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A Generation in Jeopardy

How pesticides are underminingour childrens health & intelligence

OCTOBER 2012

PESTICIDE ACTION NETWORK NORTH AMERICA


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AcknowledgementsThis report would not have been possible without the dedicated and careul work o hundreds o scientists atacademic institutions in the U.S. and around the world. The contribution o these researchers to our collectiveunderstanding o the links between pesticide exposure and childrens health is truly invaluable.

A Generation in Jeopardyalso reects the eorts and expertise o many individuals both within Pesticide ActionNetwork and among our partner organizations and institutions. Susan Kegley, Heather Pilatic, Linda Wellsand Kathryn Gilje provided useul comments and direction as the report was being developed and fnalized.Several academic reviewers representing expertise in neurodevelopmental and carcinogenic impacts o pes-ticides on childrens health provided substantive comments. Laura Cossette, Kristen Parks and Maria Reynaprovided valuable research assistance.

Thanks also go to Brenda J. Willoughby who ormatted the report or publication, Sara Knight who trackeddown images, created fgures and otherwise assisted immeasurably with production, Mateo Rutherord andRoy Rojas o Berkeley Interpretation, Translation and Transcription Services (BITTS) who translated the Exec-utive Summary into Spanish, and Janet Stephens and Kathryn Gilje or fnal proofng and copy editing.

Funding or this report was provided by The A&A Fund, the Arntz Family Foundation, the Bellwether Foun-dation Inc., The Caliornia 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 McKnightFoundation, the Roy A. Hunt Foundation and the Wallace Genetic Foundation, as well as PANs supportingmembers.

The authors bear responsibility or any actual errors. Recommendations and views expressed are those o Pesti-cide Action Network North America, and do not necessarily represent the views o our unders and supporters.

Special thanks to our colleagues at Caliornians or Pesticide Reorm (CPR), Tracey Briegerand Sarah Aird, or strategic thinking and input as the report was being conceived and drated,as well as assistance with the reports release and dissemination. PAN North America is amember o 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 Caliornia tochange statewide pesticide policies and practices. See www.PesticideReorm.org or call 510-788-9025 or moreinormation about CPRs statewide work.

Pesticide Action Network North AmericaPesticide Action Network North America (PAN North America) works to replace the use o hazardous pesti-cides with ecologically sound and socially just alternatives. As one o fve PAN Regional Centers worldwide, welink local and international consumer, labor, health, environment and agriculture groups into an internationalcitizens action network. This network challenges the global prolieration o pesticides, deends basic rights tohealth and environmental quality, and works to ensure the transition to a just and viable society.

2012 by Pesticide Action Network North America. Permission is granted to reproduce portions o this report, provided the title and publishing organization is acknowledgePrinted on recycled paper.

1611 Telegraph Ave, Suite 1200Oakland CA 94612-2130Tel 510.788.9020 Fax 415.981.1991www.panna.org www.pesticideinfo.org

Pesticide Action Network


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A Generation in JeopardyHow pesticides are undermining

our childrens health & intelligence

October 2012Pesticide Action Network North America

Kristin S. Schafer, MAEmily C. Marquez, PhD

withMedha Chandra, PhDKendra Hutchens, PhD CandidateMargaret Reeves, PhDMeriel Watts, PhD, PAN Asia-Pacifc


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5/44AGenerationinJeopardyPesticideActionNetworkNorthAmerica

A Generation in JeopardyExecutive Summary

Children today are sicker than they were a generationago. From childhood cancers to autism, birth deectsand asthma, a wide range o childhood diseases anddisorders are on the rise. Our assessment o the latestscience leaves little room or doubt: pesticides are onekey driver o this sobering trend.

As the recent Presidents Cancer Panel reports, we havebeen grossly underestimating the contribution o envi-ronmental contamination to disease, and the policiesmeant to protect us have allen ar short. Nearly 20 yearsago, scientists at the National Research Council calledor swit action to protect young and growing bodiesrom pesticides.1 Yet today, U.S. children continue to beexposed to pesticides that are known to be harmul inplaces they live, learn and play.

This report reviews dozens o recent studies that exam-ine the impact o pesticides on childrens health. Our

analysis reveals the ollowing:

Compelling evidence now links pesticide exposures with harmsto the structure and unctioning o the brain and nervoussystem. Neurotoxic pesticides are clearly implicated ascontributors to the rising rates o attention defcit/hyperactivity disorder, autism, widespread declines inIQ and other measures o cognitive unction.

Pesticide exposure contributes to a number o increasinglycommon health outcomes or children, including cancer, birthdeects and early puberty.Evidence o links to certain

childhood cancers is particularly strong.

Emerging science suggests that pesticides may be importantcontributors to the current epidemic o childhood asthma,obesity and diabetes.

Extremely low levels o pesticide exposure can cause signicanthealth harms, particularly during pregnancy and earlychildhood.

Prioritizing childrens health requiresreal changeAs a nation, we value the wellbeing o our children. Inaddition to our natural urge to protect what we love, weknow that at a societal level their successul developmentis key to a vibrant, secure uture. Poll ater poll showsmore than 80 percent o Americans consider healthychildren a top priority. We must line up our practice andpolicies with these values.

Many communities across the country have stepped upto create local or state policies to protect children rompesticide exposure. From pesticide-ree schools, parksand playgrounds to protective buer zones in agricul-tural areas, locally-driven actions are leading the way tohealthier childhood environments.

But to ensure protection o all children rom the harmso pesticides, we must dramatically reduce the use othese chemicals nationwide. An estimated 1.1 billion

Childrensdevelopingbodiesareparticularlyvulnerabletothehealthharmsofpesticides.



pounds o pesticides are used in the U.S. every year, withmore than 20,000 products on the market. This volumeo use is undermining the health o the next generationand, as the science demonstrates, derailing developmento our childrens potential.

Scientists have understood or decades that childrenare particularly vulnerable to the harms o pesticideexposure. Quickly growing bodies take in more o

everything; they eat, breathe and drink more, pound orpound, than adults. As physiological systems undergorapid changes rom the womb through adolescence,intererence rom pesticides and industrial chemicalseven at very low levels can derail the process in waysthat lead to signifcant health harms.

Reducing overall pesticide use would not only limitchildrens exposure during their most vulnerable years,it would also lower pesticide levels in the bodies o menand women o childbearing ageprotecting currentand uture generations in one ell swoop. Those pesti-

cides most harmul to children should be frst on the list.

While we must each do what we can with ood choicesand decisions about home pest control, we cannotaccomplish this goal at an individual household level.Policy change is required.

Eective policies urgently neededTo protect children rom the health harms o pesti-

cides, policymakers need much more eective tools.We believe change is most urgently needed in the waydecisions are made about these three questions:

Whichpesticidesareusedinagriculture?

Whichpesticidesareusedinplaceschildrenlive,learnandplay?

Howarefarmerssupportedastheyreducerelianceonpesticides?

OBESITY 2004171% increase, ages 611

1980

DIABETES1990 201153% increase, ages 019

1975 2004CHILDHOOD CANCERS25% increased incidence, ages 019

AUTISM2002 200878% increase, age 8

ADHD 200619973% increase every year, ages 617

17% increase overall, ages 317DEVELOPMENTAL DISABILITIES

20081997

1975 2011

Figure 1: ChildrensHealthHarmsontheRise,19752011*

Statisticsshowsteadyincreasesinmanychildhooddiseasesanddisordersoverthepast30years.Thosehighlightedherearejustsomeofthehealthharmsontherise.Sources:seeendnotes4,13,24,52and94.

* Withtheexcept ionofcancer,allother dataareprevalence data,i.e.,representingt heU.S.population orbased ondataats everalsiteswi thintheU.S.Prevalenceis totalnumberof casesina populationat agiventime,whileincidenceisameasureofthenumberofnewcasesperyear.Theautismdataarefrom14sitesintheAutismandDevelopmentalDisabilitiesMonitoringNetworkandarenotconsideredfullyrepresentativeoftheU.S.population.The1990diabetesdataarefortype1only(type2beingextremelyrareamongchildrenatthattime),while2011dataincludebothtype1and2.Prevalenceoftype2diabetesamongchildrenisdiculttodetermineforvariousreasons,includingdicultyofdiagnosis.



Preventharmfullow-levelexposures: EPA should acton existing evidence that exposures to endocrinedisrupting pesticides pose a particular danger todeveloping children; the long-delayed endocrinedisruptor screening program (EDSP) should beswitly implemented.

2. Protect children where they live, learn & play

Kid-safehomes,daycares&schools: EPA shouldwithdraw approval o existing pesticide productsand not approve new pesticides or use in homes,daycare centers or schools when scientifc evidenceindicates the chemicals are possible neurodevelop-ment or reproductive toxicants, endocrine disrup-tors or human carcinogens.

Saferparks&playgrounds: State and local ofcialsshould enact policies requiring that all publicplaygrounds, playing felds and parks be managedwithout using pesticides that studies show areharmul to childrens health.

We recommend the ollowing policy changes in each othese arenas:

1. Prevent the pesticide industry from sellingagricultural products that can harm childrenshealth

Takeswiftactiononexistingpesticides: I studiesfnd a pesticide to be a neurodevelopmental or

reproductive toxicant, endocrine disruptor orhuman carcinogenandit has been measured inhumans, in schools or homes, or as residues onood or in drinking waterEPA should targetthe pesticide or rapid phaseout, triggering USDAresources to assist rapid armer transitions to saerpest control methods.

Blockharmfulnewpesticides: EPA should notapprove any new pesticide that scientifc studiessuggest is a neurodevelopmental or reproductivetoxicant, endocrine disruptor or human carcino-

genincluding short-term conditional registra-tions.

Childhood Health Harms*

Brain &

nervous systemimpacts

Childhoodcancers

Birthdefects

Reproductive &developmental

harms

Metaboliceects

(e.g., obesity,diabetes)

Immunedisorders,

asthma

Pesticides

Herbicides442 million lbse.g., atrazine, glyphosate,

2,4-DP P P P P

Insecticides65 million lbse.g., chlorpyrifos,malathion, permethrin

P P P P PFungicides44 million lbse.g., mancozeb,chlorothalonil

P P PP PFumigants108millionlbse.g., metam sodium, methylbromide, chloropicrin

P P PResearchershavelinkedexposuretovariouspesticideswitharangeofchildhoodhealthharms.APindicates that links to the health harmare particularly well supported by scientifc evidence.

* SeeAppendixAandwww.pesticideinfo.org 2007useestimates,referstoactiveingredient.FromPesticide Industry Sales & Usage, 2006 and 2007 Market Estimates, U.S.EPA,Washington,DC,Feb2011.Seewww.epa.gov/

opp00001/pestsales/07pestsales/market_estimates2007.pdf.Table3.4.

Table 1:Pesticides &Childhood HealthHarms



3. Invest in farmers stepping o the pesticidetreadmill

Corralresourcesforfarmers:Federal and stateofcials should mobilize and coordinate exist-ing resources to help armers adopt well-known,eective pest management strategies that reducereliance on pesticides.

Increaseinvestmentininnovativefarming: Congressshould authorize signifcant unding or programssupporting armers adoption o sustainable prac-tices that reduce use o harmul pesticides.

Setusereductiongoals:EPA and USDA should setspecifc and aggressive national pesticide use reduc-tion goals, ocusing frst on pesticides that studiesshow to be harmul to children. To track progresstoward this goal, armers should work with appli-cators and pest control advisors to report theirpesticide use to a nationally searchable database.

Sourceforchildrenshealth: Food distributorsshould require that their suppliers limit use opesticides that harm childrens health.

These proposals are all common-sense measures in theace o clear evidence that our childrens wellbeing is atrisk. Its time to muster the political will to prioritize thehealth o our children, grandchildren and uture gener-ations.

Evenatverylowlevels,pesticideexposurecanderaildevelopmentandundermine the ability to learn.



The process o establishing the architecture o the humanbrain begins in the womb and continues into early adulthood.During this long window o development, many complexprocesses take place, involving tens o billions o nerve cells

making trillions o connections. Cells migrate rom onesection o the brain to another, and nerve tracts are laid as thefnal structure o the brain is created.

Many o the processes that occur during brain developmentare vulnerable to disruption rom pesticides. Exposure toneurotoxic pesticides during critical moments o etal devel-opment, even at very low levels, has been shown to unda-mentally alter brain architecture.2 Pesticides that disrupt thehormone systemand particular those aecting the unc-tioning o the thyroid, which plays a key role in brain devel-opmentcan cause lasting damage. The impacts o exposuresare oten irreversible because unlike other organs, the braincannot repair damaged cells (see sidebar).

Children whose brain inrastructure or nervous system ailsto develop normally may be disabled or the rest o their lives.Developmental disabilities include autism spectrum disorders,attention defcit disorders, hearing loss, intellectual impair-ment and vision loss. People with developmental disabilitiesare oten challenged by everyday lie activities such as lan-guage, mobility, learning and independent living. Reducedcognitive abilities can also lead to behavioral problems, romaggression and social alienation to increased risk o drugabuse.3

A Silent PandemicSome 15 percent o all U.S. children have one or more devel-opmental disabilitiesrepresenting a 17 percent increase inthe past decade. For some disorders, the numbers are risingeven more rapidly.4 Overall, researchers estimate that between

Brainpower at RiskNew studies fnd pesticides can compromise intelligence

Knowledge o environmental causes o neurodevelopmental disorders is critically importantbecause they are potentially preventable. Dr. Philip Landrigan

1

Mechanisms of HarmMisring neurons & altered brain architecture

Pesticides can interere with brain unction anddevelopment in several ways; we describe three o themost common and best understood mechanisms oharm here:

Neurotransmittercontrol:Organophosphatepesticides can block the normal unctioning oacetylcholinesterase, an enzyme that degradesand thus controlsa neurotransmitter calledacetylcholine. When the unctioning o the enzymeis blocked, acetylcholine is not degraded and neuronscontinue fring instead o shutting down ater theyveaccomplished their mission. This can cause seriousproblems in the normal unctioning o the nervoussystem.

Developingbraincells:To date, EPA assessments haverelied on acetylcholinesterase levels as a marker o

organophosphate exposure risk, yet studies now showadverse eects can occur at much lower doses thanthose that block acetylcholinesterase. For example,chlorpyrios has been shown to interere with neuralcell replication, dierentiation and survival. As thebrain structure is developingparticularly at keystages inuterochlorpyrios can disrupt the processin ways that permanently alter the architecture o thebrain.*

Sodiumowintonervecells:Pyrethroid insecticides acton neurons by perturbing voltage-sensitive sodiumchannels. These sodium gates are what allow sodiumto ow into a nerve cell, controlling how a neuron fres

and transmits signals along a nerve. Pyrethroids causethese gates to open and close more slowly, changinghow the nerve cell normally respondseither inducingrepetitive fring or causing the nerve cell not to fre at all.

* Rauh,V.A.,F.P.Perera,M.K.Horton,R.M. Whyatt,R.B ansal,X.Hao,etal. BrainAnomaliesinChildrenExposedPrenatallytoaCommonOrganophosphatePesticide.Proceedings o the National Academy o Sciences.May2012109(20):7871-6.Seehttp://www.pnas.org/cgi/doi/10.1073/pnas.1203396109.

ShaferT.J.,D.A.MeyerandK.M.Crofton.Developmentalneurotoxicityofpyrethroidinsecticides:criticalreviewandfutureresearchneeds. Environ Health Persp.Feb2005113(2):123-36.Seehttp://www.ncbi.nlm.nih.gov/pubmed/15687048. Pesticides can interere with brain unction in several ways, rom altering architect

during etal development to interering with neurostransmitter control. Gaetan Lee



400,000 and 600,000 o the our million U.S. children borneach year are aected by a neurodevelopmental disorder.5

Public health experts rom Harvard and Mt. Sinai Hospitalhave called the damage that chemicals are causing childrensdeveloping minds a silent pandemic,6 and scientists nowpoint to a combination o genetic and environmental ac-tors to explain this rapid rise o developmental, learning andbehavioral disabilities.7

Some children, or example, may have a genetic susceptibilityto attention defcit/hyperactivity disorder (ADHD) or autism,but it may only develop i the child is exposed to a trigger-ing chemical during a certain period o development. Otherchildren may be genetically programmed to produce less o acommon detoxiying enzyme, rendering their brain and ner-vous system more susceptible to lasting harm when they areexposed to neurotoxic pesticides (see sidebar, p. 25).8

Genetic mutations that occur in parents (both men andwomen) in response to chemical exposures over the course otheir lietime can also, according to recent research, raise therisk o neurodevelopmental disorders or their children.9, 10

The National Academy o Sciences now estimates that about

one third o all neurobehavioral disorders (such as autism andADHD) are caused either directly by pesticides and otherchemicals or by interaction between environmental exposuresand genetics.11 Some experts say this estimate is likely to below, as the health proession is just beginning to ully rec-ognize the contributions o environmental actors to diseaseormation.*

Whatever the mechanism o harm, recent studies leave littledoubt that exposures to pesticides during etal development,

* Seefore xamplethe2010PresidentsCancer Panelreport ReducingEnvironmentalCancerRisk:Whatwecandonowhttp://deainfo.nci.nih.gov/advisory/pcp/annualReports/index.htm.

inancy and childhood may contributesignifcantly to decline in the cogni-tive abilities o our children. A recentcomprehensive review o the science onhealth eects o pesticides by the OntarioCollege o Family Physicians oundexposure to pesticides in the womb to beconsistently associated with measurabledefcits in child neurodevelopment.12

We look here at three areas where theevidence is particularly strong: ADHD,autism and alling IQs. A ew o thekey studies are highlighted below, andmore detailed descriptionsalong withadditional studiesare provided inAppendix A.

ADHD rates continue to riseADHD is quite clearly on the rise, andthough changes in diagnosis play a role,this cannot ully explain the trend. The

number o children diagnosed withADHD increased an average o threepercent every year rom 1997 to 2006,

and an average 5.5 percent per year rom 2003 to 2007 (seeFigure 2).13,

The Centers or Disease Control and Prevention (CDC)estimates that ADHD now aects three to seven percent oall school children in the U.S.; one independent study putsthe fgure at 14 percent.14 Boys are much more likely to bediagnosed with ADHD, although the American PsychologicalAssociation notes that girls are more likely to suer rom theattention defcit part o the disorder, and their symptomsare oten overlooked.15

A variety o brain unctions are compromised in childrenexhibiting ADHD. Learning is oten impaired, and thosewith the disorder may exhibit impulsive behavior and hyper-activity, and lack the ability to sustain attention.

As with other neurodevelopmental disorders, the socialimpacts can be immense. Parents report that children withADHD have almost three times as many problems interact-ing with peers as children without. Diagnosed children arealmost 10 times as likely to have difculties that intererewith riendships, including experiencing exclusion rom peergroups.16

The ScienceResearchers estimate that rom 20 to 40 percent o ADHDcases are caused by something other than genetics.17 Studieshave ound links to a variety o environmental contaminants,including exposure to organophosphate and pyrethroid insec-ticides during pregnancy and throughout childhood.

TheCDCout linesdiagnostic criteria here:http://www.cdc.gov/ncbddd/adhd/diagnosis.html,specifyingthatchildrenmustdisplayatleastsixcharacteristicbehaviorswithinsixmonths,andthatsomesymptomsmustbepresentbeforetheageofseven.CDCexplainsshiftsindiagnosticcriteriahere:http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5810a1.htm.

0

2

4

6

8

10

19971999 20002002 20032005 20062008

8.43

9.55 9.44

10.6

2.83

3.73 3.964.39

Boys

Girls

PercentageofChildren

DiagnosedwithADHD

Year

Figure 2: ADHDPrevalenceamongChildrenAges3to17,from19972008

ThenumberofchildrendiagnosedwithADHDincreasedanaverageof3percenteveryyearfrom1997to2008.Boysaremuchmorelikelytobeaected. Source:C.Boyleetal.,TrendsinthePrevalenceofDevelopmentalDisabilitiesinU.S.Children,19972008.



Childrenwithhigherlevelsoforgano-phosphate breakdown products in theirurine were more likely to have ADHD.Researchers ound that 94 percent othe 1000+ children tested by CDC haddetectable levels o these metabolites,and those with levels above the medianwere twice as likely to be diagnosed withADHD as those with no metabolitesound.18

Organophosphatemetabolitesatlevelscommonly ound in the bodies o U.S.children are linked to increased likeli-hood o ADHD. Every 10-old increasein levels o organophosphate metabolitesin the urine o children aged eight to15 years was associated with a 55 to 72percent increased likelihood o the disor-der.19

Prenatalorganophosphateexposurehasbeen linked to attention problems. Eachten-old increase in a pregnant mothersurinary concentration o organophos-

phate metabolites led to a fve-oldincreased risk that her child would bediagnosed with ADHD by age fve.20

Childrenwithlowbirth-weightaremorelikelytohaveADHD,21 and there is considerable evidence linking re-duced birth-weight with prenatal exposure to organophos-phate pesticides.22

Mousepupswerehyperactiveafterbeingexposedtothepyrethroid insecticides pyrethrin or cypermethrin, andadult mice injected with permethrin or deltamethrin hadlong-term elevation o the dopamine transporter, a markerthat has been linked to ADHD.23

Autism rates jump 250% in one decadeThe autism spectrum includes classic autism, Aspergers Syn-drome and atypical autism. Incidence rates have risen rapidlyin recent years; in its 2012 report, CDC estimatedbasedon 2008 data on eight-year-olds rom 14 statesthat 1.1percent o U.S. children, or one in every 88, are now on theautism spectrum. Boys are more likely to have the disorder,with one in 54 aected.

Data rom the National Health Interview Surveys reveal adramatic rate o increase. Between 1997 and 2008, autismprevalence 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 o more than385% over the same period (see Figure 3).24

In Caliornia, the number o children with autism who areenrolled in statewide programs rose rom 3,864 in 1987 to11,995 in 1998, an increase o more than 210 percent in11 years.25 Other states saw similar rates o increase between2002 and 2006.26 Though shits in diagnosis account orsome o this dramatic rise, public health experts have deter-mined that diagnostic changes do not ully explain the trend.

Researchers believe autism spectrum disorders reect changes

in brain structure occurring during critical windows o devel-opment in the womb. These shits in brain architecture maybe caused by genetics, environmental insults such as chemicalexposure, or an interaction between the two.27, 28

In 2012, a group o researchers led by Dr. Philip Landrigan oMt. Sinai Medical Center released a list o ten types o chem-icals most likely to be linked to the development o autism(see Table 2), and laid out an urgent strategy or research intothe role o these contaminants and how children can be betterprotected rom them. The list includes both commonly usedorganophosphate pesticides and longlasting organochlorine

0.31

0.58

0.94

1.1

0.070 0.11

0.22

0.34

0

0.3

0.6

0.9

1.2

19971999 20002002 20032005 20062008

Boys

Girls

Year

PercentageofChildrenDiagnosedwithAutism

Figure 3: AutismPrevalenceamongChildrenAges3to17,from19972008

Rates o autism have risen dramatically in the past decade. While overall prevalence is higher amongboys, the rate o increase is higher among girls. Source:C.Boyleetal,TrendsinthePrevalenceofDevelopmentalDisabilitiesinU.S.Children,19972008.

Table 2:Chemicals Contributing to Autism

Lead

Methylmercury

Polychlorinated biphenyls

Organophosphate pesticides

Organochlorine pesticides

Endocrine disruptors

Automotiveexhaust

Polycyclic aromatic hydrocarbons

Brominatedameretardants

Peruorinatedcompounds

Thislistfrompublichealthexpertsincludesbothcommonlyused organophosphate pesticides and long lastingorganochlorine pesticides, as well as other chemicalscommonly ound in consumer products. Source:Landrigan,etal.,2012



pesticides, as well as other chemicals commonly ound inconsumer products.29

The ScienceStudies examining the links between pesticide exposure andautism suggest prenatal exposures are particularly damaging.

OnestudyinCaliforniasCentralValleyfoundthatwhenmothers were exposed early in pregnancy to the organo-

chlorine pesticides endosulan and dicool, the risk oautism among their children increased sharply. Childrenwhose mothers lived within 500 eet o felds being sprayedwere six times more likely to be on the autism spectrum.30

MothersinCaliforniascentralcoastregionwhohadhigherlevels o organophosphate metabolites in their urine duringpregnancy were much more likely to have children withpervasive developmental disorderwhich can include orbe an indicator o autism. The risk more than doubled eachtime metabolite concentrations went up by a actor o 10.31

AstudyinNewYorkCityfoundthatinfantsmostexposedto chlorpyrios inutero were signifcantly more likely tohave pervasive developmental disordersincluding au-

tismby the time they were three years old.32

AtrioofU.S.studiesexaminedlinksbetweenenvironmen-tal exposures among parents (including, but not limitedto, pesticides) and incidence o autism among their chil-dren.33 Among other fndings, the scientists reported thatolder athers are more likely to transmit tiny, spontaneousgene mutationsthat occur over a lietime in response toenvironmental stressorsto their ospring, that in turnincrease the risk o autism. Recent research in Iceland con-frmed these fndings.34

Minnesotaresearchersexploredtheinteractionofexposureto organophosphate pesticides, gene expression and dietaryactors as potential contributors to autism.35 Among otherthings, they ound that mineral defciencies linked to highructose corn syrup consumption* make developing mindsmore susceptible to the neurotoxic eects o pesticides.

These various recent studies show how complex the path toour current autism epidemic has been. But evidence suggeststhat pesticide exposureparticularly during pregnancyisimplicated in a number o ways.

Derailed brain development means falling IQsThe societal implications o reduced cognitive abilities acrossan entire generation are nothing short o staggering and havebeen a concern among public health specialists since the IQeects o lead exposure became clear in the 1970s. As Dr. TedSchettler observed back in 2000:

A loss o fve points in IQ is o minimal signifcance ina person with an average IQ. However a shit o fve IQpoints in the average IQ o a population o 260 millionincreases the number o unctionally disabled by over50 percent (rom 6.0 to 9.4 million), and decreases thenumber o gited by over 50 percent (rom 6.0 to 2.6million).36

* Highfructosecornsyrupisfoundinawiderangeofprocessedfoodsandbeverages.

Twelve years later, Dr. David Bellinger echoed this observa-tion. He pointed out that cognitive eects, oten dismissedas clinically unimportant at the individual level, becomevery signifcant across a whole society in terms o decliningintellectual capacity, lost economic productivity and increasedcosts or education and health care.

Bellinger reviewed published data linking organophosphatesand cognitive eects, and concluded that overall, exposure toorganophosphate insecticides may be responsible or lowering

U.S. childrens IQ level by 17 million pointsnot much lessthan the 23 million point loss attributed to lead poisoning.37

Bellinger argues that because the potential impacts o organo-phosphates are so widespread and signifcant to society, a riskassessment that ocuses solely on individual risk, and ails toconsider the problem in a public health context is mislead-ing and will not lead policymakers to sound and protectivedecisions.

The SciencePesticide exposure during pregnancy can have dramatic eectson cognitive development. From a wide range o animalresearch to studies tracking the intellectual development ochildren over time, the evidence points squarely at prenatalpesticide exposures as signifcantly harming the developmentand unctioning o the brain. These harms can then lead toboth lower IQ levels and neurodevelopmental delays.

AparticularlycompellingstudyusedMagneticResonanceImaging (MRI) technology to observe the developing braino inants who had been exposed to chlorpyrios duringpregnancy. Researchers observed signifcant structuralchanges, including abnormal areas o thinning and enlarge-ment. Areas o the brain related to attention, language,reward systems, emotions and control were aected.38

Threecohortstudies released in 2011 document cognitiveimpairment caused by exposure to organophosphates in thewomb. The frst study ound that higher metabolite levelsin a mothers urine late in pregnancy increased the likeli-hood o reduced cognitive development in their children.39The second study linked prenatal exposure to a seven-pointreduction in IQ by age seven.40 The third study ound thateven very low levels o chlorpyrios residues in cord bloodresulted in lower IQ and reduced working memory.41

Pregnantmothersexposedtochlorpyrifosthroughhouse-hold use (beore this use was withdrawn) had inants withlower birth weight and reduced head circumerence, bothindicators o impaired cognitive ability later in childhood.42

TheaccuracyofIntelligenceQuotient(IQ)testingtomeasureintellectualcapacityhaslongbeenasourceofcontention,butIQiscurrentlythebestindexformeasuringcognitiveabilitiesacrossapopulation.

SeesidebarinAppendixAforadescriptionofthevarioustypesofscienticstudieshighlightedinthisreport.

SeethiseditorialinEnvironmental Health Perspectivesforadiscussionoftheimportanceofthesethreestudies:StrengthinNumbers:ThreeSeparateStudiesLinkinUteroOrganophosphatePesticideExposureandCognitiveDevelopment,availableonlineat:http://ehp03.niehs.nih.gov/article/fetchArticle.action?articleURI=info%3Adoi%2F10.1289%2Fehp.1104137

Chlorpyrifoswaswithdrawnfromhomeusein2001,butremainswidelyusedinagriculturalsettingswherefarm,farmworkerandruralcommunitymothersandchildrenstillfaceexposure.Childrenalsocontinuetobeexposedfromresidueonfruitsandvegetables.



Exposuretotheorganophosphatepesticidesdiazinonandparathion during early childhood may reduce cognitiveunction, according to results rom animal studies. Low-dose exposures caused changes in the developing brainso rats known to correspond to reduced ability to learn.43Other animal studies indicate that inutero and neonatalexposure to organophosphates increases the risk o develop-mental delays.44

Childrenatthreemonthsofagewhoweremosthighlyexposed to the pyrethroid pesticide synergist piperonylbutoxide,* as assessed by personal air monitors, scored 3.9points lower on the Bayley Mental Developmental Index.These scores are predictive o school readiness, and theauthors described their results as modest, yet worrisome.45

PrenatalexposuretotheDDT breakdown product DDE isalso associated with neurodevelopmental delays in children,especially the psychomotor skills linking movement ormuscular activity with mental processes.46 And exposureinutero to DDT itsel has been associated with reducedcognitive unctioning, memory and verbal skills amongpreschoolers.47

Strong emerging evidence links childhood pesticide exposure

to other, adult-onset neurological eects such as Parkinsonsand Alzheimers diseases; these studies are not examinedhere.48

The combined, society-wide impact o the various syndromes,disorders and defcits resulting rom damage to childrensbrains and nervous systems early in lie is immense. Healthproessionals and educators across the country have indicatedconcern that our current policies dont adequately protect ourchildren as their nervous systems develop.49 Something mustbe done to address this gap, as the results o such exposureshave proound consequences or individuals, amilies andsociety as a whole.

* Piperonylbutoxide,orPBO,iscommonlyincludedinformulationsofpyrethroidpesticideproductstoincreasethepotencyoftheactiveingredient.

AgriculturalusesofDDTwerebannedintheU.S.in1972,butbecauseofitspersistence,DDTanditsbreakdownproductscontinuetoappearinhumanbloodsamples.DDTusecontinuesinsomecountriesformalariacontrolprograms.

Exposureofadevelopingfetus,infantorchildtoneurotoxicpesticidescanleadtogreaterriskoflearningdisabilitiesandsignicantdropsinIQ.


14/440 AGenerationinJeopardyPesticideActionNetworkNorthAmerica

Arican-American children have a lower survival rate than dowhite children (73 vs. 81 percent).53

For some cancers, genetics is a powerul predictor. But as

outlined by the Presidents Cancer Panel, cancers can havemultiple and oten interacting causes. In some cases geneticactors make an individual more susceptible, and exposure toenvironmental carcinogens may trigger cancer development.

The ScienceA large number o recent studies link pesticide exposure tochildhood leukemia, brain tumors and neuroblastoma. Someevidence suggests pesticide exposure may also be associatedwith other types o childrens cancer, such as non-Hodgkinslymphoma, Wilms tumor and Ewings sarcoma. Many studies

Cancer, Birth Defects &Early PubertyLatest science links many childhood health harms to pesticide exposure

I we are going to live so intimately with these chemicalseating and drinking them,taking them into the very marrow o our boneswe had better know something abouttheir nature and their power. Rachel Carson

2

Our children ace a range o health challenges that were notencountered by past generations. Public health experts areconcerned, and are increasingly ocusing on the contributingrole o environmental actors such as pesticides and otherchemicals.

The Presidents Cancer Panels 2010 report, or example,concluded that the role environmental contaminants playin contributing to cancer has been grossly underestimatedand called or urgent action to reduce the current widespreadexposure to carcinogens. The Panels chair, Dr. LaSalle Leall,urged preventative measures to protect public healtheven

in the ace o some uncertainty.*

The increasing number o known or suspectedenvironmental carcinogens compels us to action, eventhough we may currently lack irreutable proo oharm.50

Meanwhile, evidence continues to mount linking chemicalexposure to a range o childrens health harms. Below wepresent a summary o some o the growing body o recentfndings on pesticides and childhood cancer, birth deectsand early puberty. More detailed descriptions and additionalstudies are included in Appendix A.

Some childhood cancers linked to pesticidesCancer is the second most common cause o death amongU.S. children one to 14 years old. Over the past 30 years,the number o children diagnosed with all orms o invasivecancer has increased 29 percent, rom 11.5 cases to 14.8 casesper 100,000 children per year (see Figure 4).51

There are many types o childhood cancer, and incidence ratesvary widely. Leukemia and childhood brain cancers are nowthe most common cancers among children, with rates orthese two cancers rising 40 to 50 percent since 1975: leuke-mia rom 3.3 to 4.9 per 100,000 children, and brain cancersrom 2.3 to 3.2 (see Table 3).52

Survival rates have also risen. Improved cancer treatmentshave led to dramatic increases in survival o all types ochildhood cancer, particularly leukemia (rom 50 percentsurvival in 1975 to more than 80 percent in 2004) andnon-Hodgkins lymphoma (rom 43 to 87 percent survivalover the same time period.) For all types o childhood cancers,

* ThiscallforactioninthefaceofsomeuncertaintyisanexampleofthePrecautionaryPrinciple,anapproachtodecisionmakingthathasbeenadoptedbymanylocalgovernmentsintheU.S.andincountriesaroundtheworld.Foradenitionandmoreinformation,seetheScienceandEnvironmentalHealthNetworksFAQ:http://www.sehn.org/ppfaqs.html

Lethalaccidentsarethemostcommoncauseofdeath.

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Over the past 30 years, the number o children diagnosed with all orms ocancerhasincreasedfrom11.5to14.8casesper100,000childrenperyear.Source:SEER,2004

Table 3: Top 5 Childhood Cancers

Leukemia

Brainandothernervoussystemtumors

Neuroblastoma

Wilmstumor

Lymphoma

The types o cancers that occur most oten inchildrenaredierentfromthoseseeninadults.Source:AmericanCancerSociety



fnd inutero exposure during key windows o etal develop-ment or parental exposure beore conception to be particu-larly important.

Homeinsecticideuseduringpregnancycanincreaserisko childhood leukemia, according to a review o 15 studiesover the past two decades. Timing o exposure appears to beparticularly important.54

Theriskofachilddevelopingacutelymphocyticleuke-mia the most common type o childhood leukemia ishigher when the mother is exposed to home insecticidesduring pregnancy. Risk increased with the requency othe mothers exposure; the highest risk was associated withuse o household insecticides more than fve times over thecourse o gestation.55

Motherswhohaveaparticulargeneticvariantofanenzymeinvolved with the metabolic processing o wastes and toxins(including carcinogens)* are more likely to have a child withleukemia when they use pesticide products during preg-nancy.56

Severalcase-controlstudieslinkexposuretoherbicidesandhousehold insecticides during pregnancy to an increased

risk o childhood brain cancer.57

Higherriskofneuroblastoma,themostcommoncancer

among inants, was observed in children whose parentsreported garden and home pesticide use.58 An older case-control study o U.S. and Canadian children indicated in-creased risk o neuroblastoma among children whose atherswere landscapers and groundskeepers.59

Inanationalcase-controlstudyinAustralia,increasedrisko Ewings sarcoma tumors among children was linked tooccupational exposures o mothers and athers who workedon arms around the time o conception.60

Childrenwholivedinareasofhighagriculturalactivityinthe U.S rom birth to age 15 experienced signifcantly in-creased risk o childhood cancers.61 And a study in Norwayo agricultural census data ound that o 323,359 childrenunder 14, those who grew up on a armcombined witha high level o pesticides purchased by the amilywerenearly twice as likely have brain tumors.62

A number o studiesnot reviewed here explore potentiallinks between prenatal or childhood pesticide exposures andincidence o cancers later in lie. For example, according tothe Presidents Cancer Panel, girls who were exposed to DDTbeore they reach puberty are fve times more likely to developbreast cancer in middle age.63

In general, the association between pesticide exposures andchildhood cancer outcomes may be underestimated, as dataare somewhat limited and studies ocus on certain cancersmore than others. In addition, common methodologicalproblemssuch as occupational exposures being identi-fed only through sel-reporting or job title, considerationso other routes o exposure, small sample sizes, and relyingon recall to estimate exposuresmay contribute to skewedfndings.64

* TheCYP1A1genecodesfortheexpressionandactivitylevelofanenzymethathelpsclearthebodyofpotentiallyharmfulcompounds.

Birth defects rise with seasonal or occupationalexposuresBirth deects are the leading cause o inant mortality in theU.S., accounting or 19 percent o the 29,138 inant deathsin 2007. And the overall incidence o birth deects is ris-ing.65 According to CDC data, about one in every 33 babiesborn today has some kind o birth deect.66 Birth deects canaect almost any part o the body; some are mild and impactappearance only, others aect the unctioning o organs and

can be lie threatening, although overall survival rates haveincreased signifcantly since 1979.67

Incidence trends vary by specifc birth deect. Clet lip/palateis the most common birth deect reported, and incidencehas declined slightly over the last decade. Rates o DownSyndrome, gastroschisis (an abdominal wall deect resultingin protrusion o the intestines) and anencephaly (absence oportions o the brain, skull and scalp) have all increased since1999.68

Like many childrens health outcomes, a combination ogenetic and environmental actors is oten at play. CDCsresearch on environmental actors has ocused primarily on

smoking, alcohol intake, obesity and diabetes.69 Other scien-tists, however, have examined the role o parental exposureto pesticides and other chemicals beore conception, and omothers exposure to environmental contaminants duringpregnancy (see sidebar, p. 17).

The ScienceParents exposed to pesticides occupationally, rom exposuresin their community or by in-home pesticide use may increasethe risk o birth deects in their newborn. Studies indicatethat exposure o both mothers and athers, particularlyduring the period o conception, can inuence birth deect

outcomes. Several studies in agricultural areas have correlatedconception during peak pesticide spray season with increasedbirth deect risk.

A mothers exposure during pregnancy can also play a keyrole, with specifc timing once again emerging as a criticallyimportant variable.

Childrenwhosemotherswereexposedtoherbicidesandhouseholdinsecticidesduring pregnancy have an increased risk o developing brain cancer.



Amulti-year,nationalreviewofUSGSwaterdataandCDC birth deect records ound a strong seasonal associa-tion between birth deects and the presence o the herbicideatrazine in surace water. Inants conceived between Apriland July, when elevated concentrations o the herbicideare ound, have a signifcantly higher birth deect risk (seeFigure 5).70

InWashingtonstate,aseasonalanalysisoftheriskoftheabdominal wall deect gastroschisis showed prevalencepeaking when conception occurred between March andMay. The birth deect occurred most requently amonginants whose mothers lived within 50 kilometers o a sitewith high surace water concentration o atrazine.71

MalepesticideapplicatorsinMinnesotahadasignicantlyhigher number o children with birth deects, in a studyexamining 4,935 births to pesticide applicator athers overthree years. The birth deects were more common amongboy ospring than girls.72 Egyptian athers exposed to pesti-cides at work also had a greater risk o having children withcongenital malormations.73

Increasedriskofboysurogenitalmalformationssuchashy-pospadia, micropenis and cryptorchidism* has been linkedin many studies to prenatal exposure to environmental con-taminants. One recent meta-analysis o studies rom sevencountries (Canada, Denmark, Italy, Netherlands, Norway,Spain and the U.S.) indicated a 36 percent increased risko hypospadia when mothers were exposed to pesticides atwork, and a 19 percent increased risk with athers occupa-tional exposure to pesticides.74

* Hypospadiaisadefectinwhichtheurethralopeningdevelopsinthewronglocationalongtheshaftofthepenis.Micropenisisadefectwhereboyshaveseverelyreducedpenilesize,andcryptorchidismisadefectwherethetestesdescendimproperly,ornotatall.

Theriskofhavingachildwithneuraltubedefects,whichare birth deects o the brain and spinal cord, has also beenlinked to pesticide exposure. Studies indicate a higher risko this birth deect i insecticide bombs or oggers are usedin the home during the period o conception. Risk is alsohigher i women live within a quarter mile o a cultivatedfeld where pesticides are sprayed.75

Mothersexposedtopesticidesatworkduringaparticularperiod o pregnancy have a signifcantly greater risk ohaving a child with anencephaly (a rare deect involving ab-sence o a large part o the brain and skull).76 A meta-anal-ysis o studies examining athers exposure to Agent Orange

(containing the herbicides 2,4-D and 2,4,5-T) ound therisk o having ospring with spina bifda, a split spinedeect caused by incomplete ormation o the neural tube,was twice as high among those athers who were exposed.77

Many epidemiological studies over the years have ound noassociation between pesticide exposure and birth deects.It must be considered, however, that these studies may nothave taken timing o exposure into account, a variable that isproving to be a critical actor in birth deect outcomes. And aswith cancer studies, results may be skewed by use o inap-propriate surrogates or pesticide exposure (e.g. job title) orinaccurate subject recall.

Changes in puberty timing linked to low-levelexposuresYoung girls in the U.S. are moving rom childhood to ado-lescence at an ever-younger age. Changes in the timing osexual development over the past two decades have been sowidespread that the age o normal puberty onset has beenredefned by health proessionals.78

AgentOrangewaswidelyusedasadefoliantduringtheVietnamWarandwasoftencontaminatewithdioxinswhichhavealsobeenlinkedtobirthdefects.Oneoftheherbicideingredients,2,4-D,isstillinuseintheU.S.,andaproposaliscurrentlyunderconsiderationforageneticallyengineeredvarietyofcorndesignedtoallowincreased2,4-Dapplication.

Farmworker Families & Pesticides

As a community organizer and health educator inNorth Carolina, Ana Duncan Pardo works with manycommunities directly aected by pesticides.

When we spoke with Ana about her experienceworking with armworkers, she described a particularinstancewhen she was setting up or a presentationto armworker parentsthat awoke her to the healthharms aced by many o these amilies:

Within fve minutes I had noted multiple cletpalates and several children with apparent DownSyndrome. It was shocking and disturbing towalk into a room with a group o parents andchildren that easily represented three to ourtimes the national average or birth deects.

Farmworkers and their amilies ace unique risks, as theharmul chemicals applied in the feld ollow workershome on their skin, shoes and clothing, and may alsodrit into their homes rom the nearby felds. And, like

all amilies, the ood they eat every day may containpesticide residues.

Ana Duncan Pardo is the armworker organizer & communicationscoordinatorforToxicFreeNorthCarolina,andamemberofPANsboard.

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Figure 5: AtrazineSeasonalExposure&BirthDefects

Seasonalexposuretopesticidesduringpregnancyhasbeenlinkedtoincreasedro birth deects. Source:Winchester,P.D.,J.HuskinsandJ.Ying.AgrichemicalsinsurfacewateranddefectsintheUnitedStates.ActaPaediatrica.200998:664669.



Dr. Herman-Giddens and her colleagues frst documentedthis acceleration in 1996, in a study fnding that the numbero girls having some sign o puberty onset beore the age oeight was substantially higher than previously ound.79

These initial fndings o early puberty were corroborated in2010 by researchers who ound that by age seven, 10 percento white girls, 23 percent o black non-Hispanic girls, and15 percent o Hispanic girls had begun the process o breastdevelopment, also known as thelarche.80 Some changes in

pubertal development in boys have also been documented.

Changes in puberty timing are concerning or several reasons.For both boys and girls, sel-esteem and body image issues cansometimes lead to sel-destructive behaviors and poor peror-mance in school. Additionally or girls, both early pubertyand obesity (a contributing actor or early puberty) havebeen linked to health impacts later in lie, increasing the riskor breast cancer and later reproductive health issues such aspolycystic ovary syndrome.81, 82

These changes cannot be ully explained by ethnic, geo-graphic, or socioeconomic actors, and thus a growing bodyo research has turned to examining the role o endocrine-dis-

rupting chemicals in accelerating puberty in children.83

The ScienceAlthough the number o studies is relatively small, researchershave ound some associations between pesticide exposureeither during etal development or early childhoodandeects on puberty.

Most studies ocus on inutero exposures to pesticides withendocrine-disrupting eects that can interere with thehealthy development o the reproductive systempar-ticularly i exposure occurs at certain times in the process

(see sidebar).84

The majority o studies ocus on precociouspuberty in girls, but a ew studies have also ound linksbetween pesticide exposure and changes in the timing opuberty among boys.

Much o the research to date examines impacts o long-lastingorganochlorine pesticides. Some o these are chemicals thathave already been banned in the U.S. (e.g., DDT, hex-achlorobenzene); others are in the process o being phased out(e.g., lindane, endosulan); but all are still present in our oodsupply, environment, and in our bodies.85, * Though ew stud-ies have yet examined the connections, pesticides currently inuse are also implicated in some studies.

Prenatalexposuretotheherbicideatrazinewaslinkedtodelayed pubertal development in both male and emale ratsin a recently released animal study.86

Danishgreenhouseworkersexposedtoarangeofpesticidesduring pregnancy were more likely to have daughters show-ing breast development rom 611 years old.87 Increasedlikelihood o early puberty in girls in Jerusalem was oundto coincide with seasons o intensifed pesticide usage.88

* CDCsamplingfrom19992000,forexample,foundDDTsbreakdownproductinbloodsamplesof99percentofU.S.population.Seehttp://www.cdc.gov/exposurereport/.

DaughtersinMichiganweremorelikelytoreachpubertyat a younger age i their mothers had higher blood levels othe DDT breakdown product, DDE. Participants in thisstudy included women who regularly consumed fsh romthe Great Lakes, which or years have been heavily contami-nated with industrial pollutants such as PCBs and DDT.89

HigherbloodlevelsofhexachlorobenzeneandDDEwereassociated with early puberty among Flemish boys.90 Tworecent studies o boys in India and Russia linked exposureto the pesticide endosulan and the industrial by-productdioxin to delayed puberty among boys.91

Thepyrethroidinsecticideesfenvalerate has shown endo-crine-disrupting eects related to puberty timing in emalerats. Rats exposed to low levels (hal o EPAs no observableeect level) or seven days showed signifcant delays inonset o puberty.92

As evidence mounts that developmental exposures to pesti-cides can have an eect on puberty timing, additional studiesare now ocusing on such endocrine-disrupting eects opesticides currently in use.

EsfenvalerateislistedforTier1screeningunderEPAsEndocrineDisruptorScreeningProgram.Seehttp://www.regulations.gov/#!documentDetail;D=EPA-HQ-OPP-2009-0634-0001.

Mechanisms of HarmEndocrine disruption = development derailed

The term endocrine reers to systems in the bodythat are controlled by hormones, such as braindevelopment, growth, reproduction and puberty.Hormones are proteins synthesized in the body thatbind to receptors to trigger actions at the cellular level

resulting in physiological changes. Once their job isdone they are released and ree to act again.

Some pesticides act as endocrine disruptors thatmimic hormones and can interere with systemsnormally controlled by hormonal action. I suchdisruption occurs at times during development knownas windows o vulnerability,such as when thereproductive system is coalescing, brain or nervoussystems are developing, immune system is ormingor puberty is getting underwaythe process can bederailed in signifcant ways, sometimes with lie-longeects.

Because hormones themselves act at extremely low

levels, biological processes controlled by hormones aretremendously sensitive. This means there oten is nothreshold or sae dose when it comes to endocrinedisrupting compounds.*

* Zoeller,R.T.,T.R.Brown,L.L .Doan,A.C. Gore,N.E.Sk akkebaek,A.M. Sotpetal.Endocrine-DisruptingChemicalsandPublicHealthProtection:AStatementofPrinciplesfromTheEndocrineSociety. EndocrinologyJune2012.Seehttp://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,etal.HormonesandEndocrine-DisruptingChemicals:Low-DoseEectsandNonmonotonicResponses.Endocrine Reviews.March201233(3):378-455.



Many o the health challenges acing childrentoday have strong genetic and/or behavioralcomponents. The rise in childhood obesity, orexample, in part reects the increasingly sed-entary habits o many U.S. children.* But itsbecoming increasingly clear that personal liestylechoices do not tell the whole story.

The speed and scope o the society-wide rise inchildhood health problems suggest a complexinteraction o genetic, behavioral and environ-mental variables. Researchers are beginning totease apart these interactions to more ully under-stand how exposure to environmental contami-

nants are involved.

We examine here the rapidly emerging scienceexploring how pesticides may contribute to therecent rise in childhood obesity, diabetes andasthma. Additional studies are included anddescribed in Appendix A.

Childhood obesity, diabetes & disruptedmetabolismThe recent dramatic rise in childhood obesityin the U.S. has the ocused attention o health

specialists and the public. The number o clini-cally obese children has more than tripled in thepast 30 years, with obese children ages six to 11jumping rom seven percent o the total in 1980to nearly 20 percent in 2008. The percentage oobese adolescents (1219 years old) increasedrom fve to 18 percent over the same period (seeFigure 6).93,

Obesity is closely linked to childhood diabetes, which is alsoon the rise. According to the National Institutes o Health,about 215,000 Americans under the age o 20 had diabetes in2010up rom roughly 123,000 in 1990.9495

In addition to increasing related health risks, both obesity anddiabetes can have a negative eect on quality o lie in termso ability to engage in physical activities, societal acceptanceand sel-image.

* CDCpointstoestimatesthatU.S.childrenspendanaverage4.5hoursadaywatchingtelevisionand7.5hoursusingentertainmentmedia(TV,computers,videogames,cellphonesandmovies)asacontributingfactortochildhoodobesity.Seehttp://www.cdc.gov/obesity/childhood/problem.html

SeeCDCsHistoryofStateObesityPrevalenceshowingtrendsinadultobesitybystatefrom2000-2010,atthebottomofthispage:http://www.cdc.gov/obesity/data/adult.html

The ScienceSo much new science exists around the links between obesityand environmental contaminants that a new term, obesogen(like carcinogen) has emerged in the literature. Findingsincreasingly suggest that exposures to pesticides and otherchemicals play a role by altering developmental programmingin ways that raise the likelihood o obesity and related meta-

bolic eects such as diabetes.96

In 2002, Baillie-Hamilton reviewed data suggesting that theobesity epidemic coincided with the marked increase in usageo industrial chemicals, including pesticides, over the past 40years (see Figure 7). The author suggested that pesticides andother industrial chemicals potentially cause weight gain byaecting the hormones that control weight, altering sensitivity

SeeWendyHoltcampsreviewarticle,Obesogens:AnEnvironmentalLinktoObesity(Environmental Health Perspectives,Feb.2012)foranoverviewofthecurrentliterature.Availableonlineathttp://ehp03.niehs.nih.gov/article/info%3Adoi%2F10.1289%2Fehp.120-a62#r13.

Emerging ScienceObesity, diabetes& asthma

Chemicals that disrupt hormone messages have the power to rob us o rich possibilities thathave been the legacy o our species and, indeed, the essence o our humanity. Teo Colburn

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Figure 6: Prevalence o Obesity among Children Ages 2 to 19between19762008

PrevalenceofobeseU.S.childrenages6-11jumpedfrom7percentin1980to20percentin

2008,whilethepercentageofobeseadolescentsincreasedfrom5to18percent. Source:CenterforDiseaseControl,PrevalenceofObesityAmongChildrenandAdolescents:UnitedStates,Trends1963-1965Through

2007-2008.



to neurotransmitters, or altering the activity o thesympathetic nervous system.97

In the 10 years since this review, many studies havelinked exposure to endocrine-disrupting chemicalswith increased incidence o obesity and diabetes.98The National Institutes o Health is oering grantsto study the role o environmental chemical expo-sures in the development o obesity, type 2 diabetesand metabolic syndrome,99 and the National

Childrens Study, an ongoing 21-year prospectivestudy o 100,000 U.S. children, is now exploringthe hypothesis that prenatal exposures to endocrinedisruptors are linked to obesity.100

Inoneanimalstudy,ratsexposedtolow-leveldoses o the organophosphate pesticide chlorpy-rios early in lie developed metabolic dysunc-tion resembling pre-diabetes.101

InDenmark,childrenexposedprenatallytopesticides through their mothers work in green-houses had signifcantly higher BMI (body massindex) scores than greenhouse worker mothers

who were not occupationally exposed, withhighly exposed children also having larger skinolds and higher body at percentages.102

Exposuretothepesticidelindane* during childhoodhas been linked with increased abdominal at, increasedwaist circumerence, higher BMI and at mass percent-age in adults.103

Organochlorinepesticideexposure can be a predictoro developing type 2 diabetes later in lie, particularlyamong obese individuals. Serum concentrations oorganochlorines were strongly associated with type 2diabetes, and the association was stronger among obesepersons than non-obese persons.104

Obesechildrenaremorelikelytohavehigherconcentra-tions o 2,5-DCP in their urine, a metabolite o the pes-ticide ound in mothballs (p-dichlorobenzene). This cor-relation was observed in data rom the National Healthand Nutrition Examination Survey (NHANES).105

A number o specifc genes have been identifed as con-tributing to obesity, with several thought to specifcallycontribute to obesity in children. Such genes may play arole in regulating metabolic hormones.106

Scientists are now investigating the role o environmentalactors (such as exposure to pesticides) in inuencing theexpression o such genes. Such epigenetic changes caninclude the expression o genes that are typically silent,or inactivation o a gene that is normally active. Research-ers are fnding that some o these changes can be passedrom one generation to the next (see sidebar).107

* Lindane,anorganochlorineinsecticide,isslatedforglobalphaseoutundertheStockholmConventiononPersistentOrganicPollutants.AgriculturaluseswerephasedoutintheU.S.in2006;pharmaceuticaluses(liceshampoosandscabiestreatments)werephasedoutinCaliforniain2001,butarestillallowedinotherstates.

MostorganochlorinepesticidesarenowbannedintheU.S.,andmanyhavebeentargetedforinternationalphaseoutundertheStockholmConvention.Rapidimplementationofthistreatywillreducefurtherexposuretotheselonglastingchemicalsthatcontinuetotraveltheglobeonairandwatercurrents.

Figure 7. Chemical production & the percentage o overweightadults in the U.S.

Researchers note that the obesity epidemic coincides with the increase in use oindustrial chemicals, including pesticides, over the past 40 years. Source:Baillie-Hamilton,P.F.Chemicaltoxins:ahypothesistoexplaintheglobalobesityepidemic.J Altern Compleme nt Med.20028:185192.

Mechanisms of HarmChanging gene signals

Many environmental pollutants can strip or addchemical tags to DNA, locking the expression o geneson or o and changing how they unction. These

changes are called epigenetic tags, and have beenlinked to various health eects including early puberty,disrupted ovarian unction, death o sperm-ormingcells and changes in metabolic rate.

Recent studies suggest that some chemicals can evenoverride the genetic reset button that usually protectsa developing etus rom such changes being passedrom one generation to the next.



Asthma epidemic aects more than seven million

childrenAsthma is a chronic disease o the pulmonary system thatcauses wheezing, breathlessness, chest tightness and coughing.The number o U.S. children with asthma today is muchhigher than it was 30 years ago, rising rom 2.1 million in1980 to 7.1 million in 2009.108 Today, it is the most commonchronic childhood disease in the U.S. (see Figure 8).

Asthma is the leading cause o hospital admission amongurban children, with over 200,000 hospitalizations every year.Asthma is also the top cause o days lost rom school, withmore than 10.1 million school daysmissed every year.109 Missed school daysin turn negatively impact academic

perormance, such that children withsevere asthma symptoms are more likelyto suer academically than childrenwith milder symptoms.110

Asthma disproportionately aectspeople o color. Data rom 2009 showthat roughly one in six (17 percent)non-Hispanic black children hadasthma in 2009, the highest rate amongany racial/ethnic group. Overall, boysare more likely than girls to suer romasthma (11.3 vs 7.9 percent) rom birth

through adolescence. As adults, womenare more likely to be asthmatic thanmen.111, *

The ScienceMany studies have explored the relativeimportance o common respiratory

* InMay2012,thePresidentsTaskForceonEnvironmentalHealthand SafetyRisk stoChildrenreleasedtheCoordinated Federal Action Plan to Reduce Racial and Ethnic Asthma Disparities.Theeortlaysoutaplantoaddressthiscrucialpublichealthchallengeduringthenextthreetoveyears.Seehttp://www.epa.gov/asthma/childrenstaskforce.

Figure 8: AsthmaPrevelencebyAgeandSexinU.S.,20012009

irritants in the home environment to triggering the onset oasthma, including cockroaches, dust mites, molds and air pol-lutants. Many pesticides are considered respiratory irritants,and studies suggest that pesticide exposures may play a role intriggering asthma attacks, exacerbating symptoms, or height-ening the overall risk o developing asthma.112

Pesticides may also play a role in increasing asthma inci-dence by aecting the bodys immune system, triggeringeither hypersensitivity or suppression o the bodys immune

response. Allergic responses, or example, are a hyper-sensitivity o the immune system to an allergen in theenvironment.113

Numerous studies have documented the association opesticides and asthma incidence or adults, and more recentstudies have examined potential links to both asthma inci-dence and triggering or exacerbation o wheezing episodesamong children.

Inastudyofover4,000childrenfrom12southernCalifor-nia communities, exposure to pesticides in the frst year olie signifcantly increased the risk o being diagnosed withasthma by age fve.114

Across-sectionalstudyof3,291Lebaneseschoolchildrenound a potential association between childhood asthmaand parental occupational exposure to a range o currentuse pesticides.115

InSpain,childrendiagnosedwithasthmaatagesixhadhigher levels o cord serum DDE at birth than childrenwithout asthma. And in a study o 343 German childrenaged 710 years who had the DDT breakdown product

SeetheRecognition and Management o Pesticide PoisoningspageofEPAsNationalPesticideInformationCentersite:http://npic.orst.edu/health/child.html

Today,morethansevenmillionchildrenhaveasthma,upfromjustovertwomillion 30 years ago.

SourceCentersforDiseaseControlandPrevention,VitalSigns:AsthmaintheU.S.Seehttp://www.cdc.gov/VitalSigns/Asthma/index.html,viewedMay2012.



DDE present in their blood, the risk o havingasthma was signifcantly higher.116,*

Childhoodexposuretoorganophosphate,carbamateand pyrethroid insecticides may trigger or exacerbateasthma symptoms among children by promotingbronchial constriction.117

Recognizing the rising prevalence o asthma amongU.S. children, Dr. David Schwartz recently calledon ellow researchers to ocus more attention on thepotential links between exposure to air pollutants andenvironmental contaminants like pesticides and child-hood asthma.118

* Thesemeasurementsweretakenfrombloodserumandwerethoughttorepresentearlylifeorprenatalexposures,buttheactualrouteofexposurewasnotknown.

Traditional toxicology relied or years on the mantra thedose makes the poison. We now know that this statementis, in many cases, simply inaccurate. It assumes that thelevel o harm always increases as the level o exposuregoes up (i.e., that every dose response curve ollows a

linear pattern). Assuming a higher dose is always moredangerous, policymakers oten base regulations on alevel below which no health risks is expecteda saethreshold. The reality, as scientists now understand, isquite dierent.

For some pesticides, the linkage between exposure andeect actually ollows a-shaped curve. In this scenario,a very low dose elicits a high level o response or healthharm. At a higher dose that is along the bottom o the, this same chemical elicits little or no response. Thenat the highest doses, the eects increase again. For otherpesticides, an inverted -shaped curve can occur, whereintermediate doses cause the greatest response, and testing

at high doses can completely miss the eect.Given these complex dose-response patterns, picking athreshold dosebelow which exposure can always beconsidered saeis simply not possible. Throw into themix the dramatic dierences in how sensitive individuals

may be to chemical exposures, plus the vulnerabilities ochildren at particular times during development, and itquickly becomes clear that it is much more than the dosethat determines how much harm a pesticide will cause.*

* Vandenberg,L.,T.Colborn,T.Hayes,J.Heindel,D.Jacobs,D.H.Lee, etal.HormonesandEndocrine-DisruptingChemicals:Low-DoseEectsandNonmonotonicResponses. EndocrineReviews.March201233(3):378-455.

High

Low

Low High

Dose

Response

Rethinking SafeWhy the dose does not make the poison


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when pesticides are used in homes or daycare acilities,exposure is a near certainty. Inhaling spray droplets, vaporsor pesticide-contaminated dust rom indoor use o pesticideproducts is one o the primary routes o exposure or manyU.S. children. Pesticides used to control ticks and eas onpets are another important source o childrens exposure.125

One Massachusetts study ound residues o DDT in housedust many decades ater use o the chemical had been discon-tinued.126 Even pesticides that are relatively short-lived in theenvironment are more persistent indoors; one study ound thesemi-volatile insecticide chlorpyrios to be longer lasting thanexpected in closed apartments, detectable or more than twoweeks on rugs, urniture, sot toys and pillows.127 Pesticidevapors oten settle ater application indoors, so levels tend tobe highest in the inant breathing zone.128

Exposure rom home lawns and gardens or outdoor play areasat daycare centers can also be signifcant. Children oten rolland play on lawns and sit or lie on bare soil, and toddlers areknown to put dirt directly into their mouths.129 I pesticideshave been used in these areas, the likelihood o ingestion orinhalation is high.

In rural communities, the risk may be compounded by dritrom nearby agricultural felds. A study conducted in Wash-ington State ound residues o several agricultural pesticidesincluding chlorpyrios and ethyl parathionin outdoor playareas.130 Air monitoring studies using PANs Drit Catcher in

Caliornia and Minnesota have documented a range o agri-cultural pesticides in backyards and play areas as well.131, 132

Rural inants and toddlers also ace potential exposure romdrit directly into their homes, and rom pesticide contami-nation o water supplies. Water sampling results rom Illi-nois, Nebraska, Iowa and Minnesota detected the commonherbicide atrazine at levels above those linked to low birthweight.133 Young children in armworker amilies ace addi-tional exposure rom residues carried into the home on thebodies and work clothes o working amily members.134

At school & on playgroundsPesticides used in school buildings can settle on desks, books,counters and walls. When children touch contaminatedsuraces, they may absorb chemical residues that can remain

in the school environment or days. Herbicides used to keepplaying felds ree o weeds may be picked up on childrenshands, bodies, clothes and tennis shoes, or drit into class-rooms ater application.

According to one recent national review, o the 40 pesticidesmost commonly used in schools, 28 are probable or possi-ble carcinogens, 26 have been shown to cause reproductiveeects, 26 damage the nervous system, and 13 have beenlinked to birth deects.135

In rural areas, pesticides oten drit into schoolyards duringand ater spraying on nearby felds. Community air monitor-ing studies across the country using the Drit Catcher device

have documented pesticides in or near school grounds in agri-cultural communities,136 and incidents o pesticide poisoningsin schools are not uncommon. For example:

InFlorida,highschoolstudentsusedaDriftCatchertomeasure the pesticides endosulan, diazinon and triuralin*driting into the school rom nearby cabbage felds.137

* EndosulfaniscurrentlybeingphasedoutintheU.S.,andalsogloballyundertheStockholmConventiononPersistentOrganicPollutants.Seehttp://www.epa.gov/oppsrrd1/reregistration/endosulfan/endosulfan-cancl-fs.html.

Children as Farmworkers

Some children are exposed to pesticides as they workin agricultural felds. Specifc rules vary rom state tostate, but ederal law allows children under 12 to dofeld work outside o school hours on arms where theirparents are employed.*

Age restrictions or hazardous work such as applying

pesticides are more lenient in the agriculture sector,and age restrictions simply do not apply or childrenworking on arms owned or operated by a parent orguardian.

Documenting the exact number o child workersin U.S. agriculture is difcult, and estimates varywidely. A Human Rights Watch report published in2000 put the number somewhere between 300,000and 800,000. The nonproft group Toxic Free NorthCarolina recently documented the experience andvoices o young armworkers acing pesticide exposurein the feld; the stories can be viewed at www.panna.org/youngarmworkers.

* U.S.Dept.ofLabor.ChildLaborRequirementsinAgriculturalOccupationsUndertheFairLaborStandardsAct.June2007.Seehttp://www.dol.gov/whd/regs/compliance/childlabor102.htm.

HumanRightsWatch. Fingers to the Bone: United States Failure to Protect ChildFarmworkers. Washington:HumanRightsWatch,2000.

NationalCenterforFarmworkerHealth.Child Labor. Buda,Texas.2009.Seewww.ncfh.org/docs/fs-Child%20Labor.pdf

Davis,S.andJ.B.Leonard,The Ones the Law Forgot: Children Working in Agriculture,FarmworkerJustice,WashingtonDC.2000.

Evidenceshowsthatwhenpesticidesareusedathome,onpetsorindaycarecenters,childrensexposureisanearcertainty.


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Why children are particularly vulnerableSo what do all o these well-documented pesticide exposurepathwaysmeanforchildrenshealth?

In their frst six months o lie, children take in roughly 15times more water than the average adult per pound o bodyweight.147 Children also inhale more air. Up to around age12, a childs breathing rate is roughly twice that o an adult,which means a child will inhale roughly double the dose o apesticide in the air rom spray drit or household use.148

Exposure to pesticides occurs largely through touching, inhal-ing or ingesting. For each o these routes, children are muchmore likely to absorb what they come into contact with thanadults. The skin o inants and young children, or example,is particularly permeable, and the skin surace area relative tobody weight is much greater in children than adults.149 Thelung surace area relative to rate o breathing is also higheramong children,150 and absorption levels in the gastrointes-tinal tract are also greater (especially or alkaline pesticides),as adult levels o gastric acid are not reached until a child isabout two years old.151

As noted above, the brain and nervous system are especiallyvulnerable during etal development and or the frst sixmonths o lie. During this period the blood-brain barrier,*which provides the adult nervous system some protectionrom toxic substances, is not yet ully developed.152

Finally, young bodies are less equipped to process and excreteharmul chemicals as the liver and kidneysthe bodysprimary detoxiying organsare not yet ully developed. Lev-els o enzymes that help the body process chemicals are alsonot yet at ull strength (see sidebar). Genetic variations leadto tremendous range in the production o these protectiveenzymeswith some newborns as much as 164 times morevulnerable to chlorpyrios than less sensitive adults.153

According to researchers, this fnding alone means that most,i not all inants and toddlersas well as a subpopulation oadultsare much more likely to have adverse health eectsrom organophosphate exposure. Policies that dont accountor this variability ail to protect the most vulnerable, leavingmany children in harms way.

* Theblood-brainbarrierismadeupofhigh-densitycellsthatprotectthebrainfrompotentiallyharmfulsubstancescirculatinginthebloodstream.

Mechanisms of HarmWhen enzymes dont detoxiy

Enzymes are proteins that catalyze reactions ona molecular level, and there are many that occurnaturally in the human body. Without enzymes tocatalyze reactions, some o the chemical reactions thatmake up the normal unctioning o our body could

take much longer, or not happen at all.One key human enzyme, known as paraoxonase 1 (orPON1), catalyzes the metabolic process that rendersorganophosphate pesticides and other compoundsless harmul to our systems. Researchers say inantshave very low levels o this enzyme up to age two, andchildren dont reach adult PON1 levels until about ageseven.* This suggests that children are less protectedrom harmul contaminants by enzyme activity, andnewborns may be especially vulnerable.

There is also tremendous natural variability in thelevel and eectiveness o the PON1 enzyme, whichmeans some individuals are much more susceptible to

health harms o organophosphate pesticides and othercontaminants.

* HuenK.,K.Harley,A.Bradman,B.Eskenazi,N.Holland.LongitudinalchangesinPON1enzymaticactivitiesinMexican-Americanmothersandchildrenwithdierentgenotypesandhaplotypes. Toxicol Appl Pharmacol.2010.244(2):181-9.Seehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2846980/?tool=pubmed

Holland,N.,C.Furlong,M.Bastaki,R.Ricther,A.Bradman,K.Huen,etal.ParaoxonasePolymorphisms,Haplotypes,andEnzymeActivityinLatinoMothersandNewborns.Environ Health Persp.July2006114(7):985991.Seehttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC1513322/.

The human body undergoes rapid growth and development throughoutchildhood, with many processes vulnerable to disruption rom pesticides andother chemicals.


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Pesticide use at homeWhile 80 percent o all pesticides are applied in agriculturalfelds, use in homes, gardens, playgrounds, schools, hospitalsand other buildings is also signifcantand as noted above,such uses pose a particular risk to childrens health.

In 2007, an estimated 78 million pounds o pesticides(measured by active ingredient) were applied in homes andgardens across the country, with the herbicides 2,4-D andglyphosate (RoundUp) topping the list.161 The household

pesticide product industry has an estimated annual net wortho $1.4 billion; according to EPA, more than 78 millionhouseholdsroughly 74 percent o all households in theU.S.report using pesticides at home (see Table 5).162

Many home-use insecticides contain pyrethroids, and thechemicals are used extensively in homes where the potentialor exposure to children is very high. Researchers rom EmoryUniversity and the CDC ound that even children ed anexclusively organic diet had pyrethroid metabolites in theirsystems ater their parents had used pyrethroid insecticides intheir homes.163

Neonicotinoid products are widely used in pet products tocontrol eas and ticksanother use which poses particularlyhigh exposure risks or children.164

Safer pest control at schools & daycare centersMore than 3,000 pesticide products are currently approvedor use in schools;165 yet current national pesticide rules donot address the use o pesticides in and around schools ordaycare centers. The ederal School Environmental Protec-tion Act (SEPA) was frst introduced in November 1999 inan attempt to address this oversightand it continues to bedebated in Congress today.

In the non-proft sector, the national Childrens Environmen-tal Health Network (CEHN) moved to fll this gap by creat-ing the Eco-Healthy Child Care (EHCC) program to provide

Herbicides are the most commonly used type opesticide in the U.S., with 531 million pounds o activeingredientappliedin2007.Source:Pesticide Industry Sales &Usage, 2006 and 2007 Market Estimates,U.S.EPA,Washington,DCFeb

2011.Seewww.epa.gov/opp00001/pestsales/07pestsales/market_

estimates2007.pdf.

tools that acilities need to create environmentally healthyspaces or children. Today, the program endorses over 1600

Eco-Healthy daycare acilities across the country and pro-vides this list to parents online.*

Meanwhile, several states are moving orward with policiesdesigned to protect children rom pesticides in these earlyenvironments.

In2005Connecticutlawmakersprohibiteduseofpesti-cides on K8 lawns and playing felds; in 2009, the law wasextended to daycare center grounds. Through this policy,schools have successully implemented organic tur pro-grams in various municipalities.166

NewYorkfollowedsuitin2010,signingtheChildSafePlaying Fields Act into law to ban the cosmetic use o pesti-cides on playgrounds and sports felds at schools (includinghigh schools) and daycare centers.167

* Seehttp://www.cehn.org/ehccformoreinformationaboutthisprogram.

Table 5: Households Using Pesticides

Pesticide Type # Households

Insecticides 59 million

Fungicides 14 million

Herbicides 41 millionRepellents 53 million

Disinectants 59 million

Any pesticides 78million

Table 4: Pesticide Usage in All MarketSectors,2007

Pesticide Class Active Ingredient

Herbicides 531 million lbs

Insecticides 93 million lbs

Fungicides 70millionlbs

Fumigants/Nematicides 133 million lbs

Other 30 million lbs

Total 857 million lbsAccordingtoEPA,morethan78millionhouseholdsroughly74percentofallhouseholdsintheU.S.usepesticides at home.Source:EPAestimatesbasedonthe1992EPANationalHomeandGardenSurveyand2000U.S.CensusBureau

populationestimates(www.quickfacts.census.gov/qfd/states).

Toprotectchildrenshealth,severalstateshaveputpoliciesinplaceprohibitingthe use o pesticides on playing felds and playgrounds.



ManyschooldistrictsinCaliforniahavesignicantlyreduced pesticide use ater a 2000 state law requiredpesticide reporting and provided incentives oradoption o IPM. School districts in Los Angeles, SanFrancisco, Santa Barbara and Palo Alto have madeparticular progress.168

In2001,Californialegislatorspassedalaw(AB947)allowing county agricultural commissioners to restrictpesticide spraying near sensitive sites, includingschools and daycare acilities. Under this provision,communities in Tulare County won new rules in 2008requiring a quarter mile buer zone banning the aerialapplication o restricted-use pesticides around schoolswhen they are in session or due to be in session within24 hours, occupied arm labor camps and residentialareas.169 Kern, Stanislaus, Merced and Fresno countiesenacted similar rules in subsequent years.

Pesticide-free school lunchesCurrently, neither state nor national policies are inplace to reduce pesticide residues in school lunches. Butmany communities across the country are leading the

way to provide children with nutritious school lunchesincluding resh (sometimes locally produced) ruits andvegetables ree rom pesticides.

InWashingtonstate,theOlympiaSchoolDistricthas implemented an Organic Choices Salad Bar (25percent o the produce is purchased directly rom localarms and 50 percent o the salad bar is organic), andthe Orcas Island Farm-to-Caeteria Program integratesproduce rom local, organic armers and a schoolgarden, and hosts student che competitions.

InMinnesota,theWhiteEarthLandRecoveryProjectadded a arm-to-school component in the 20072008school year to their Mino-miijim (Good Food) Pro-

gram to help reach their goal o ood sovereignty onthe reservation and promote access to resh, local andorganic ingredients.170

Berkeley,CaliforniasEdibleSchoolyard(ESY)Projectbegan as a one-acre interactive classroom providingprimarily organic, resh ruits and vegetables or stu-dents meals at King Middle School. It has grown intoan online initiative building and sharing a ood curric-ulum, and it has inspired similar programs across thecountry.171

Many o these programs are part o the National Farm toSchool Network (NFSN), which connects K12 schools

across the country with local arms in an attempt toserve healthy meals at school lunch tables while support-ing local, oten organic, armers.172

Parks & playgrounds without pesticidesCommunities across the country are choosing to managepublic parks and playgrounds without harmul pesti-cides. In the Pacifc Northwest, 17 cities are phasingout pesticide use with the creation o 85 pesticide-reeparks and playgrounds, building momentum or strongpolicies at the local level despite legislative hurdles (seesidebar on ollowing page).173

At What Cost?Economic impacts o health harms

The impact on amilies o caring orand sometimeslosinga child in ill health cannot be reected in monetaryterms. Nor can the incalculable costs o lowered IQ, lostopportunities and social alienation that can accompanydevelopmental eects. But actual costs o providing medicalcare or a child with a chronic condition or illness can becalculated, and according to public health ofcials, healthcare costs or childhood diseases are signifcant. Here aresome examples:

ADHD: Researchers estimate annual ADHD health carecosts in the U.S. to be between $36 and $52 billion (in2005 dollars).*

Autism: One analyst at the Harvard School o PublicHealth estimates that it costs $3.2 million to care or anautistic person over their lietime.

Cancer:The total costs per case o childhood cancerrom treatment, to laboratory costs to lost parentalwagesis an estimated $623,000 per year. This

translates into a society-wide cost o roughly $6.5 billionannually or the 10,400 newly diagnose

kids health report oct 2012

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