Pesticide use data California pesticide use reporting: calpip.cdpr.ca.gov EPA Pesticide Industry Sales & Usage: www. epa.gov/opp 00001 /pestsales USDA National Agricultural Statistics Service: www.nass.usda.gov Pesticide health harms Agency for Toxic Substances & Disease Registry, ToxFAQs: www. atsdr. cdc.gov/az1c. html Collaborative on Health & the Environment, Toxicant & Disease Database: www.healthandenvironment.org/tddb EPA Pesticides & Human Health Issues: www.epa.gov/0pp00001/health/human.ht?n EPA Recognition & Management of Pesticide Poisonings: npic.orst.edu/rmpp.htm Ontario College of Family Physicians, Systematic Review of Pesticide Human Health Effects: www. ocfp.on. ca/docs/pesticidespaper/pesticides paperpdf PAN International Highly Hazardous Pesticides: www.panna.org/ issues/publication/pan-international-list-highly-hazardous pesticides PAN's pesticide database: www.pesticideinfo.org Physicians for Social Responsibility, Pesticides & Human Health: A Resource For Health Care Professionals: www.psr-la. org/resources/reports-training-materials/#Pesticides The Endocrine Disruption Exchange (TEDX): www.endocrinedisruption.com/Pesticides.introduction.php Pesticides & children's health Beyond Pesticides, Learning/ Developmental Disorders resource page: www.beyondpesticides.org/health/learningdevelopmental.htm Center for Environmental Research & Children's Health: cerch.org/research programs/chamacos EPA Pesticides & Children: www. epa.gov/opp 00001 /health/children. htm National Academy of Sciences: www. nap. edu/catalogphp?record id=2126 PAN's Children's health page: www.panna.org/children Pesticide food residues FDA Total Diet Study: www.fda.gov/Food/FoodSafety/ FoodContaminantsAdulteration/TotalDietStudy/default. htm Whats On My Food? database (also includes health effect data): www.whatsonmyfood.org USDA Pesticide Data Program: www.ams.usda.gov/AMSv1.0/pdp Childhood disease & disorders American Academy of Pediatrics: www.aap.org CDC Child Health Statistics: www.cdc.gov/nchs/fastats/children.htm Children's environmental health Children's Environmental Health Network: www.cehn.org—A national multidisciplinary organization whose mission is to protect the developing child from environmental health hazards and promote a healthier environment. Children's Environmental Health Project: www.cape.ca/children—A project of the Canadian Association of Physicians for the Environment, CEHP is intended to introduce clinicians (and their patients) to children's environmental health issues. Information on the health effects from environmental exposures is presented in a systems approach. Healthy Child, Healthy World: healthychild. org— Protecting children's health and wellbeing from harmful environmental exposures through education and prevention strategies. Healthy Kids: www. healthy -kids. info —Provides resources and programs to help educators, health professionals, community officials, organiza- tions, policy makers and parents work together to ensure schools are safe for children's healthy development. Learning & Developmental Disabilities Initiative: www.healthandenviron- ment.org/initiatives/learning—An international partnership foster- ing collaboration among LDD organizations, researchers, health professionals and environmental health groups to address concerns about the impact environmental pollutants may have on children's neurological health. Making our Milk Safe (MOMS): www.safemilk.org—A national grassroots movement of mothers working to create a healthier, safer environ- ment for children, MOMS engages in education, advocacy and corporate campaigns. Pediatric Environmental Health Specialty Units: www.aoec.org/PEHSU. htm—ATSDR and EPA support this network to provide education for health professionals, public health officials and others about the topic of children's environmental health. Physicians for Social Responsibility: www.psr. org/resources/pediatric-toolkit. html—PSR has developed a pediatric environmental health toolkit that combines easy-to-use reference guides for health providers and user-friendly health education materials on preventing expo- sures to toxic chemicals and other substances that affect infant and child health. The toolkit is endorsed by the American Academy of Pediatrics. Safer Chemicals, Healthy Families: www.saferchemicals.org—A coalition pressing for reform of national chemicals policy. SCHF represents more than I I million individuals including parents, health pro- fessionals, advocates for people with learning and developmental disabilities, reproductive health advocates, environmentalists and businesses. The Children's Environmental Health Institute: cehi.org—Works to identify, validate and develop solutions to address adverse health effects to children occurring as a consequence of exposure to hazardous envi- ronmental substances. A Generation in Jeopardy • Pesticide Action Network North America 39 1. Pe mCiWOf K 1611 Telegraph Ave, Suite 1200 ® Oakland CA 94612-2130 510.788.9020 COUNTY CLERK COUNTY OF HAWAII RECEIVED Time 9.*o&PM BY Date 2015 '0 4 P/ EMC BILL 71 COMM. 392 PESTICIDES IN PARADISE HAWAI`I'S HEALTH & ENVIRONMENT AT RISK HAWAII i CENTER FOR FOOD SAFETY MAY /-'U ii SUBMITTED BY: JENNIFER RUGGLES ABOUT CENTER FOR FOOD SAFETY CENTER FOR FOOD SAFETY (CFS) is a non-profit public interest and environmental advocacy membership organization established in 1997 for the purpose of challenging harmful food production technologies and promoting sustainable alternatives. CFS combines multiple tools and strategies in pur- suing its goals, including litigation and legal petitions for rulemaking, legal support for various sustainable agriculture and food safety constituencies, as well as public education, grassroots organizing and media outreach. ACKNOWLEDGEMENTS Authors: Bill Freese, Ashley Lukens, Ph.D. and Alexis Anjomshoaa Copy Editior: Sharon Perrone Legal Consultant: Sylvia Wu Design: Hummingbird Design Studio Figures: Patrick Riggs Report Advisor: Andrew Kimbrell This abridged summary highlights the key points of a comprehensive, fully documented report of the same title by Center for Food Safety, available at: www.centerforfoodsafety.org/reports HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK CONTENTS SUMMARY OF KEY FINDINGS 3 PART I: PESTICIDES & GE SEEDS IN HAWAII Introduction 5 Transition from Sustainable Agriculture to Plantation Agriculture 6 Rise of the Seed Crop Industry and Decline of Hawai'i's Food Security 7 Employment and Economic Contribution 8 Land Use and Food Security 8 Missed Opportunities 9 Genetically Engineered Crops in Hawai'i 10 Pesticide and Fertilizer Use in GE Seed Corn Production 12 PART II: IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT Reported Health Harms from Pesticide Use in Hawai'i 17 Lessons from History 17 Pesticide Drift in Hawai'i 18 Health Impacts of Pesticide Exposure 22 Farmers and Farmworkers at Risk 22 Cancer 22 Parkinson's Disease 23 Depression 24 Endocrine Disruption 24 Our Keiki at Risk 24 Childhood Cancers 25 Neurobehavioral and Cognitive Deficits 25 Adverse Birth Outcomes 26 Asthma 27 Health Harms Specifically Linked to Pesticide Drift 27 Acute Pesticide Exposure Can Cause Lasting Harm 28 Additional Exposure to Agrochemicals in Food and Water 28 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 1 Environmental Impacts of Agrochemical Use in Hawaii 29 Atrazine 30 Chlorpyrifos 30 Synthetic Pyrethroids 31 Neonicotinoids 31 Impacts of Multiple Pesticides 32 PART III: TAKING CONTROL OF OUR FUTURE Regulation Does Not Prevent Harms 33 County Regulatory Initiatives Consistent with State Law 33 Deficient Federal Pesticide Regulation 34 Momentum Building to Protect Kids from Pesticide Drift 35 Conclusion 36 Endnotes 37 References 38 FIGURES + TABLES Figure 1: Area Planted to Vegetables, Fruits 9 (excl. Pineapples) and Seed Crops in Hawai'i Figure 2: Share of Fresh Fruit and Vegetable Markets 9 Supplied by Hawai'i Produce Figure 3: GE Crop Field Tests in Hawaii 11 Figure 4: GE Crop Field Trial Permits for Selected Traits in Hawai'i 11 Figure 5: DuPont -Pioneer Pesticide Use on Kaua'i 14 Figure 6: Average Annual Sales of Restricted Use Pesticides on Kauai 16 Figure 7: Pounds of Restricted Use Pesticides 16 (a.i.) Applied on Kaua'i by Month Table 1: Land Used for Seed Crop Operations in Hawai'i 7 Table 2: Key to DuPont -Pioneer Pesticides Used on Kaua'i 14 2 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK SUMMARY OF KEY FINDINGS 0 N OAHU, KAUAI, MAUI, AND MOLOKAI, chemical and biotechnology companies Monsanto, Syngenta, DuPont -Pioneer, Dow Chemical, and BASF have purchased prime agricultural land, taking advantage of Hawai`i's isolation and year-round growing season, in order to field test crops that have been genetically engineered (GE) to withstand greater applications of pesticides. As the report details, the onslaught of pesticide -promoting GE crops on the Hawaiian Islands raises three main areas of concern: the impacts of pesticide exposure on public health, the threat to native biodiversity, and food inde- pendence for the people of Hawaii. Our in-depth analysis of pesticide risks and impacts to the communities and environment of Hawaii revealed the following findings. SEED INDUSTRY FOOTPRINT IN HAWAII ❖ Since 1987 Hawaii has hosted more cumulative field trials (3,243) than any other state. In 2014 alone, 178 different GE field tests were conducted on over 1,381 sites in Hawaii (vs. only 175 sites in California). •:• Due to Hawai`i's small size, it has a much higher density of field tests than other states. As a result, more people in Hawaii live in closer proximity to field test sites than residents of any other state and run a higher risk of experiencing pesticide drift. The seed industry's footprint (24,700 acres) is 72% of the total area planted to crops other than sugarcane or pineapple (34,400 acres). ❖ The majority (91%) of the plants being tested are corn and soy—not niche crops such as papaya or banana. •: Herbicide -resistance was the most frequently tested trait in GE crop field tests in Hawaii over the past five years. This means that plants genetically engineered in Hawaii, by and large, are engineered to resist ever greater application of herbicides. ❖ Despite claims that the seed industry is a pillar of Hawai`i's economy, it only employed 1,397 workers in 2012, representing just 0.23% of total Hawaii jobs. PESTICIDE USE DuPont -Pioneer applied 90 different pesticide formulations containing 63 different active ingredients on Kauai from 2007 to 2012. The company sprayed on two-thirds (65%) of the days over this period and made from 8.3 to 16 applications per application day on average. •,• The third -most frequently applied class of pesticides is also among the most toxic: the organophosphate insecticide chlorpyrifos was sprayed an average of 91 days each year. •:• Restricted Use Pesticides (RUP) sales data for Kauai show that 22 RUPs containing 18 active ingredi- ents were applied in agriculture from 2010 to 2012. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 3 SUMMARY OF KEY FINDINGS ❖ 81% of RUP active ingredients by weight were applied to corn and 19% to coffee, with negligible amounts used on ornamentals, soybeans, sugarcane, tomatoes, and turf. PESTICIDE EXPOSURE RAISES SERIOUS HEALTH CONCERNS ❖ In general farmers, farmworkers, pregnant women, and children are at greatest risk: farmers are more highly exposed than the general population; and children are more susceptible to the harmful effects of pesticides than adults. ❖ The American Academy of Pediatrics recently published a major report entitled "Pesticide Exposure in Children" that reviewed 195 medical studies; their chief concerns were that pesticides are linked to child- hood cancers, neurobehavioral and cognitive deficits, adverse birth outcomes, and asthma. ,eIn adult populations, pesticide exposure has been linked to Non -Hodgkin's lymphoma, bladder and colon cancers, Parkinson's disease, depression, and disrupting our hormonal or endocrine systems. REGULATION NEEDED TO ADDRESS PUBLIC HEALTH RISKS We would all like to believe that the Environmental Protection Agency (EPA) protects us from pesticide harms, but this is often not the case. ❖ EPA requires safety testing only on the pesticide product's active ingredient, even though "inert ingredients" in pesticide formulations can be toxic in their own right, or increase the active ingredient's toxicity. ❖ In a failed attempt to better protect human health and the environment from pesticide drift, EPA proposed improved pesticide labeling in 2001, but has yet to finalize and enact the policy. ❖ EPA began to phase-out residential use of the toxic insecticide chlorpyrifos in 2000, specifically to protect children.Yet, rural children remain at risk, as ambient air levels of chlorpyrifos have been found to exceed health standards in agricultural areas. ❖ As of 2014, at least nine states had established no -spray buffer zones around sensitive areas such as schools, hospitals, and public parks, and while eleven states have established notification requirements for pesticide applications near schools. These policy actions evince growing awareness of the serious health threats posed by pesticide drift. ❖ Residents of three Hawaii counties have demanded that their local governments take action, under the counties' authority to regulate agriculture, ensure the welfare of its residents, and fulfill its duty to protect public resources. Despite making miniscule contributions to employment and the economy, Hawai`i's pesticide/seed industry occupies significant prime farmland, even as Hawaii supplies ever less of its food needs. GE seed corn exper- imentation and production involves heavy, frequent, year-round use of toxic agrochemicals. Pesticide drift threatens both public health and Hawai`i's incredible biodiversity. Hawai`i's state officials must join this growing movement and protect citizens from the irresponsible practices of agrochemical -seed firms by enacting sensible, prudent restrictions. In the longer term, the state's agricultural policy must be re -directed from supporting continued expansion of GE seed corn operations towards increasing sustainable local food production, the only realistic means to reverse Hawai`i's steadily declining food security. 4 1 HAWAI'I CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAPI'S HEALTH & ENVIRONMENT AT RISK PART ONE: PESTICIDES & GE SEEDS IN HAWAII INTRODUCTION N NOVEMBER 2013, thousands of people took to the streets of Kauai in sup- port of a proposed ordinance that would require chemical -seed companies to disclose the amount, location, and frequency of the pesticides they spray, as well as observe modest no -spray buffer -zones around sensitive areas including homes, schools, hospitals, and waterways. That same year, on Hawaii Island, the County Council passed Ordinance 13-121, providing farmers and residents of Hawaii, their property, and the environment important protections from the impacts of genetically engineered (GE) crops and associated pesticide drift, while also banning the planting and outdoor testing of new GE crops. In 2014, the county of Maui passed a temporary moratorium on GE crop operations pending a company -funded environmental and public health impact assessment. These historic actions are the work of a powerful and growing community -driven movement to protect citizens, especially our children, from the irresponsible practices of the multinational chemi- cal -seed companies that operate across the state of Hawaii. Despite these policy and electoral victories, some policy -makers are still confused as to why so many residents in our state would demand greater regulation of the GE In November 2013, thousands of people took to the streets of Kauai in support of a proposed ordinance that would require chemical -seed compa- nies to disclose the amount, location, and frequency of the pesti- cides they spray, as well as observe modest no -spray buffer -zones around sensitive areas including homes, schools, hospitals, and waterways. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'1'S HEALTH & ENVIRONMENT AT RISK I 5 PART ONE PESTICIDES AND GE SEEDS IN HAWAI I The State of Hawaii actively promoted expansion of the seed industry onto land abandoned by the pineapple and sugar industries. For instance. the Agribusiness Development Corpora- tion has helped the agrochemical multi- nationals gain control of former sugarcane lands on Kauai As the world's seed firms were acquired by agrochemical companies in the 1980s and 1990s, there was a rapid transition of Hawai`i's seed industry from conventional to genetically engineered seeds. Today, five of the Big Six pesticide -seed conglomerates' grow primarily GE seed corn on Kauai, Oahu, Maui, and Molokai, much of it engineered for resistance to herbicides.' The State of Hawaii actively promoted expansion of the seed industry onto land abandoned by the pineapple and sugar industries. For instance, the Agribusiness Development Corporation, created in 1994 as an agency of the Hawaii Department of Agriculture, has helped the agrochemical multinationals gain control of former sugarcane lands on Kauai (Eng 2012). This raises an important question. Has the state's promotion of the seed crop industry been good for Hawai`i's agriculture and economy? Or has it foreclosed other options that would have provided more benefits? Below, we explore these questions with respect to employment, economic contri- bution, land use, and food security. Employment and Economic Contribution Agricultural employment in Hawaii has declined by 32% since 1990, and today comprises only 1.06% of Hawai`i's jobs, 27% less than the national average.The seed industry employs just 1,397 workers, or 0.23% of Hawai`i's work force, which comes to just one of every 435 jobs (Loudat and Kasturi 2013, HDBEDT 2013). Nearly half (43%) of these positions are part-time and so presumably provide too little income to support a family (Loudat and Kasturi 2009). What about economic impact? There is increasing emphasis on the seed industry's rapid growth in "value" (Loudat and Kasturi 2009, 2013), yet this increasing value merely reflects the astro- nomical rise in GE seed prices these firms are charging U.S. farmers (Hubbard 2009), which is certainly no cause for celebration. And despite its growth, the Hawaii seed industry's share of the state's overall gross domestic product (GDP) is estimated at just 0.18% (HDBEDT 2015). Land Use and Food Security The seed industry arrogates rich farmland that would generate more employment, contribute more to the economy, and increase Hawai`i's food security if it were instead devoted to local food production. In fact, the area planted to seed crops has grown ten -fold since 1982, while land growing vegetables and fruits (excluding pineapples) has declined more than 50% since the late 1990s (Figure 1). As a result, Hawaii grows only one-third, and imports two-thirds, of the fresh produce consumed 8 1 HAWAPI CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART ONE PESTICIDES AND GE SEEDS IN HAWAII on the Islands. That a tropical paradise like Hawaii should be so dependent on imported fruit must be counted a major failure of state agricultural policy. And the situation is getting worse rather than better: in fact, the locally produced share of the Hawaiian market in fresh fruit fell by nearly half between 1990 and 2008, from 57% to 32% (Figure 2). About 85% of the land occupied by the Big Five pesticide -seed firms is leased. The lessors—large landowners and the State itself—are thus actively ceding valuable farmland to pesticide -intensive seed crop operations that make zero contribution to Hawai`i's food security, and only miniscule contribu- tions to employment and the economy. Missed Opportunities According to University of Hawaii agronomist Hector Valenzuela and Molokai activistWalter Ritte, the State and the University of Hawaii failed to follow through on promises to foster small-scale, diversified agricul- ture on former plantation lands in the 1990s (Mitra 2014). Novice farmers received little or no training and support. Instead, then -governor Ben Cayetano encouraged further expansion of the seed industry. What opportunities has Hawaii missed with these misplaced priorities? It is estimated that replacing all imports of beef, pork, eggs, fresh milk, fresh fruits, and vegetables with local production would create 14,629 jobs, over 10 times the number employed by the seed industry, and generate $303 million in earnings and $39 million in state taxes. A more modest goal of replacing just 10% of the food currently imported into the state would keep $313 million now spent v a N C C 7 0 Figure 1: Area Planted to Vegetables, Fruits (excl. Pineapples), and Seed Crops CO OOD ODm 00 W pa) M M comm m m ooi0000O000000O 9-1 5D 5) 5192 Of mmOf 21 m m OI O ON 0 0 0 0 0 0 0 0C14 NNNNNNNN �N Vegetables & Melons Fruits (excl. pineapples) Seed Crops (footprint) -- Seed Crops (harvested) Sources: Hawaii Agricultural Statistics (HASSa various years). Figure 2: Share of Fresh Fruit and Vegetable Markets Supplied by Hawaii Produce: 1990-2008 50 v 40 a s `m 30 E 2 a 20 10 0 1990 1995 2000 2005 2008 Fruits (excl. pineapple) *Vegetables Sources: Hawaii Agricultural Statistics (HASSb various years). overseas in the local economy. This would generate $188 million in sales, $37 million in earnings, $6 million in state taxes, and over 2,300 agricultural jobs, 65% more than the seed industry employs (Leung and Loke 2008, Hawaii Food Security 2012).These projections show clearly that increasing Hawai`i's food security is not only the right thing to do, but also makes economic sense. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 9 PART ONE PESTICIDES AND GE SEEDS IN HAWAI'I Hawaii is ground zero for experimentation with genetically engineered crops. The state has had more outdoor field releases of GE crops than any other state in the nation. Because Hawaii is much smaller than Midwestern states where GE crops are also frequently tested It has a much higher density of field tests. GENETICALLY ENGINEERED CROPS IN HAWAII Hawaii is ground zero for experimentation with genetically engineered crops. The state has had more outdoor field releases of GE crops than any other state in the nation (ISB Locations 2015). Because Hawaii is much smaller than Midwestern states where GE crops are also frequently tested, it has a much higher density of field tests. For instance, Hawaii has had 9.2 times more GE crop field releases per unit land area than Illinois, suggesting that more people in Hawaii live in closer proximity to field test sites than people in other states. Field releases of experimental GE crops are carried out under perfunctory permits issued by the United States Department of Agriculture's (USDA) Animal and Health WHAT IS A GENETICALLY ENGINEERED CROP (A.K.A. GMOP Genetic engineering involves the splicing of foreign genes, most derived from bacteria, into plants to generate new "traits." Virtually all GE crops grown commercially today have only one or both of two traits: herbicide -resistance' (HR) and/or insect - resistance (IR). Insect -resistant GE crops generate up to 7 insecticidal toxins in all their tissues. HR crops survive direct application of certain herbicides that would otherwise kill them, and lead to sharply increased herbicide use. HR traits are roughly twice as common as IR traits in the world's GE crops. 10 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART ONE PESTICIDES AND GE SEEDS IN HAWAII Inspection Service (APHIS).While USDA once carried out environmental assessments under the National Environmental Policy Act (NEPA) prior to issuing permits, this is rarely done today. In fact, the last full environmental assessment of a GE crop field release in Hawaii was conducted in 1994 (ISB EA 2015). The GE crops grown in Hawaii mirror those grown on the mainland. GE corn and soybeans dominate mainland fields, and comprise 91% of field releases in Hawaii, with corn tested nearly three times more fre- quently than soybeans (Figure 3). Herbicide -resistance is the trait that characterizes the most widely grown type of mainland GE crop, and it is also the most commonly tested type in Hawaii. Over two-thirds (689/6) of GE field releases over the past five years, and 82% over the past two years, involved herbicide - resistant crops (ISB Release 2010-2014).4 Despite rhetoric about nutritional enhancement and disease resistance, the pesticide -seed firms have conducted extremely few field trials of such GE crops, and there are hardly any such GE crops grown commercially (Figure 4). The Big Five pesticide -seed firms conducted 97% of GE field tests in Hawaii over the past five years, while public sector institutions were responsible for only 1% (ISB Release 2010-2014). The dominance of pesti- cide firms explains why herbicide -resistance is the most frequently tested trait in GE crop development. Because these firms are the major producers of her- bicides, and genetically engineered crops with HR traits dramatically increase herbicide use, these com- panies profit twice: first from the sale of expensive GE seeds, and then again from the vastly increased sales of the herbicide(s) used in conjunction with them. Herbicide -resistant corn, soybeans, and cotton alone Figure 3: GE Crop Field Tests in Hawaii: 2010-2014 600 500 400 v a p 300 v n Z) 200 Z 100 0 67% 0 Corn Soybean 0 Tobacco 0 Wheat 0 Rice O Other 0 Sorghum Source: ISB Release (2010-2014). Figure 4: GE Crop Field Trial Permits for Selected Traits in Hawaii: 2010-2014 Herbicide Resistance Disease Resistance Nutritional Quality Source: ISB Release (2010-2014). Nutritional quality refers to permits for GE crop field Vials involving the phenotype (trait) "nutritional quality improved." Disease resistance comprises three distinct trait categories: fun- gal resistance, virus resistance, and bacterial resistance. have increased overall herbicide use by a massive 527 million lbs. in the 16 years from 1996 to 2011 (Benbrook 2012).The USDA confirms that herbicide use has more than doubled on soybeans over same the period, when GE soybeans became dominant (USDA NASS 2014). Most of this additional herbi- cide is glyphosate, the active ingredient in Monsanto's Roundup, and is applied to the company's GE Roundup Ready crops. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 11 PART ONE PESTICIDES AND GE SEEDS IN HAWAII Hawaii is a major test ground for the pesticide companies' short-sighted response to these resistant weeds: namely, "next - generation" GE crops resistant to a host of This massive use of glyphosate has triggered a raging epidemic of glyphosate -resistant weeds, just as overused antibiotics breed resistant bacteria. Hawaii is a major test ground for the pesticide companies' short- sighted response to these resistant weeds: namely, "next -generation" GE crops resist- ant to a host of toxic herbicides that will still kill them, at least for a time (Kilman 2010). As noted above, 82% of GE field releases in toxic herbicides that Hawaii over the past two years have involved crops resistant to one or more herbi- will still kill them, at cide(s). Because 63% of Hawaii permits had herbicide -resistance traits hidden as least for a time. "confidential business information" (CBI),5 GE crops resistant to unidentified chemicals are also being tested. The major "next -generation" HR crops are resistant to 2,4-D (Dow Chemical) and dicamba (Monsanto), and will come stacked with resistance to glyphosate as well (Mortensen et al. 2012). USDA has issued multiple permits allowing field testing of corn and soybeans resistant to 2,4-D and/or dicamba in Hawaii (ISB Release 2010-2014). Widespread adoption of these HR crops is expected to boost agricultural use of 2,4-D by three- to seven -fold (CFS 2014a); and that of dicamba by 11 -fold (CFS 2014b). These crops will generate still more intractable weeds resistant to multiple herbicides, driving herbicide use to new heights, both on Hawai`i's test fields and on the mainland, putting agriculture in a "crisis situation" (Keim 2014). However, intensive use of herbicides on herbicide -resistant GE crops is just one com- ponent of the chemical onslaught involved in growing GE seed crops in Hawaii. PESTICIDE AND FERTILIZER USE IN GE SEED CORN PRODUCTION The vast majority of Hawai`i's seed crops are GE corn, as indicated by the following two facts: seed corn comprised 95.6% of the "value" of the state's seed crop industry in 2011 (Loudat and Kasturi 2013); and 93% of U.S. corn is genetically engineered. GE field corn grown on the mainland involves intensive use of chemicals: half of the herbicide and nearly half of the nitrogen and phosphorous fertilizer applied in all of U.S. agriculture is used on corn (USDA ERS 2013, 2014). Growing seed corn is still more chemical -intensive because the inbred varieties grown for breeding purposes are less vigorous and more vulnerable to pests and disease than the more robust hybrids that mainland farmers grow (Thomison undated). To compensate for these vulnerabilities, seed corn growers make heavier applications of fertilizer and pesticides (Ibid, Rinehold 2011). Hawaii corn breeder James L. Brewbaker describes the chem- ical -intensive practices employed by the seed corn firms. Fertilizer is applied heavily to compensate for Hawai`i's soils, which are not well-suited to corn. This creates 12 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART ONE: PESTICIDES AND GE SEEDS IN HAWAI I "[t]he potential for leached nitrate to pollute groundwater .... a serious environmen- tal concern" (Brewbaker 2003). Pesticides are also used intensively because the temperate varieties grown by the pesticide companies have no resistance to local pests and diseases. Dr. Brewbaker, famous for breeding pest- and disease -resistant Hawaii sweet corn varieties (see inset), is diametrically opposed to the seed industry in this respect: "There is no thought of trying to grow such valuable but unadapted germplasm pesticide -free! "' The" [u]nique pesticide regimes ... imposed by the seed industry" on Hawaii kill off beneficial insect predators that would otherwise control the pests (Brewbaker 2003, p. 69). Corn seeds are treated with pesticides; insecticides are applied to the soil during planting; and as the corn grows, insecticides and fungicides are applied every 5 to 7 days. BREEDING FOR RESISTANCE ... AND FOOD It is ironic that Hawaii, a leading center of pesticide -intensive, GE seed corn production, is at the same time the breeding ground for the world's leading "pesticide-free"5 conventional corn. Dr. James Brewbaker, known in Hawaii as the King of Corn, has bred a multitude of sweet corn varieties with excellent resistance to diseases and insect pests. These varieties are credited with saving HawaiTs sweet corn industry, and are also widely grown in Thailand, Australia, and many other countries (Salkever 2003). The University of Hawaii has developed field corn varieties with similarly broad- spectrum resistance. The key to Dr. Brewbaker's success is breeding without insecticides and fungicides, the precise opposite of pesticide company practice: "Using no pesticides, a continuing evolution occurred between diseases, pests, and HawaiTs home-bred corn. Today, Waimanalo-bred corns effectively can be grown with- out pesticides, having high levels of resistance to a host of diseases, pests, and stresses peculiar to the Hawaiian Islands" (Brewbaker 2003, p. 4). University of Hawaii breeder James C. Gilbert has employed similar techniques to breed resistant tropical varieties of tomatoes, eggplant, edamame soybeans, and other crops (Brewbaker 2010), and breeding without pesticides is known to be an effective means to develop pest- and disease - resistant strains of most crops (e.g. see Robinson 1996). By slashing insecticide and fungicide use, such crops would be cheaper to produce, which in turn would help make Hawai'i produce more cost -competitive with offshore production. Every acre of pesticide -intensive seed corn replaced by a resistant food crop would thus have multiple benefits—reducing the human health and environ- mental impacts of pesticides while increasing local food production. The work of Dr. Brewbaker and others shows that this is not only a desirable path, but also a feasible one, if only HawaiTs gov- ernment and large landowners would commit to plant breeding in the public interest, provide proper financial and technical support to aspiring farmers, and withdraw subsidies and leases to the agrochemical -seed industry. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 13 — 120 v T 100 a a e0 T V w 60 LL 40 0 a 20 a PART ONE PESTICIDES AND GE SEEDS IN HAWAI I Figure 5: DuPont -Pioneer Pesticide Use on Kauai: 2007-2012 These authoritative accounts of intensive pesticide use associated with GE seed corn production in Hawaii are borne out by hard numbers. Records obtained from DuPont -Pioneer in a lawsuit show that this single company applied 90 different pesticide formulations containing 63 different active ingredients' on Kauai from 2007 to 2012 (Jervis and Smith 2013). Consis- tent with Dr. Brewbaker's description above, these pesticides are used quite frequently. The company sprayed on two-thirds (65%) of the days over this six - ,P a ra`e voce Hca\ \be coF \J,c �a'-e �a`e \J tea .r o ati&0 year period; and made from 8.3 to 16 applications per co ear yQ \ac o mac o o a a 1 0 coQcoyQ Q��acoQroG���� Gto�rotoaoca`�a�F '�io Gam Ga�� 5�N11C �� �� application day, on average, in various years of this (' period (Jervis and Smith 2013). The third -most fre- quently applied class is also among the most toxic: Source: Jervis and Smith (2013). Chart based on data released by DuPont - Pioneer regarding its pesticide use practices on its seed corn and GE crop organophosphate insecticides SUCK as chlorpyrifos test fields near the town of Waimea, Kauai. See Table 2 below for key. (discussed below) , which were sprayed on average 91 days each year (see Figure 5 and Table 2). If one con- siders the additional pesticide use by Dow Chemical, Syngenta, and BASF, there are likely 30 or more spray operations most days of the year on Kauai. Even if one accounts for the fact that applications are made to only portions of the companies' overall seed fields, this represents extremely intensive pesticide use. TABLE 2: KEY TO DUPONT-PIONEER PESTICIDES USED ON KAUAI PESTICIDE CLASS PESTICIDE TYPE EXAMPLES OF ACTIVE INGREDIENTS Organophosphorous Herbicide Glyphosate, glufosinate Pyrethroid Insecticide Permethrin, zeta-cypermethrin Organophosphate Insecticide Chlorpyrifos Macrocyclic lactone Insecticide Avermectin Microbiological Insecticide Bacillus thuringiensis Chloroacetanilide Herbicide S-metolachlor, alachlor Quaternary ammonium Herbicide Paraquat dichloride Strobilurin Fungicide Azoxystrobin Carbamate Insecticide Methomyl Sulfonylurea Herbicide Chlorimuron Triazine Herbicide Atrazine Nicotinoid Insecticide Imidacloprid Conazole Fungicide Propiconazole 14 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART ONE' PESTICIDES AND GE SEEDS IN HAWAI'I The only other available data on pesticide use on Kauai applies only to "restricted use pesticides" (RUPs), an Environmental Protection Agency (EPA) designation for pesticides whose "toxicity exceeds one or more ... specific hazard criteria.."8 RUP sales data for Kauai show that 22 RUPs representing 18 active ingredients were applied in agriculture from 2010 to 2012. Assuming that sales are roughly equivalent to usage, an average of 20,801 lbs. of agricultural RUPs (weight of active ingredients only) were applied annually over this period (Figure 6). Eighty-one percent (819/6) of RUP active ingredients by weight were applied to corn, 19% to coffee, with neg- ligible amounts used on ornamentals, soybeans, sugarcane, tomatoes, and turf. Major users of agricultural RUPs were Dow Chemical (and its subsidiary Agrigenetics), Syngenta, DuPont -Pioneer, BASF, and Kauai Coffee Company. Total pesticide use is likely four times greater, or over 80,000 lbs. annually. This is based on the fact that DuPont -Pioneer applies over four times as many pesticide products (90) as RUP products applied by all major RUP users (22). All other things being equal, total pesticide use would be 90/22 or 4 times greater than RUP use. Estimation is our only recourse in the absence of Kauai Ordinance 960, which would have required all major RUP users to report their use of all pesticides, not just RUPs. Because of Kauai citizens' demand for more transparency concerning pesticide use associated with GE seed corn operations, some additional data have become available since December 2013. After the mayor of Kauai vetoed Bill 2491 (subsequently passed as Ordinance 960), a program was brokered where the five largest users of RUPs (Dow Chemical, DuPont -Pioneer, Syngenta, BASF, and Kauai Coffee Com- pany) now voluntarily disclose their RUP use in Kauai to the Hawaii Department. Growing seed corn is still more chemical - intensive, because the inbred varieties grown for breeding purposes are less vigorous and more vulnerable to pests and disease than the more robust hybrids that mainland farmers grow. To compensate for these vulnerabilities, seed corn growers make heavier applications of fertilizer and pesticides. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK I 1s PART ONE PESTICIDES AND GE SEEDS IN HAWAII Figure 6: Average Annual Sales of Restricted Use Pesticides on Kauai: 2010-2012 (lbs. a.i.) 'Iexc \o� be 05 �o� ay ce 0 oc 'I of cr of i. o'c ie of �o Q< :e a Qa�a co\� t1K r�o�Q� Pa e`er ear �2yo� `ia� \Qa�a Fe 5� Source: Based on "Restricted Use Pesticides Sold on Kauai: 2010-2012,"a spreadsheet obtained from Kauai County Council member Gary Hooser. RUPs converted to pounds active ingredient based on EPA -approved labels for the respective pesticides. "Synthetic pyrethroids" are restricted use insecticides that include permethrin, tefluthrin, esfenvalerate, lambda- cyhalothrin, zeta-cypermethrin, beta-cyfluthrin, and bifenthrin. Because some pesticides are much more potent than others (applied at much lower rates), lesser use does not necessarily mean less concern for human health or environmental impacts. For instance, methomyl is a carbamate insecti- cide with high acute toxicity to humans. Figure 7: Pounds of Restricted Use Pesticides (a.i.) Applied on Kauai by Month: 2014 Jan Feb Mar Apr May Jun Herbicides % Annual of Agriculture, who then release it to the public under the Orwellian name of "Kaua`i Good Neighbor Pro- gram."This program provides the only data on use (vs. sales) of RUPs in the state, although specifics on loca- tions where the pesticides are applied are not provided. The data discussed below are for the 12 months of 2014. We first compare the use intensity of the ten restricted use insecticides (RUIs) applied to Kauai seed corn to that of the same RUIs on mainland corn (USDA NASS 2011). When one considers both the propor- tion of acres treated and the amounts applied, Kauai seed cornfields receive 17 times more RUIs than main- land corn: 0.188 versus 0.011 lbs. /acre/year. While 0.188 lb./acre may not sound like much, one must consider how potent some of these RUIs are. For instance, beta-cyfluthrin and lambda-cyhalothrin are applied at the vanishingly low rates of 0.01 to 0.02 pound (about 1 to 2 teaspoons) of active ingredient per acre. According to their labels, these insecticides may be fatal if swallowed; are harmful when inhaled or absorbed through the skin; and are also extremely toxic to aquatic organisms and bees. The nerve toxin chlorpyrifos comprises two-thirds of RUI use. Health and environmental impacts of PUPS and other pesti- cides are discussed further below. Figure 7 shows that PUPS are sprayed throughout the year, meaning that there are many more opportunities for harmful drift episodes to occur than in the Mid- west, where spraying on corn is confined primarily to narrow windows in the spring and early summer. In general, RU herbicides are applied more heavily in the spring and especially in the fall. RU insecticides are applied more consistently throughout the year, though with a very strong spike in the winter months Jul Aug Sep Oct Nov Dec (December to February). It is likely no accident that Insecticides % Annual two of the higher -profile pesticide drift poisoning Source: Kauai Good Neighbor Program PUP data for 2014. episodes on Kauai ( iscusse e ow) occurre in November (Gregg 2006) and January (Leone 2008), when spraying of RU herbicides and insecticides, respectively, were likely near peak levels based on these 2014 data. 16 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE, HAWAI'I'S HEALTH & ENVIRONMENT AT RISK O PART TWO: IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT KL:PORTED HEALTH HARMS FROM PESTICIDE USE IN HAWAII Lessons from History AWAITS PLANTATION HISTORY has given its citizens ample exposure to toxic pesticides, and more than enough reason to doubt industry and government assurances of safety. EPA shut down drinking water wells in the Oahu town of Kunia in 1980, and later designated the area a Superfund site, due to hazardous levels of several pesticides used in pineapple pro- duction.These included a Dow Chemical nematicide (DBCP) infamous for causing sterility or impaired fertility in tens of thousands of farmworkers around the world (Gonzalez and Loewenberg 2003). In 1982, milk on Oahu was found to be con- taminated with hazardous levels of the pesticide heptachlor,' and elevated levels were also found in human breast milk (Smith 1982). These toxic pesticides, which have also been linked to breast cancer (Allen et al.1997), continued to be used in Hawaii pineapple production 5-6 years after EPA had otherwise banned them. The industrial food system externalizes much of its true costs by passing them on to society and the environment. These costs stem from the systems reliance on temporary chemical "fixes." and include adverse public health impacts, contamination of ground and surface water, soil degradation and erosion, and biodiversity loss. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 17 PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT Star Advisor—September 18, 2014 Pesticide Odor Closes Big Isle Schools, Sends 50 to Hospitals HAWAII NEWS NOW -2008 School Samples Test Positive for Pesticide 1\PI',1, HAWAI6I NEWS -APRIL 13, 2006 Pesticide Forces School Evacuation These episodes teach important lessons. First, pesti- cides initially approved as "safe" are found to be hazardous only after years of use and thousands are harmed. Second, powerful agricultural interests often succeed in keeping hazardous pesticides on the mar- ket even after their toxicity is well-understood.Third, Hawaii state officials have a history of covering up pesticide contamination and denying clear health risks to citizens in order to protect agricultural interests (e.g. heptachlor contamination, see Smith 1982). These lessons are still relevant today because haz- ardous pesticides continue to be applied today on the GE corn fields that have largely replaced the planta- tions. And these operations are run by some of the very firms that produced the plantation -era pesticides and long assured us of their supposed safety, for instance Dow Chemical. While the crops and chem- ical names have changed, Hawaii residents continue to be threatened by pesticides—not only in the water, but in the very air we breathe. At least three similar episodes have been reported on Oahu. In 2007,15 students were sickened by pesticide drift at Kahuku Intermediate and High Schools, forcing closure of the school for three days, while other students reported ill effects from the use of the insecticide malathion at St. Joseph School in Waipahu in 2008 (Hillyer 2008, Leone 2008). In 2014,31 students and staff at Kahalu`u Elementary School experi- enced nausea, burning eyes, shortness of breath, dizziness, sore throat, and coughing, and 26 were evacuated to and treated at nearby hospitals, due to a strong chemical odor that the Fire Department linked to reports of pesticide spraying in the area 18 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK Pesticide Drift in Hawaii Many pesticide Communities in Hawaii are rightly concerned about pesticide drift that occurs from drift incidents go open-air GE seed corn operations. Teachers and schoolchildren in Waimea on Kauai became sick on at least three separate occasions following chemical applications to a unreported. Hawaii nearby seed corn plot (Leone 2008). In a 2008 episode, 60 children and at least two does not have a teachers experienced headaches, dizziness, nausea, and/or vomiting; 10 or more chil- "pesticide poisoning dren were treated at an emergency room; several were put on a nebulizer to relieve surveillance program " respiratory distress; and one was given an anti -vomiting medication intravenously. A of the sort established teacher who was also affected firmly rejected the explanation given by Hawaii offi- cials and Syngenta that "stinkweed" was the culprit, saying that she was familiar with in eleven other states. stinkweed's odor and that this was not the cause (Leone 2008, Hillyer 2008). At least three similar episodes have been reported on Oahu. In 2007,15 students were sickened by pesticide drift at Kahuku Intermediate and High Schools, forcing closure of the school for three days, while other students reported ill effects from the use of the insecticide malathion at St. Joseph School in Waipahu in 2008 (Hillyer 2008, Leone 2008). In 2014,31 students and staff at Kahalu`u Elementary School experi- enced nausea, burning eyes, shortness of breath, dizziness, sore throat, and coughing, and 26 were evacuated to and treated at nearby hospitals, due to a strong chemical odor that the Fire Department linked to reports of pesticide spraying in the area 18 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT (Kalani and Fujimori 2014). These symptoms are all commonly reported effects of exposure to pesticides (AAP 2012: Table 2). These media reports likely represent a small fraction of actual pesticide poisoning cases, for several reasons. Many pesticide drift incidents go unreported (EPA 2001). Hawaii does not have a "pesticide poisoning surveillance program" of the sort established in eleven other states (CDC 2014). And even when drift victims do seek medical atten- tion, many physicians lack the training to recognize the effects of pesticide poisoning, and so do not report it (CA PISP Fact Sheet, AAP 2012). Physicians concerned about pesticide drift in west Kauai encounter "almost daily reports of respiratory symptoms in patients that have no history of these respiratory illnesses...," and report that many do not recover despite healthy lifestyle changes or pharmacological interventions.They also report recurring nose bleeds in children and recurring dermatitis, among other symptoms (Kaua`i Physicians 2013).Waimea residents are frequently afflicted with "fugitive dust" blowing into their town, which is down- wind of a 1,000 -acre DuPont -Pioneer seed corn operation (see photo above) (Jervis and Smith 2013). Fine dust can penetrate the lungs and cause bronchitis (CCOHS 2012), and is still more harmful if the dust is laden with pesticides (USGS 2003). Evidence from other states also suggests that pesticide drift is a frequent occurrence. A study of pesticide exposure at schools in eight states from 1998 to 2002 identified 2,593 individuals who had experienced acute pesticide -related illnesses. Of the 406 cases for which more detailed information was available, nearly one third (31%) Physicians concerned about pesticide drift in west Kaua'i encounter "almost daily reports of respiratory symptoms in patients that have no history of these respiratory illnesses ...;' and report that many do not recover despite healthy lifestyle changes or pharmaco- logical interventions. HAWAI'I CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 19 PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT Kaua'i physicians and involved pesticide drift from farmland while the others involved pesticide use at the residents have noted school (Alarcon et al. 2005). a "cancer cluster" in Pesticides may also be a factor in still more serious health threats. Dr. James Raelson and Waimea -37 cases in a his colleague Dr. Chatkupt, practicing pediatricians in Kaua'i, have noted an unusually neighborhood of just high incidence of rare birth defects involving malformations of the heart in Kauai 800—which is said over the past seven years, at roughly ten times the national rate (Raelson 2013).They to be 10 times the note that Hawai'i has not had surveillance for birth defects since 2005, and have statewide cancer rate called for unbiased epidemiology studies by the U.S. Centers for Disease Control and HawaiTs Department of Health to better understand the causes. Kaua'i physicians and residents have also noted a "cancer cluster" in Waimea -37 cases in a neighbor- hood of just 800—which is said to be 10 times the statewide cancer rate. Although a one-page report by the Hawai'i Department of Health disputes the existence of a cancer cluster on Kaua'i, the author conceded that her analysis was inconclusive, and reportedly said: "If I lived there, it would concern me" (Skolnick 2013). These parcels of land (identified in pink) are known RUP users confirmed through Honolulu, Maui, and Kauai County Real Property Assessment Division websites. Schools are marked with red, green, and yellow flags with a half mile and one mile buffer zones identified by blue circles. Nursing homes are marked by orange stars with a half mile and one mile buffer zones identified by orange circles. Schools and residen- tial areas are in dangerous proximity to agrochemical operations. [GIs MAPS: ADRIAN RAMIREZ] 20 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 21 PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT In a 2008 episode. 60 children and at least two teachers experienced head- aches, dizziness, nausea, and/or vomiting; 10 or more children were treated at an emergency room: several were put on a nebulizer to relieve respiratory distress; and one was given an anti -vomiting medica- tion intravenously. HEALTH IMPACTS OF PESTICIDE EXPOSURE Pesticides have a long history of having negative, often unforeseen, impacts on human health. People are exposed to certain pesticides in their food and water; farmworkers take in pesticides via dermal contact and inhalation of spray. Pesticide drift represents an important additional exposure pathway (Goldman et al. 2009). In general, farmers, farmworkers, pregnant women, and children are at greatest risk: farmers are more highly exposed than the general population; and pregnant women and children are more susceptible to the harmful effects of pesticides than adults. Pesticides cause acute health problems such as nausea, dizziness, vomiting, headaches, abdominal pain, muscle aches, and skin or eye irritation (AAP 2012, Owens and Feldman 2004), and can also have long-term impacts, as discussed below. Farmers and Farmworkers at Risk CANCER: Cancer rates in the U.S. have nearly doubled since 1950, corresponding to the period of rapid growth in use of pesticides and other industrial chemicals (Clapp et al. 2006). Significant associations between agricultural chemical use and cancer deaths have been found in 1,497 rural U.S. counties (Steingraber 2010). National Cancer Institute scientists have found that famers in the U.S. and elsewhere suffer from higher rates of certain cancers—including leukemia, non-Hodgkin's lym- phoma, multiple myeloma, and brain cancer—than the general population, even though they have fewer cancers and are healthier overall (Blair and Zahm 1995). These findings drove considerable research into potential causes, particularly pesticide exposure. Non -Hodgkin's lymphoma (NHL) is a terrible cancer of the immune sys- tem that kills 30% of those who contract it. A large number of studies have associated 22 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAPI'S HEALTH & ENVIRONMENT AT RISK PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT NHL with exposure to chlorophenoxy herbicides like 2,4-D (Zahm et al. 1990, Cantor et al. 1992, Blair and Zahm 1995, Mills et al. 2005); dicamba herbicide (Can- tor et al. 1992, McDuffie et al. 2001); glyphosate (Hardell et al. 2002, De Roos et al. 2003, Schinasi and Leon 2014); and to organophosphate insecticides (reviewed in Schinasi and Leon 2014). In a landmark ruling, the World Health Organization's International Agency for Research on Can- cer recently determined glyphosate to be a probable human carcinogen (Guyton et al. 2015).This is the major organophospho- rous herbicide, the most frequently applied class on Kauai (Figure 5). These findings are especially concerning when one considers the intensive use of these toxic herbicides on GE crops resistant to them (see above), and the fact that they are prone to drift (AAPCO 1999, 2005). Exposure to imidazolinone herbicides has been strongly associated with bladder and colon cancer in the Agricultural Health Study (Koutros et al. 2009), and BASF has field-tested imidazolinone-resistant corn and soybeans in Hawaii. Exposure to the organophosphate insecticide chlorpyrifos has been linked to lung cancer (Lee et al. 2004), colorectal cancer (Lee et al. 2007), and non-Hodgkin's lymphoma (Schinasi and Leon 2014). PARKINSON'S DISEASE: Several major meta-analyses10 have demonstrated a strong association between pesticides and Parkinson's disease. For instance, Priyadarshi et al. (2000) assessed 19 studies published between 1989 and 1999, and found that the majority reported that pesticide exposure elevated the risk of Parkinson's disease. Brown et al. (2006) made similar findings, which were "strongest for exposure to herbicides and insecticides, and for long durations of exposure"A review by van den Mark et al. (2012) came to the same conclusions. Particular classes of pesticide impli- cated in Parkinson's disease include paraquat and rotenone (Tanner et al. 2011), chlorophenoxy herbicides (Brighina et al. 2008, Elbaz et al. 2009), and 2,4-D (Tanner et al. 2009). Paraquat is one of the most heavily used RUPs on Kauai (Figure 6). Besides the association with Parkinson's disease, it is also one of the most acutely toxic herbicides in use, and is banned in 32 countries, including the European Union and Switzerland, home of Syngenta, its major producer (Watts 2011). It is responsible for thousands of deaths, both accidental poisonings and suicides (Watts 2011). While ingestion of as little as a teaspoon of concentrate is fatal, paraquat is 1,000 -fold more toxic when inhaled due to its extreme toxicity to lung tissue (Ames et al. 1993). Kentucky agricultural extension agent Gordon Johnson reports that paraquat can drift for miles Qohnson People are exposed to certain pesticides in their food and water: farmworkers take in pesticides via dermal contact and inhalation of spray. Pesticide drift represents an important additional exposure pathway. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 23 PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT While exposure to 2008). Paraquat drift sickened dozens of people in a small California agricultural many pesticides causes community, inducing respiratory distress, nausea, and diarrhea, among other symp- acute neurological toms (Ames et al. 1993). symptoms. such as DEPRESSION: Several studies have also found a positive relationship between pes- headaches and ticide exposure and depression (reviewed in Bienkowski 2014, see also Beard et al. dizziness, a spate of 2014). Higher rates of clinically diagnosed depression were found in both farmers recent studies builds an with high cumulative exposure and those who reported pesticide poisoning (Beseler et al. 2008, Beseler and Stallones 2008).A study in France found nearly double the irrefutable case that rate of depression in agricultural workers exposed to herbicides, with greater risk long-term, low-level from longer-term exposure (Weisskopf et al. 2013). The troubling implication of exposure to organo- many of these studies is that acute poisoning episodes can have chronic, long-term phosphate insecticides consequences for mental health. In early life (particu- larly in utero) has ENDOCRINE DISRUPTION: Pesticides can also disrupt our hormonal or endocrine systems. Extremely low levels of atrazine, a restricted use herbicide applied heavily profoundly negative in Hawaii (Figure 6), have been shown to cause feminization of male frogs —a impacts on children's process described as chemical castration (Hayes et al. 2011). Because human hormonal neurological systems are similar to those of amphibians, these animal findings suggest that atrazine development. may be hazardous to human health as well. Atrazine is discussed further below. OUR KEIKI AT RISK It is well-established that the young are more susceptible to the harmful effects of pesticides than adults (National Research Council 1993, Roberts and Karr 2012). First, infants and children are more highly exposed to pesticides, because they con- sume more food and water on a body-weight basis, and have a higher breathing rate, than adults. Secondly, children have greater hand-to-mouth activity, increasing oppor- tunities for exposure to pesticide residues in dirt and dust. Finally, the immature, developing physiological systems of children are more susceptible to disease -causing disruption, particularly neurological impacts and cancer (NRDC 1997). Exposure of pregnant women to pesticides is particularly hazardous, since pesticides can be potent disruptors of fetal development, meaning our future generations will face a lifetime of impacts due to exposure in the womb. The American Academy of Pediatrics (AAP) recently published a major report enti- tled "Pesticide Exposure in Children" that comprehensively reviewed 195 medical studies on the subject (see Roberts and Karr 2012).They found that pesticide expo- sure was strongly linked to four types of disease: 1) Childhood cancers, especially leukemia and brain tumors; 2) Neurobehavioral and cognitive deficits, such as reduced IQ and attention deficit/hyperactivity disorder; 24 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAII S HEALTH & ENVIRONMENT AT RISK PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT 3) Adverse birth outcomes, including preterm birth, low birth weight, and congenital anomalies; and 4) Asthma. We briefly discuss each of these impacts below, with reference to the AAP's compre- hensive review. Childhood Cancers Five of six recent case -control studies found a statistically significant relationship between pesticide exposure and leukemia (Roberts and Karr 2012). Maternal expo- sure to pesticides between the periods of preconception through pregnancy was the primary risk factor. Maternal use of either herbicides or insecticides was associated with nearly double the risk of childhood leukemia (Infante -Rivard et al. 1999). A meta-analysis (Wigle et al. 2009) and a study of parents exposed to pesticides in Costa Rica (Monge et al. 2007) arrived at similar results. A high-quality study entitled "Parental Occupational Exposure to Pesticides and Childhood Brain Cancer, involving 321 cases, demonstrated that maternal exposure to insecticides before or during pregnancy was associated with a 90% greater risk of astrocytoma (a type of brain cancer) in the child, as well as a trend to higher risk in children of exposed fathers (van Wijngaarden et al. 2003). Neurobehavioral and Cognitive Deficits While exposure to many pesticides causes acute neurological symptoms, such as headaches and dizziness, a spate of recent studies builds an irrefutable case that long- term, low-level exposure to organophosphate insecticides (OPs) in early life Chlorpyrifos is the most heavily sprayed Restricted Use insecticide on Kauai, and DuPont -Pioneer alone sprays OPs on Kauai once every four days. Air sampling at Waimea School consis- tently detected chlorpyrifos. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 25 PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT Chlorpyrifos is the most heavily sprayed restricted use insecticide on Kauai. and DuPont -Pioneer alone sprays OPs on Kauai once every four days. Air sampling at Waimea School consistently detected chlorpyrifos (particularly in utero) has profoundly nega- tive impacts on children's neurological development. The National Institutes of Health and the EPA are sponsoring three large-scale studies into this subject, two in urban settings and one in a rural commu- nity (Roberts and Karr 2012).Women were enrolled during pregnancy, and their expo- sure to OPs carefully measured. Their children were tested for neurological devel- opment in the following years. At two to four years of age, higher prenatal OP exposure was associated with "significantly poorer mental development," "pervasive developmental disorder," and in one group "increased scores for attention- deficit/hyperactivity disorder" (Rauh et al. 2006, Eskenazi et al. 2007). At seven years of age, kids more highly exposed to OPs in the womb had lower IQ scores in all three groups (Rauh et al. 2011, Bouchard et al. 2011, Engel et al. 2011). Bouchard et al. (2010) similarly found increased rates of attention-deficit/hyperactivity disorder in eight to fifteen -year olds whose urine had higher levels of OP breakdown prod- ucts, a sign of greater exposure. These findings are even more concerning when one considers the intensive use of chlor- pyrifos in Hawaii's seed corn operations, coupled with its propensity to drift. Chlorpyrifos is the most heavily sprayed RU insecticide on Kauai (Figure 6), and DuPont -Pioneer alone sprays OPs on Kauai once every four days (Figure 5). Air monitoring in Cal- ifornia and Washington has found levels of chlorpyrifos exceeding health limits on several occasions (Goldman et al. 2009), and chlorpyrifos is one of the most frequently cited culprits in drift -related pesticide poisioning episodes in California (CA PISP 1992-2011). Air sampling at Waimea School consistently detected chlorpyrifos (Li et al. 2013). Based on these multiple lines of evidence, there is every reason to expect that chlorpyrifos drift is adversely affecting the mental health of Hawaii residents living near GE seed corn fields. Adverse Birth Outcomes Two studies in Minnesota have revealed a higher rate of birth defects in children fathered by male pesticide applicators in areas of the state where chlorophenoxy her- bicides (e.g. 2,4-D) and fungicides are most heavily apphed.These studies also found a seasonal effect, with children conceived in the spring, when herbicide use is heav- iest, exhibiting the highest birth defect rates (Garry et al. 1996, Garry et al. 2002). Six additional studies described by Roberts and Karr (2012) found higher risk ratios for birth defects in children of mothers exposed to pesticides, with three of them showing statistically significant effects. A study of expectant mothers carried out in New York demonstrated an association between exposure to chlorpyrifos and 26 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT reduced birth weight and length (Perera et al. 2003). Wolff et al. (2007) also found reduced birth weight in infants born to mothers exposed to OPs during pregnancy, but only in those children with a mutation that reduces their ability to detoxify OPs. Another study found that in utero exposure to OPs was associated with reduced gestation time (Eskenazi et al. 2004). Prenatal atrazine exposure has been associated with suppression of fetal growth (Cheerier et al. 2011), and exposure to chlorophenoxy herbicides and certain other classes of herbicide, such as triazines (e.g. atrazine), with increased risk of spon- taneous abortion (Arbuckle et al. 1999, 2001). All of these pesticides are heavily used in Hawaii seed corn operations. Asthma Asthma is estimated to affect 300 million people worldwide and cause a quarter of a million deaths each year (Strina et al. 2014). Asthma is characterized by intermittent breathing difficulty, including chest tightness, wheezing, and cough.There have been few studies of pesticides and asthma in children, but those conducted raise serious concerns. For instance, exposure to either herbicides or insecticides in the first year of life was strongly linked to a diagnosis of asthma before the age of five in a study carried out in southern California—an over four -fold higher risk from herbicide and more than two -fold greater risk from insecticide exposure (Salam et al. 2004). Studies of adults provide similar evidence. Farmers are at high risk of asthma and other respiratory diseases (Hoppin 2002), and exposure to organophosphate and car- bamate insecticides has been linked to asthma in Canadian farmers (Senthilselvan et al. 1992). Hoppin et al. (2002) found a higher incidence of wheezing in farmers exposed to the herbicides atrazine, alachlor, and paraquat, as well as the OP insecti- cides chlorpyrifos, parathion, and malathion. These findings take on added weight when one considers the testimony of Kauai physicians that Westside residents are very frequently afflicted with symptoms of respiratory distress. HEALTH HARMS SPECIFICALLY LINKED TO PESTICIDE DRIFT A growing body of research finds increased risk of disease in those living near pesti- cide -sprayed agricultural fields. Costello et al. (2009) have found that exposure to paraquat and maneb within 500 meters of the home increased the risk of Parkinson's disease by 75%, with those under 60 years of age at higher risk. Roberts et al. (2007) found that expectant mothers residing within 500 meters of fields sprayed with organochlorine insecticides during early pregnancy had a six -fold higher risk of bear - Expectant mothers residing within 500 meters of fields sprayed with organochlorine insecticides during early pregnancy had a six -fold higher risk of bearing children with autism spectrum disorder than mothers not living near such fields. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 27 PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT It is often assumed ing children with autism spectrum disorder than mothers not living near such fields. that people suffer no Shelton et al. (2014) found a 60% increased risk of autism spectrum disorder (ASD) in children of mothers who lived near fields sprayed with organophosphate insecticides permanent harm from at some point during their pregnancies, with much higher risk when exposure a single (acute) occurred in the second trimester of their pregnancies. Similarly increased risk—for pesticide exposure, both ASD and developmental delay—was found for children of mothers near fields but research is proving treated with pyrethroid insecticides just prior to conception or during their third this to be untrue. trimester. Proximity to carbamate -treated fields was also linked to higher risk of developmental delay. Most of the insecticides at issue in this California study are used on Kauai and likely on other islands as well: chlorpyrifos; the pyrethroids permethrin, lambda-cyhalothrin, cypermethrin, and esfenvalerate; and methomyl (Figures 5 & 6 and Table 2). ACUTE PESTICIDE EXPOSURE CAN CAUSE LASTING HARM All of the symptoms reported above in Hawai`is schoolchildren are among those typically caused by pesticide drift, which include headaches, dizziness, difficulty breathing, nausea, vomiting, weakness, chest pain, fatigue, rashes, and eye ailments (Owen and Feldman 2004, CA PISP 1992-2011). It is often assumed that people suffer no permanent harm from a single (acute) pesticide exposure, but research is proving this to be untrue. For instance, many studies have found increased rates of lasting depression (e.g. Stallones and Beseler 2002, Beseler and Stallones 2008), impaired cognitive functioning (Rosenstock et al.1991), and reduced neuromuscular control (Kofinan et al. 2006) in people exposed acutely to certain toxic pesticides. This means that children and adults exposed just a single time to a pesticide, even though they may appear to fully recover, in certain cases go on to develop chronic, long-term illnesses that may persist throughout their lives. ADDITIONAL EXPOSURE TO AGROCHEMICALS IN FOOD AND WATER Exposure to pesticides via drift must be considered together with other pathways, especially water and food. Both surface water (e.g. streams, rivers, lakes) and ground- water (e.g. source of well water) are regularly polluted with agrochemicals. As noted above, heavy nitrogen fertilizer use on corn can contaminate drinking water supplies with toxic nitrates (Brewbaker 2003, Charles 2015). The U.S. Geological Survey (LJSGS) monitors the nation's water bodies for pollutants. In the 1990s, USGS studies found one or more pesticides or their breakdown products in sampled streams more than 90% of year; and that the mean annual concentrations of one or more pesticides exceeded a human health benchmark in about 10% of the 83 agricultural streams that were sampled. Pesticide concentrations in groundwater (wells) also sometimes exceeded health standards (e.g. Gilhom et al. 2006). Atrazine is among the most com- monly detected pesticide contaminants in our streams and drinking water (Wu et al. 28 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAPI'S HEALTH & ENVIRONMENT AT RISK PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT 2010). Monitoring data reveal that an esti- mated 33 million Americans are exposed to atrazine in tap water (Duhigg 2008). Atrazine was detected in 80% of the 24 watersheds and streams recently tested by Hawaii health and agricultural officials (Grange 2014), and in 90% of base flow samples tested in an earlier investigation by USGS on Oahu (Anthony et al. 2004). Pesticide residues from the direct or indirect spraying of food crops is another major exposure pathway. Organically grown foods have substantially lower residue levels than conventionally grown foods (Baker et al. 2002). Lu et al. (2008) showed that breakdown products of organophosphate insecticides (OPs) practically disappeared in the urine of urban and suburban children after they were switched from a diet of conventional fresh fruit and vegetables to their organic counterparts. This shows that for (sub)urban children, diet is the major exposure pathway for OPs. Children exposed to OPs via spray drift as well as their diets will have higher cumulative expo- sure and thus a still greater risk of health impacts. As noted above, OPs have been found to cause serious neurobehavioral and cognitive deficits in infants and children. A recent Government Accountability Office (GAO) study found that the Food and Drug Administration (FDA) is testing an ever smaller proportion of produce for pes- ticide residues (GAO 2014). FDA tests too few samples to estimate either the frequency or magnitude of pesticide residue violations in the U.S. food supply. FDA does not test produce for 6 of the 25 most commonly used pesticides with set tol- erances," including glyphosate, 2,4-D, methyl bromide, and paraquat. The GAO report reveals that Americans cannot rely on our nation's food safety agency to protect us from excessive pesticide residues in the U.S. food supply. ENVIRONMENTAL IMPACTS OF AGROCHEMICAL USE IN HAWAII Beyond the considerable threat that RUPs pose to the health of Hawaii residents, these chemicals also threaten Hawai`i's unique and biodiverse environment, which is home to about 9,500 species found nowhere else on the planet (Evenhuis and Eldredge 2002).While Hawaii is considered a biodiversity hotspot, it has also been named the "endangered species capital of the world" (Scheuer and Clark 2001).The Islands represent just 0.2% of land area in the United States, and yet they are home to over one-third of the nation's federally endangered species (Holt 2001). Roughly 75% of documented species extinctions in the U.S. have occurred on Hawaii (Allison and Miller 2000), and 437 species on the islands are listed as either threatened or endangered (USFWS 2012). m Atrazine was detected z A in 80% of the 24 water - 0 sheds and streams m recently tested by Hawaii health and agricultural officials, and in 90% of base flow samples tested in an earlier investigation by USGS on O'ahu. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 29 PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT While Hawai'i is consideree a biodiversity hotspot, it has also been named the "endangered species capital of the world." The Islands represent just 0,2% of land area in the United States, and yet they are home to over one-third of the nation's federally endangered species. Below, we discuss the environmental harms associated with several classes of pesticide heavily used in Hawai`i's seed corn operations. Where available, we discuss studies and information specific to the Hawaii context. ATRAZINE As discussed above, atrazine is the most heavily used RUP on Kauai (Figure 6) and the most frequently detected pesticide contaminant in Hawai`i's surface waters.Atrazine is toxic to coral (Jones et al. 2003), and atrazine runoff has been pro- posed as one possible cause of coral reef decline on the north shore of Kauai (D'Angelo 2013). Atrazine is also extremely toxic to amphibians at low concentra- tions that are found in nature. For instance, male tadpoles exposed to atrazine concentrations as low as 0.1 part per billion (ppb) developed hermaphroditic char- acteristics (multiple male and female gonads); and exposure to as little as 1.0 ppb reduced larynx size, which could reduce fitness in the wild (Hayes et al. 2002). Low- dose exposure to atrazine consistently suppresses the immune systems of fish and amphibians, predisposing them to infection with pathogens and parasites (Rohr and McCoy 2010). Atrazine may also harm aquatic organisms indirectly by killing off vegetation and so degrading habitat (EPA 2006). C H LO R PY R I FOS is an organophosphate, and by far the most heavily applied restricted use insecticide on Kauai (Figure 6). Chlorpyrifos is very highly toxic to birds, aquatic invertebrates, freshwater fish, other estuarine and marine organisms, and bees (NPIC 2009). Like other pesticides, chlorpyrifos is washed out of the atmosphere in rainfall events to contaminate bodies of water. In 2001, the U.S. Geological Survey found chlorpyrifos in "toxic rainfall" and in rivers in California at levels exceeding the pro- posed state guidelines for protection of aquatic life in most samples (USGS 2003). 30 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT Chlorpyrifos is also a terrestrial threat. It has been shown to kill or injure substantial numbers of both adult and larval bees at lev- els that are found in the environment (Williamson et al. 2013). Chlorpyrifos is currently being reassessed together with other insecticides for their impacts on endangered species (USFWS 2014). SYNTHETIC PYRETHROIDS are a class of neurotoxic insecticides derived from an extract (pyrethrum) of the chrysanthemum, but they have been chemically altered to be both more potent and more persistent in the environment (BP Pyrethroids). At least seven are used in Hawai`i's seed corn operations: permethrin, tefluthrin, esfenvalerate, lambda-cyhalothrin, zeta-cyperme- thrin, beta-cyfluthrin, and bifenthrin. They form the second -most frequently used class of pesticide (Figure 5). Although generally less acutely toxic to human beings than organophosphate insecticides, several pyrethroids carry label statements warning of possible death upon ingestion and harm from inhalation. Permethrin, zeta-cypermethrin, and bifenthrin are possible human carcinogens (BP Pyrethroids). Infants are more susceptible to pyrethroids because they lack the ability to efficiently detoxify them. Pyrethroids also cause respiratory and dermal allergies in sensitive individuals (BP Pyrethroids). Pyrethroids are extremely toxic to fish, aquatic invertebrates, oysters, lobsters, and shrimp, which can be killed at levels rang- ing from just 2 parts per trillion to 1 part per billion (BP Pyrethroids, Weston and Lydy 2010). Pyrethroids are also extremely toxic to bees, which are killed not only by direct exposure to spray, but also by residues on blooming crops and weeds that have been previously sprayed.The U.S. EPA in its registration of permethrin acknowl- edges that it is "likely to reduce the numbers and possibly eliminate populations of beneficial insects" (EPA Permethrin 2009). N E O N I C OT I N 01 D S are a class of neuroactive insecticides that are often applied to seeds; they are absorbed by the growing seedling, making the plant itself toxic to insects. Pollinators such as bees can be exposed when collecting pollen or nectar. Nearly all corn seed in the U.S. is treated with neonicotinoids (Krupke et al. 2012). Massive bee kills have resulted upon exposure of bees to neonicotinoid-laden dust from seed corn at planting time (Krupke et al. 2012, Stokstad 2013). Bees exposed to sublethal levels of neonicotinoids experience problems with flying and navigation, reduced taste sensitivity, and slower learning of new tasks, which all impact foraging ability (Hopwood et al. 2012). Neonicotinoids also make honey bees more susceptible to parasites and pathogens, including the intestinal parasite, Nosema, that is one cause Chlorpyrifos is vee highly toxic to biro-, aquatic invertebrates, freshwater fish, of i ( ) estuarine and marire organisms, and bees. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 31 PART TWO IMPACTS ON HUMAN HEALTH + THE ENVIRONMENT Massive bee kills have resulted upon exposure of bees to neonicotinoid-laden dust from seed corn at planting time. Bees exposed to sublethal levels of neonicotinoids experience problems with flying and navigation, reduced taste sensitivity: and slower learning of new tasks, which all impact foraging ability of colony collapse disorder (Hopwood et al. 2012, Di Prisco et al. 2013). Nosema is one of the major causes of the dramatic loss of both domesticated and feral bees in Hawaii in recent years (Edwards -Hunt 2011). Neonicotinoids are frequently found in sur- face waters around the world, often at levels that exceed water quality guidelines (Mor- rissey et al. 2015). Imidacloprid, a leading neonicotinoid, is highly toxic to freshwater invertebrates. Ground beetles are killed or impaired when they consume slugs that have been contaminated with neonicoti- noids through ingestion of treated seedlings (Douglas et al. 2014). Birds may also be poisoned by neonicotinoid exposure.A single kernel of corn coated in neonicotinoids can kill a songbird (Mineau and Palmer 2013), and neonicotinoids also appear to harm birds by reducing populations of insects they feed on (Hallemann et al. 2014). Many birds are threatened by extinction, and 34 bird species, including many species of Hawaiian honeycreeper, are listed as endangered (USFWS 2015). Seed corn in Hawaii is treated with pesticides (Brewbaker 2003), and this almost certainly includes neonicotinoids; but since they are not RUPs, they are exempt from Kaua`i's voluntary RUP reporting system. Hawai`i's pilot program to monitor pesti- cide contamination of surface waters did not include testing for neonicotinoids. Testing for these compounds is absolutely necessary to make a realistic assessment of the environmental impacts of their use in Hawaii. IMPACTS OF MULTIPLE PESTICIDES Humans and other organisms are often exposed to numerous pesticides, which can have additive effects or interact in various ways that make them more toxic than exposure to one of them alone. Several studies have shown that organophosphate insecticides like chlorpyrifos are more toxic to aquatic invertebrates and frogs when low levels of atrazine are also present (Belden and Lydy 2000). Bumblebee colonies exposed to both a neonicotinoid and a pyrethroid suffered higher losses of worker bees than colonies exposed to either chemical alone (Gill et al. 2012). Synthetic pyrethroids are often formulated with a substance (piperonyl butoxide) that inhibits enzymes that would otherwise break down the pyrethroids, thus making them more toxic (BP Pyrethroids). Some fungicides likewise suppress detoxifying enzymes (Stok- stad 2013). The intensive and frequent use of many different pesticides in seed corn fields increases the opportunities for additive and synergistic interactions that poten- tiate their toxic effects on Hawai`i's wildlife. 32 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART THREE: TAKING CONTROL OF OUR FUTURE REGULATION DOES NOT PREVENT HARMS County Regulatory Initiatives Consistent with State Law OUNTIES HAVE AUTHORITY to regulate local impacts of agriculture, lack- ing protection from state and federal agencies, various counties in Hawaii have taken action to protect the health and welfare of their people and natural environment. Kauai County passed Ordinance 960 to require basic transparency via disclosure, and shelter from pesticide drift and spray through the impo- sition of buffer zones, among other measures. In response, the chemical corporations filed a lawsuit, alleging every claim of which they could conceive, rather than simply complying with the County's urgently -needed, reasonable, and limited ordinance. Hawaii County Ordinance 13-121 provides farmers and residents of Hawaii, their property, and the environment important protection from the impacts of genetically engineered crops, such as transgenic contamination and associated pesticide drift. However, Hawaii County was also sued by chemical corporations, and Ordinance 13-121 was similarly determined as invalid, under state law, even though no Hawaii Counties have author- ity to regulate local impacts of agriculture, lacking protection frorn state and federal agencies, various counties in Hawaii have taken action to protect the health and welfare of their people and natural environment. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAITS HEALTH & ENVIRONMENT AT RISK 1 33 PART THREE TAKING CONTROL OF OUR FUTURE We would all like t o law speaks to any requirements for any GE organisms. The case is also currently on believe that the EPA appeal before the Ninth Circuit. More recently, the County of Maui passed a mora - protects us from pesti- torium on genetically engineered crops, in response to which chemical companies again filed a lawsuit, leading to a temporary hold on the moratorium. cide harms. but this is often not the case. Despite these setbacks, the district court rulings make one thing clear: counties have Fundamental flaws in authority to regulate agricultural activities for the protection of its residents and the EPA's regulatory environment.The legislature granted the counties the authority to protect health, life, and property in HRS § 46-1.5(13), and also the power to enact and enforce process ensure that the ordinances to address public nuisances. There is no Hawaii constitutional provision Agency regularly or law that expressly precludes county regulation of agriculture, and no court has approves pesticide held that any law does so implicitly. Moreover, the district court's decision in the products that are Kaua'i litigation makes clear that such county initiatives are not prohibited by federal hazardous to human law. The federal pesticide law and the federal plant law applied to GE crops did not Prohibit county regulation.Thus, the decision supported the conclusion that, in other health and the states, federal law would not prohibit counties from protecting themselves the way environment. Kaua'i did, and regulation pesticides and GE crops via disclosures and buffer zones. Deficient Federal Pesticide Regulation We would all like to believe that the EPA protects us from pesticide harms, but this is often not the case. Fundamental flaws in EPA's regulatory process ensure that the Agency regularly approves pesticide products that are hazardous to human health and the environment (see e.g. Jacobs and Clapp 2008).These flaws include: 1) Tests conducted on one pesticide at a time, even though in the real world we are exposed to multiple pesticides that can have additive or synergistic effects; 2) Tests conducted only on the active ingredient (a.i.), even though so-called "inert ingredients" 12 in pesticide formulations can be toxic in their own right, or increase the a.i.'s toxicity; 3) Testing is biased to acute effects and is not geared to detect most impacts from long-term exposure to lower levels of the pesticide; 4) Near exclusive reliance on animal experiments conducted by the financially inter- ested pesticide company, with little or no attention paid to more relevant human epidemiological studies carried out by independent medical scientists; 5) Assumption of perfect compliance with a host of complicated label directions that are often unworkable and not followed. The deficiencies in EPA's regulatory regime are demonstrated by the long history of presumably "safe" pesticides that have had to be taken off the market, but only after harming many thousands of people and the environment. These include the planta- tion era pesticides DBCP and heptachlor (see "Lessons from History" above), and two pesticides used on Hawai'i as recently as 2012—methyl parathion and sulfuryl 34 1 HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK PART THREE TAKING CONTROL OF OUR FUTURE fluoride (Figure 6). Although long known to be toxic, these pesticides are only now in the process of being phased out (EPA Methyl Parathion, EPA Sulfuryl Fluoride 2011). Even when EPA acknowledges a pesticide's toxicity, its use can continue for many years. EPA phased out all residential uses of chlorpyrifos beginning in the year 2000, specifically to protect children, yet rural kids remain unprotected (Goldman et al. 2009). Chloryprifos is the most heavily used insecticide in U.S. agriculture (EPA 2011) and the most heavily applied restricted use insecticide in Hawaii (Figure 6). These examples, as well as the hundreds of medical studies showing harm from approved pesticides (some discussed in this report), demonstrate clearly that EPA can- not be relied upon to protect Hawaii residents or the environment from intensive pesticide spraying by agrochemical -seed firms. Momentum Building to Protect Kids from Pesticide Drift EPA regulation is especially deficient in the area of pesticide drift. Requirements intended to mitigate drift are often not followed; for instance, applicators often violate pesticide labels by spraying pesticides when it is too windy (AAPCO 2002). Recog- nizing its deficient regulation of drift, EPA proposed improved pesticide labeling in 2001, but the proposal was never finalized and is not in effect (Goldman et al. 2009). Neither does EPA take drift exposure into account when it registers or re -registers individual pesticides. EPA's very definition of drift is deficient, in that it leaves out vapor drift and pesticide -laden dust, considering only the form of drift that occurs during application. Public interest and farmworker groups formally challenged EPA for its inaction, and petitioned the Agency to establish regulations to protect children from pesticide drift (Goldman et al. 2009). An official policy statement of The American Academy of Pediatrics lists the establishment of no -spray buffer zones around schools as one of several local approaches to protect children from pesticide drift (AAP 2012). Medical scientists from the federal and state governments also support "adoption of pesticide spray buffer zones around schools" (Alarcon et al. 2005). Hundreds of medical studies showing harm from approved pesticides, demonstrate clearly that EPA cannot be relied upon to protect Hawaii residents or the environment from intensive pesticide spraying by agrochemical -seed firms. HAWAII CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK 1 35 PART THREE TAKING CONTROL OF OUR FUTURE Because federal regulators do not protect citizens from pesticidal harms, a growing number of states and counties— including Maui, Hawai'i Island, and Kaua'i— Momentum is building to protect kids from pesticide drift, including measures such as those found in Kauai County Ordinance 960. As of 2004, at least seven states had established no -spray buffer zones around schools, hospitals, nursing homes, public parks, and playgrounds (Owens and Feld- man 2004). More recent information shows that nine states (Hurley et al. 2014) and fourteen counties in California (CPR 2010) have taken matters into have established such no -spray buffer zones. States with notification requirements their own hands by for pesticide applications near schools have increased in number from eight in 2004 requiring environmen- to eleven today (Owens and Feldman 2004, Hurley et al. 2014).These policy actions t a l and public health evince growing awareness of the serious health threats posed by pesticide drift. impact assessments, banning outdoor GE CONCLUSION field tests, establishing Hawaii is at a cross roads in its economic, ecological, and agricultural development. no -spray buffer zones After over 150 years of export -oriented commodity production, the last 50 of which have involved the intensive use of pesticides, its land and food system are dangerously around schools, and insecure. While Hawaii imports 88% of its food, the GE Seed industry uses 72% of requiring notification its total crop area, largely (upwards of 80%) for the field testing of new crops that and disclosure have been genetically engineered to resist one or more herbicides; these industrial of pesticide use. agriculture practices threaten public and environmental health. It is in the face of this tipping point that communities across the state have started to push back against the untempered expansion of GE field trials on our prime agri- cultural land. While questions of the safety of GE foods in the food supply have also been subject to political debate in the U.S., most popularly through the question of labeling, the debate in Hawaii is significantly different. Given the amount of agri- cultural land dedicated to GE field trials in Hawaii, combined with the integral role pesticides play in this industry, we are questioning whether the development and testing of GE seeds is safe for our communities and our environment. This report examines the available data and literature that communities need to answer this question. Rather than turning to farmers and pesticide applicators for the answers to these questions, it has been critical for us to shed light on the medical literature that examines the epidemiological impacts of pesticides on human health. In adult populations, pesticide exposure has been linked to Non -Hodgkin's lym- phoma, bladder and colon cancers, Parkinson's disease, depression, and disrupting our hormonal or endocrine systems. More frightening are the links associating children and pregnant women exposed to pesticides with childhood cancers, neurobehavioral and cognitive deficits, adverse birth outcomes, and asthma.This literature is unequiv- 36 1 HAWAI'i CENTER FOR FOOD SAFETY PESTICIDES IN PARADISE: HAWAI'I'S HEALTH & ENVIRONMENT AT RISK ocal in its findings: pesticides threaten the long-term health of children, farmworkers, and other individuals who are exposed. Pesticides also threaten native biodiversity and ecological services by degrading soils, water, and killing beneficial microorganisms, insects, and pollinators. The GE seed industry warrants unprecedented public concern in Hawaii because it is largely devoted to testing and develop- ing seeds that have been genetically engineered to resist the application of new herbicide combinations, and uses growing methods that require the near daily application of insecticides and fungicides. Because of the rapid expansion of this industry in our state, we lack the appropriate regulatory framework to protect families and environment from these potential harms. This is why our counties have stepped forward to act. The State of Hawaii must follow suit. The public has the right to know what chemicals are applied, par- ticularly because they are applied so closely to places of work and play; doctors need this information to make informed medical decisions for their patients; and policy makers, without a clear picture of what pesticides are being used, cannot develop regulations that adequately protect public and environmental health. As we gain more clarity on the amount of pesticides applied in the state, and the locations of these practices, we also need to ensure that we reduce the likelihood that children and pregnant women will be exposed. Buffer zones, around homes, schools, and hospitals are a moderate first step in mitigating exposure risk.These are the concerns of community members working on the issues of pesticides and genetic engineering in our state.Together, we can ensure that the agricultural systems of Hawaii promote the health and well-being of our islands now and for future generations. ENDNOTES I Monsanto, DuPont -Pioneer, Dow Chemical, Syngenta, and BASF. 2 These companies, which account for two-thirds of combined seed and agro- chemical sales in the world today (ETC 2011), are referred to variously as agrochemical, pesticide, and seed firms in this report. 3 Also incorrectly called "herbicide tolerance" by the agrochemical -seed firms and those who follow their faulty naming convention. The Weed Science Society ofAmerica dearly defined such GE crops as "herbicide -resistant" in 1998 (WSSA 1998). 4 It should be noted that a single permit often covers a field release in which sev- eral different types of traits are tested. 5 Note that many individual permits authorize testing of more than one herbi- cide -resistance trait (e.g. one with the herbicide identified and a second one hidden as CBI). 6 In this informal usage, pesticide refers only to insecticides and fungicides, not herbicides. Pesticides threaten the long-term health of children, farmworkers. and other individuals who are exposed. Pesticides also threaten native biodiversity and ecological services by degrading soils, water, and killing beneficial microorganisms, insects, and pollinators. 7 An "active ingredient" (a.i.) is the put -killing component of a pesticide formu- lation that contains many other ingredients (some hidden as trade secrets) as well. 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