overexposed || organophosphate insecticides in children's food

7/30/2019 Overexposed || Organophosphate Insecticides in Children's Food

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W O R K I N G G R O U PT M

E N V I R O N M E N T A L Richard Wiles Kert Davies Christopher Campbell

OverexposedOverexposedOverexposedOverexposedOverexposedOrganophosphate Insecticides in

Childrens Food


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Acknowledgments

Special thanks to Molly Evans who designed and produced the report, and to Allison Daly for coordinating therelease ofOverexposed. We are grateful to Ken Coo k and Mark B. Childress for ed iting an d insight.

Overexposedwas m ade po ssible by grants from The Pew Charitable Trusts , the W. Alton Jones Foun dation, the

Joyce Foun dation, and the Wo rking Assets Funding Service. The op inions e xpressed in this rep ort are those of theauthors an d d o n ot ne cessarily reflect the views o f The Pew Charitable Trusts or other sup po rters l is ted abo ve.Environm ental Working Grou p is respo nsible for an y errors of fact or interpretation contained in this rep ort.

Copyright January 1998 by the Environm ental Working Group /The Tides Center. All r ights reserved.Manu factured in the United States of Ame rica. Printed on recycled pap er.

Environmental W orking G roup

The Environmental Working Group is a nonprofit environmental research organization based in Washington,D.C. The Environm en tal Workin g Group is a pro ject of the Tides Center, a Californ ia Public Ben efit Corpo rationbased in San Francisco that provides administrative and program support services to nonprofit programs and

projects.

Kenneth A. Cook, Presiden tMark B. Childress, Vice Preside nt for Po licyRichard Wiles, Vice President for Research

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FO R EW O RD . . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . i

EXECUTIVE SU M M A R Y . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . 1

C H APTER 1 . IN T R O D U C T I O N . . . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . 9

C H APTER 2 . O R G A N O P H O S P H A T E TO X I C I T Y . . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . . . . . . . . .. 13

C H APTER 3 . D A TA SO U R C E SA N D M E T H O D O L O G Y . . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . 21

C H APTER 4 . FI N D I N G S . . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . . 33

REFEREN CES . . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . .. . . . . . . . . . . . . . .. . . . . . . . . . . . . . 45

Contents

O verexposed


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iEN V I R O N M E N T A L W O R K I N G G R O U P

Foreword

O verexposed

With Oprah Winfreys fooddisparagement trial underway asthis study goes to print, were notsure if we sho uld send repo rters apress release o r read them theirMiranda rights.

We all have the right to remainsilent about risks in the food sup-ply; silence w ou ld suit ma ny inthe a gribu sine ss wo rld just fine .In publishing Overexposed, EWGhas emphatically chosen insteadto exercise our First Amendmentright to highlight concerns aboutfood safety, specifically, that manydifferent types of foodspeaches,

apples, nectarines, and popcorn,to name the top of the listareroutinely contaminated with levelsof organop hosp hate insecticidesthat are unsafe for infants andchildren u nde r the age o f 5 yearsold. Based on more than 80,000government lab test results fromrecent years, and detailed data onchildrens food consum ption hab -its, our a nalysis sho w s that the

average 25po und one -year-oldcould receive an unsafe dose ofneurotoxic pesticides from eating

just a fe w b ite s o f so m e o f th emore contaminated foods.

It is possible, even likely, thatexposure to organopho sphateinsecticides in the most contami-

nated food is even now produc-ing imme diate, flu-like symp -toms of ne urotoxic p oisoningamong some unlucky children:he ada che s, nau sea, irritability.The mo re wo rrisome threat, of

course, is the more subtle, longterm damage that may becaused from comb inations o f 13different organo ph osph ate in-secticides foun d b y governme ntlab tests in a wide array offoo ds. The risk is that harmmay be don e to many thousandsof children over many years,starting in the wo mb . The orga-nophosphates are related chemi-

cally to nerve gases like Sarin(used to lethal effect by terror-ists in Tokyos sub w ay), andcause all man ner o f problems tothe nervous system, up to an dincluding brain dam age an d im-pairment of intelligence.

The EPA must act immedi-ately to eliminate the threatthese insecticides pose to chil-

dren and the rest of us. Thestep s w e o utlinebann ing a lluse of these comp ound s for bugcontrol in the home and oncrops used to make bab y food,for startersare prudent andnecessary measures in line witha ne w pe sticide law Congresspassed unanimously in 1996.

The EPA m ust actimmediately toel iminate the threatthese insecticides poseto children and therest of us.

W e plan to keeptalking about these

poisons and the foo dsthey contaminate unti lEPA h as don e its job.


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i i O V EREXPO SED : O R G A N O P H O S P H A T E IN SECTICID ES IN C HILDREN S FO O D

That law mend ed some majorholes in the regulatory safety netfor pe sticides in food .

Now that the law is in effect,

EPA has all the tools it needs to

end the overexpo sure of chil-dren to organop hosphate bugkillers. We plan to keep talkingabout these poisons and thefoods they contaminate until EPA

has do ne its job.

Kenneth A. Coo k

President

Environ me ntal Working

Group


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1EN V I R O N M E N T A L W O R K I N G G R O U P

Executive Summary

O verexposed

Every day, nine out of tenAme rican children betwe en theages of 6 months and 5 years areexpo sed to com binations o f 13

differen t ne urotoxic insecticide sin the foo ds the y eat. While theamounts consumed rarely causeacute illness, these organophos-phate insecticides (OPs) havethe potential to cause long termdamage to the brain and the ner-vous system, which are rapidlygrowing and extrem ely vulner-able to injury du ring fetal de vel-opment, infancy and early child-

h o o d .

Based on the most recentgovernme nt data available onchildren s e ating pa tterns, p esti-cides in food, and the toxicity oforganop hosp hate insecticides,we estimate that:

Eve ry da y, m o re th a n on emillion children age 5 and

und er (1 out o f 20) eat anunsafe dose of organo-ph osph ate insecticides.One hundred thousand o f these children exceed theEPA safe d ose, the so-called reference dose (seep. 3), by a factor of 10 ormore.

For in fan ts six to twelvemo nths of age, com me rcialbaby food is the dominantsource of unsafe levels of

O P insecticides. O Ps inbaby food app le juice,pears, applesauce, andpeaches expose about77,000 infants each day, toun safe levels of O P insecti-cides.

This estimate very likely un-derstates the n um ber o f childrenat risk because our analysis does

not include residen tial and otherexposures to these comp ound s,wh ich can be substantial, andbecause EPAs estimates of a safedaily do se (the so-called refer-ences do se or RfD) are based onstudies on adult animals or adulthum ans, and almost never in-clude additional protections toshelter the young from the toxiceffects of OPs.

Our analysis also identifiedfood s that exp ose youn g childrento the most toxic doses of thesepe sticides. We found that:

O n e o u t o f e ve ry fo u r tim e sa child age five or undereats a peach, he or she is

O rganophosphateinsecticides have thepotential to cause longterm dam age to the

brain and the nervoussystem , w hich arerapidly growing andextremely vulnerableto injury during fetaldevelopment, infancyand early childhood.


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2 O V EREXPO SED : O R G A N O P H O S P H A T E IN SECTICID ES IN C HILDREN S FO O D

Likelihood of being

exposed to an unsafeFoods dose of O Ps

Peaches 2 4 . 8 %

A p p l e s 1 2 . 9 %

Ne c t a r i n e s 1 2 . 2 %

Po p c o rn 8 . 5 %

Pears 7 . 5 %

Cornbread 5 . 6 %

App lesauce 5 . 2 %

G ra p e s 5 . 1 %

C o r n C h i p s 4 . 5 %

Pears (baby foo d) 3 . 8 %

Rais ins 3 . 3 %

Cher r ies 3 . 2 %

K i w i 2 . 9 %

Peaches (baby food) 2 . 4 %

Ap p le Ju ice (baby food ) 2 . 0 %

Table 1. O ne out of every four t imes a child under 6 eatspeac hes, he or she is expo sed t o an unsafe dose oforganophosphate insecticides.

exposed to an unsafe levelof O P insecticides. Thirteenpe rcent of the app les, 7.5percent of the pears and 5pe rcent of the grapes in theU.S. foo d sup ply expo se theaverage youn g child eatingthese fruits to u nsafe levelsof O P insecticides (Table 1).

A sm a ll b u t w o r riso m e p e r -cen tage o f the se fruits 1.5 to 2 percent of theapples, grapes, and pears,and 15 percent of thepeaches are so contami-nated w ith OPs that the av-erage 25 pound one year

old eating just two grapes,or three bites of an ap ple,pe ar, or pe ach (10 gramsof each fruit) w ill excee dthe EPA (adult) safe daily

dose of OPs.

Th e fo o d s th at ex p ose th emost children age sixmo nths through five yearsto unsafe levels of OPs(because they are moreheavily consum ed) areapp les , peaches ,app lesauce, popcorn ,grapes, corn chips, and

ap ple juice. Just over halfof the children that eat anunsafe level of OPs eachday, 575,000 children, re-ceive this unsafe dose fromapple products alone(Table 2).

Ma n y o f th e se e xp o su re sexceed safe levels by widemargins. OPs on apples,

peaches, grapes, pear babyfood and pears cause85,000 children e ach day toexceed the fede ral safetystandard by a factor of tenor m ore (Table 2).

This Environmental WorkingGrou p study utilizes detailedgovernmen t data on food con-sump tion patterns and pe sticide

residues to conduct the firstcomprehensive analysis of thetoxic dose that infants an d ch il-dren receive when the entireorganop ho sphate family of in-sect killers is assessed in com bi-nations, an d a t levels, that actu-ally occur in the food supply.

So u r c e : EW G , c o m p i l e d fr o m U SD A f o o d c o n su m p t i o n d a ta 1 9 8 9 - 1 9 9 5 ,U SD A and FD A pest i c i de r esidue d a ta 1991-1 996 and re fe renc e do ses (RfD s) ob ta ined f r om EPA in January 19 98 .


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Children exceeding

C hildren exceeding ten t im es the

"safe" dose/ day "safe" dose/ day

A p p l es 4 0 8 ,6 8 0 3 4 ,6 0 0

Peac h es 7 7 ,4 4 0 3 0 ,9 0 0

A p p l esau c e 7 0 ,1 5 0 0

Po p c o rn , p o p p ed i n o i l 6 8 ,3 7 0 8 8 0

G rap es 5 4 ,6 3 0 1 2 ,5 6 0

C o rn Ch ip s 5 3 ,0 8 0 7 1 0

A p p l e Ju ic e 4 6 ,0 6 0 1 8 0

O at Rin g Cereal 4 5 ,6 0 0 0

A p p l e Ju ic e (b ab y fo o d ) 4 3 ,4 0 0 0

Pears (b ab y fo o d ) 3 3 ,0 6 0 4 ,6 1 0

C o rn b read 2 7 ,8 1 0 3 ,7 0 0Raisi n s 2 1 ,8 0 0 2 ,2 3 0

Pears 1 7 ,4 2 0 4 ,0 4 0

A p p l esau c e (b ab y fo o d ) 1 0 ,9 8 0 0

Peac h es (b ab y fo o d ) 1 0 ,9 7 0 0

A pple products total 5 7 9 ,3 0 0 3 4 ,8 0 0

Total (all foods) 1 ,1 4 2 ,5 0 0 1 0 6 ,6 0 0

Table 2. App les and apple products account for over half of theunsafe organoph osphate e xposure for child ren u nder six.

So u r c e : EW G , c o m p i l e d f r o m U SD A f o o d c o n su m p t i o n d a ta 1 9 8 9 - 1 9 9 5 , U S D A a n d F D Ap esti c i d e re si d u e d ata 1 9 9 1 -1 9 9 6 an d re fe re n c e d o ses (Rf D s) o b ta i n ed fr o m EPA i nJanuary 1 998 .

EPAS SAFETY ST A N D A R D S: TH E REFEREN CE D O SE

This repor t is based o n the m ost recent ly ca lcu la ted re ference d ose va lues used b y EPAscient is ts, obta ined d i rect ly f rom the EPA in January 1 99 8. A re ference do se is theagency s determ inat io n o f a safe da i ly do se o f a pest ic id e, exp ressed in m i l l i g rams ofpest ic id e per k i l ogram o f bo dy w eight per day (m g/kgbw /day) . A l l o f these re ference dosesrepresent f ina l agency dec ision s, except that fo r ch lorp yr i fos . In ear ly January 1 99 8, the

re ference dose co m m it tee o f the O f f ice o f Pest ic id e Programs recom m ended that there ference do se for ch l orpy r i fos have an add i t ion a l ten- fo ld safe ty fac tor , per therequ i rem ents o f the Foo d Q ual i ty Pro tection Ac t to pro tect in fants and ch i ld ren f rompest ic id es. The re ference dose com m it tee is the pest ic id e program c om m it tee o f sc ient is tsch arged w i th m aking recom m endat ion s for pest ic id e safety standards un der the FQ PA.G enera l l y , r ecom m enda t ions fr om the reference dose com m i t tee have been ado p ted asagency hea l th standards.


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H

ypotheticalExposure

to

O

Ps(dose)

EPA "Safe" D ose (RfD )

O rganophosphate insect icides w ere

regulated individual ly pr ior to 199 6 Food

Q ual i ty Protect ion Act

U n d er 1 9 9 6 F Q PA :

Cum ulat ive exposure to

O Ps is now regulated

Figure 1. U nder the 19 96 Food Q uality Protection Act, theEPA now m ust regulate cum ulative exposure to pesticidesw ith sim ilar health effects.

The s tudy w as prompted b ythe 1996 Food Quality ProtectionAct, which requires the govern-me nt, for the first time, to co n-sider the total risk posed to hu-

mans wh en they are expo sed toany and all pesticides that have acomm on mo de o f toxic actionan d a similar type o f effect. Priorto 1996 law, the governme nt de-termined a separate, safe levelof exposure for each of the d oz-ens of registered pesticides foundin food, but did not regulate as agroup chem icals that prod uce thesimilar he alth problem s. The

new law further required specificpro tection s for infants and chil-dren, who are more vulnerableto pesticides and other toxins.

Rece ntly, the Environ me ntalProtection Agen cy (EPA) con -cluded that the organophos-phates have a common toxicmechanism, and that exposure tocombinations of the chemicals

should b e co nsidered in sett ing asafe dose (Figure 1).

FQ PA M andates Extra Protect ionfor Kids

The Food Quality ProtectionAct (FQ PA) req uires EPA to actto protect infant and child health,even in the absence of total sci-entific certainty regarding the

toxicity or exposure of pesticidesto the fetus, infant or youngchild. This is a dra m atic reve rsalof previous statutory require-ments whe re EPA had n o m an-date, and a rguably could no t actto p rotect the pu blic he alth, evenchild h ealth, in the absen ce ofcomp lete data on the risk from a

So u r c e : En v i r o n m e n t al W o r k i n g G r o u p .

Before FQ PA

AfterFQ PA


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pe sticide. Now the law is clear.In the absence of complete andreliable data on pre- and po stna-tal toxicity and exposure to ape sticide, the EPA must err on

the side of child safety and ap-ply an add itional ten-fold m arginof safety to food tolerances forthe p esticide (FQ PA section408(b)(2)(C)(ii)(II)).

Contrary to the clear require-ments of the law, the EPA hasdevised and imp lemen ted anofficial policy in response toFQPA that d isregards the re-

quirement for a ten-fold safetyfactor (SAP 1997, EWG 1998,Cushma n 1997). This p olicyplainly unde rmines protection ofthe n ation s children from pe sti-cide s. If the ne w ten-fold safetyfactor were applied to all orga-nop hosp hate insecticides foundin food, we estimate that nearly3.6 million children age 5 andunder w ould be expo sed to lev-

els of the se p esticides in foodthat would exceed the n ew s tan-dard .

H igh Risk Pesticid es

Analysis of more than 80,000samples of food inspe cted bythe federal government for pesti-cide residues from 1991 through1996, revealed that 13 organo-

ph osph ate insecticides w erefound in or on food by the Foodand Drug Administration and theU.S. Department of Agriculture.

The h ighest risk O P com-pounds are methyl parathion,dimethoate, chlorpyrifos,pirimipho s methyl, and azinp hos

methyl which account for morethan 90 percent of the risk fromOP insecticides in the infant andchild diet.

Achieving a safe food supplyfor children, however, is not assimple as banning the five high-est risk OPs. Hom e and othernon-food uses must be consid-ered, as well as the fact that otherOPs will likely substitute forthose that are ban ned in the firstw ave of standard setting. Andmo st imp ortantly, infant an d childsafety must be me asured in terms

of safety standards designed toprotect these children, not interms of the current adult-basedstandards.

Conclusions

American children are rou-tinely exposed to unsafe levels ofOP insecticides in the food theyeat. On an y given day we esti-

mate that mo re than o ne millionchildren u nde r age six exceedfed eral safety standard s for OPs.One hund red thousand o f thesechildren e xceed these sam e stan-dards by a factor of 10 or more.The potential public health im-pact of these expo sures is sub-stantial, but as yet is not preciselyunders tood.

For perspective, it is helpful toview the situation with OPsthrough the lens of expe riencewith lead. For years lead wasknown to be toxic, but its specialhazards to children, while sus-pe cted, w ere difficult to co nfirm.On ly recently has science bee nable to bring into focus the

Am erican children areroutine ly exposed tounsafe levels of O Pinsecticides in thefood they eat .


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subtle, yet profound learning defi-cits that result when infants andchildren are exp osed to levels oflead tha t are p erfectly safe foradu lts, and that we re thought, un-

til recently to be safe for childrenas well.

In some ways, the situationwith OPs may be worse than leadbecau se significant nu mb ers ofinfants and children receive dailydoses of multiple OPs that far ex-ceed the safe do se for an adult . Itis proba ble that these high OPexposures early in life are causing

long term functional and learningdeficits that scientists are just be-ginning to un derstand.

Given this overwhelming evi-dence of unsafe exposure to orga-nop hosp hate insecticides in thediet, EPA has little choice but toact to protect infants and children.The solution to the p roblem ofunsafe levels of OPs in food,

how ever, is notfor children to eatless fruits and vegetab les. Infants,children and pregnant wom enshould be able to eat a diet rich infruits and vegetables without anyconcern about short term illnessor long term brain and nervoussystem d amage that may resultfrom unsafe levels of OP pesti-cides on these food s. The solu-tion is to rid the se h ealthful foo ds

of the m ost toxic pesticides.

Recommendations

To begin to mee t the req uire-ments of FQPA and retain thegreatest number of safe pesticidesfor farme rs, several de cisive b ut

reasonable steps must be made.These actions w ould redu ce riskfrom O Ps to a level dee me d ac-ceptable un der current EPApo licy. We must emp hasize

again, however, that current EPAsafety standards do not yet in-corporate e xplicit or ad equ atepro tection s for infants and chil-dren . Until reliable data on fetaland infant toxicity are availablefor all OPs, the actions recom-mended here, while significant,must be viewed as first steps inan o ngoing p rocess of protectinginfants and children from OP

insecticides.

First, all home and otherstructural use of O P insecticide smust be banned. These usesput a small but significant num-ber of infants and toddlers atextremely high risk, and in do-ing so jeopardize current agricul-tural uses of these co mp oun ds.Indeed , if food uses of any O Ps

are to be retained, all non-fooduses w ith po tential to e xpo sepregna nt wo men , infants or tod-dlers must be banne d.

Second, at least five high riskOPs, me thyl parathion,dimethoate, chlorpyrifos,pirimipho s methyl, and azinph osmethyl, must be banned imme-diately for all agricultural use.

Third, all OPs mu st bebanned for use in food that endsup in commercial baby food.

Fourth, EPA must require de-velopmental neurotoxicity stud-ies for all the remaining OPs

G iven th isoverwhelmingevidence of unsafeexposure toorganophosphate

insecticides in thediet, EPA has littlechoice but to act toprotect infants andchildren.


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foun d in the food supp ly.Promp t action can ensure thatthis critical informa tion is avail-able by the time EPA must takeregulatory action on OPs in Au-

gust 1999. At that tim e, the re-quired additional ten-fold levelof protection mu st be ap plied toany OP for which a develop-mental neurotoxicity study is notperformed.

Fifth, food tolerances for allOPs mu st be low ered to levelsthat are safe for infants and chil-dren. To quo te the Nationa l

Resea rch Cou ncil rep ort, Pesti-cide s in the D iets of Infants an d

Children, Children shou ld beable to eat a healthful diet con-taining legal residues withoutencroaching on safety margins(NRC 1993, p p 8-9). Tha t is to

say, legal residue s, or tolerance s,must be safe for infants and chil-dren . There is simp ly no scien -tific justification for retaining le-gal limits for pesticides in foodthat allow hugely unsafe levels ofexposure, just because most chil-dren d o no t receive this exp o-sure. This no nsen sical no tion islike leaving th e sp ee d limit at 500miles pe r hou r just because m ost

people would still drive at 65.

U nti l rel iable data onfetal and infanttoxicity are availablefor all O Ps, the actionsrecommended here,

w hile significant, m ustbe view ed as firststeps in an o ngoingprocess of protectinginfants and child renfrom O P insecticides.


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Introduct ion

Ch apter O n e

O n Augu st 3, 1996, Presiden tClinton signed the Food QualityProtection Act (FQPA), ne w leg-islation go verning the regulationand u se of pe sticides. This leg-islation enacts a strict, uniform,

and una mb iguou s safety stan-dard for allowable levels of pes-ticides in food and from all otherroutes of expo sure. Under thelaw, a pesticide will not be al-low ed in the food supp ly if thetotal exposure to the pesticide(exposure from food, water, andho me u se) is not safe. Safe isdefined as a reasona ble cer-tainty that no harm will come

to exposed individuals, includinginfants and ch ildren . For car-cinogens, reasonable certainty ofno h arm is defined as a one inon e m illion risk, or less, of can-cer (FQPA House Report 1996).

The organophosphate (OP)insecticides w ill be o ne of thefirst group of che micals regu -lated u nd er FQ PA. This distinc-

tion is w ell de served. Infantsand children are exposed tomany different OPs via manydifferen t rou tes, occasiona lly atrelatively high leve ls. Animalstudies, as well as evidence fromhuman poisonings show that thefetus, infants an d ch ildren areoften mo re susceptible to OP

toxicity than adu lts. And pe rhap smost important, organophosphatecompounds are toxic to the ner-vous system, a critical, sensitive,and developing organ system inthe very youn g.

A N e w M a nd at e

The sweeping new mandate of FQPA requires both a new assess-men t of health risks, and a neworientation to risk m anagem ent.

First, the Act requires the EPAto protect infants and childrenfrom pe sticides. In the past,

regulations had been based onaverage exp osures across thewho le p opu lation and on s tudiesprimarily conducted on sexuallymatu re (adu lt) anima ls. Now ,before a p esticide can be allow edon food , it must be foun d to besafe for infants and children,based on reliable scientific data.Further, the finding that exposureto a p esticide is safe m ust includ e

a thorough assessme nt of allroutes of exposure to that pesti-cide, as well as exposure to allo ther comp ound s with a comm ontoxic m echan ism.

Second, after 25 years of risk-ben efit balancing w here theagency was required to weigh

In the past, regulationshad been based onaverage expo suresacross the w holepopulat ion and onstudies prim arily

conduc ted on sexuallym ature (adult)animals. N ow , beforea pesticide can beallow ed on food, itmust be found to besafe for infan ts andchildren, b ased onreliable scientific data.


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1 0 O V EREXPO SED : O R G A N O P H O S P H A T E IN SECTICID ES IN C HILDREN S FO O D

farmer profits against the risks tothe public health, FQPAprohibitsthe use of economic argumentsas a rationale for exposing infantsand children to risks that exceed

the health standard of the Act.

Third, FQPA requires EPA toactin the absence of total scien-tific certainty regarding the toxic-ity or exposure of pesticides tothe fetus, infant or young child.This is a d ramatic reversal of pre-vious statutory requirements.Prior to FQPA, EPA had no man-date, and a rguably could no t act

to p rotect the pu blic he alth, evenchild h ealth, in the ab sence o fcomp lete data on the risk from ape sticide . Now the law is clear.In the absence of complete andreliable data on pre- and po st-natal toxicity and exposure to ape sticide , the Admistrator m ustapply an additional a ten-foldma rgin o f safety to foo d toler-ances for the pesticide (FQPA

section 408(b)(2)(C)(ii)(II)).

The O Ps: A C ritical Test Case

Every imp ortant new require-me nt of FQPA comes to b ear insome important way on the regu-lation of the OPs.

FQPA requ ires tha t pes ti-cides be safe for infants and

children, defined as a rea-sonable certainty that noharm w ill com e to an y ex-posed individual.Organphosphate com-po und s are typically mo retoxic to fetal and infant an i-mals than to adult animals,both in terms of cholinest-

erase effects and other in-creasingly well docu-mented b rain and nervoussystem toxicity (see chap-ter one ). There are excep -

tions to this rule, but ingeneral because the OPsare toxic to the n ervoussystem, the FQPA require-ment to protect the youngfrom pe sticide s is particu-larly relevant.

All n o n -o c cu p a tio n a lroutes of expo sure to p esti-cides m ust be con sidered

when food tolerances areset, including risks to in-fants from pe sticide indrinking water, the h om e,school, and garden . Per-haps mo re than any o thergroup of chemicals, infantsand children are exposedto OPs via multiple routes,in food, around the house,at schoo l or in the garde n.

U nd e r FQ P A, Ex p o su re toall pesticides with a com-mon mechanism of toxicityor similar toxic action onthe body must be com-bined when establishingsafe levels of tho se p esti-cides in food. O Ps are allneurotoxins, acting on thesame enzyme in the ner-

vous system. Two sep a-rate scientific review pa n-els agree that organophos-phate insecticides share acommon mechanism of toxicity (ILSI 1997, SAP1997), and that, for p ur-poses of protecting infantsand children, exp osure to

FQ PA requir es EPA toact in the ab sence oftotal scientificcertainty regarding thetoxicity or expo sure of

pesticides to t he fet us,infant or young child.This is a dramaticreversal of previou sstatutory r equirem ents.


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1 1EN V I R O N M E N T A L W O R K I N G G R O U P

these p esticides mu st beconsidered in aggregate.

Roadblocks

Since the pa ssage o f FQ PA in1996, the application of the ten-fold safety factor has emerged asthe key obstacle to successfulimp lem entation of the law .Other important issues relevantto OPs whether they share acomm on me chanism of toxicityand the consideration of allroutes of exposure have beendecided by the EPA in favor of

children . Not so with the ten-fold safety factor. (Based on aread ing of the reco rd an d EPAspo licy p ositions b efore the Sci-entific Advisory Panel (SAP), itapp ears that OPs will be con sid-ered to share a common toxicmech anism and that all routes ofexpo sure will be incorporatedinto risk a ssessmen ts.)

FQPAs req uireme nt for anadd itional ten-fold level o f pro-tection for infants and children isclear. To quo te the law :

In the case of thresholdeffects, for purposes ofclause (ii) (I) an a dd itionalten-fold m argin of safetyfor the pesticide chemicalresidue shall be applied for

infants and children to takeinto accou nt p otential pre-and po st-natal toxicity andcomp leteness of the datawith respect to e xpo sureand toxicity to infants an dchildren. Notwithstandingsuch requirements for anadd itional m argin of safety,

the administrator may use adifferent margin of safetyfor the pesticide chemicalonly if, on the basis of reli-

able data, such margin will

fully protect infants andchildren . [Emph asis add ed ]

In spite o f this unam biguouslegal requirement, the EPA andits sp ecial p esticide Scientific Ad-visory Pane l (SAP) ha ve co n-cluded that the agency need notapply a ten-fold safety factor topesticide tolerances, even in theabsence of reliable data on toxic-

ity or exposure as the law sop lainly sets forth. The SAP re-spon se to the EPA prop osal dated Decem ber, 1996 plainlyarticulates the agency policyagainst implementation of theten -fold safety factor. Acco rdingto the SAP: The Agency positionthat a ten -fold u nce rtainty factor(UF) shou ld n ot be app lied inevery case is reasonable.

Justifying this p osition , theSAP invokes a logic that standsthe m anda te of FQPA on itshead . The SAP does not chal-lenge the fact that data on pre-and post-neonatal toxicity andexposure are unreliable; This isa growing area of toxicology inwhich there are numerous datagap s an d un certainties (SAP

1997) Instead , w ith total disre-gard for the letter of the law andthe p ublic he alth e thic of precau -tion on which it is based, theyargue that the un reliability of ex-isting d ata is the p recise re asonnot to invoke the ten-fold safetyfactor required by law; Withoutadditional information or the use

Im portant issuesrelevant to O Ps w hether they share acommon mechanismof toxicity and the

consideration of allroutes of exposure have been decided bythe EPA in favor ofchildren. N ot so w iththe te n-fold safetyfactor.

The EPA an d itsspecia l pesticide

Scientific AdvisoryPanel (SAP) h aveconcluded that theagency need not applya ten-fold safety factorto pesticidetolerances, even in theabsence o f reliabledata on toxicity orexposure as the law soplainly sets forth.


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of add itional testing, it wou ld bedifficult to assign a narrow ly de-fined uncertainty factor (UF).Or put another way, The cir-cumstances under which greater

or lower UFs would be made areno t clear an d coge nt (SAP 1997).Inde ed , it is exactly the recog-nized lack of information on theprecise level of additional protec-tion nee ded by infants and chil-dren that led the Congress to re-qu ire a ten -fold safety factor u ntilsuch time as reliable data be-come available.

FPQA requires protections un-like those in an y other federalen vironm en tal law. The lawmandates that the combined ef-fects of all exp osure s to a p esti-cide must be safe for infants andchildren , including the effectsthat may result from in-utero ex-po sure. Furthe r, FQPA shifts theburde n of proo f. Under the law,pe sticide man ufacturers m ust

pro ve that a p esticide is safe forinfants and children, as op po sedto prior law where EPA had toprove that the risks of a pesticideoutweighed its benefits to farm-ers. And last, to ensure thatthese obligations are achieved,FQPA adds the requiremen t thatEPA mu st err on the side of childhealth in the face of scientificun certainty. If registrants do no t

provide reliable information toprove the safety of a pesticide,FQPA stipulates clearly that foodtolerances for pesticides mustinclude an additional ten-foldmargin of safety, i.e. that infant

and child exposure must be re-duce d b y a factor of ten.

Congress did not enact thisma nd ate un w ittingly. D uring

the three year period betweenthe release of the National Acad-emy of Sciences (NAS) study(Pesticides in the Diets of Infantsand Children , NRC 1993) andthe unanimous p assage of FQPA, num erous he arings we reheld on the report, its findingsand the recommendations of thecom mittee for legislative reform.The Congress, and particularly

the Comm erce Comm ittee of theHou se that produce d the bill,wa s well aware of the state ofthe science at the time of enact-me nt. The decision by the Con-gress to require additional safetyfactors in the a bsen ce o f reliabledata was m ade with a full und er-standing of the paucity of thecurrent database regarding pe sti-cide toxicity and exposure to

infants and children.

When it comes to p rotectingchildren from pe sticides, the lawand the intent of the Congressare exce p tion ally clear. Und erFQPA, pesticide manufacturersnow have two choices: they canprovide reliable data on pre- andpo st-neona tal toxicity and exp o-sure to their pesticides, or they

can accept a ten-fold redu ctionin the allowable levels of thatpe sticide in the food supp ly.Congress has taken a stand; no wit is up to EPA to imp leme nt thelaw.

The decision by theCongress to requireadditional safetyfactors in the absenceof rel iable data w as

made w i th a fu l lunderstanding of thepaucity of the currentdatabase r egardingpesticide toxicity andexposure to infantsand children.


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O rganopho sphate Toxicity

Chapter Tw o

Organophosphate insecticides(OPs) share a comm on m echa-nism of toxicity, identified asinhibition of acetylcho line sterase(AChE) in the ne rvous system,leading to a spectrum of cholin-

ergic symptoms (EPA 1997, ILSI1997). The role of ace tylcho linein nervous system function,how ever, is not comp letely un-de rstoo d. What is clear is thatthis ubiquitous enzyme is essen-tial to smooth operation of boththe central and pe riph eral ner-vous system . An EPA review ofthe science offered the followingob servation s on the critical role

of ace tylcho line :

Most impressive is the sin-gular fact that acetylcholineis the only substance thatcan influence every physi-ological or behavioral re-sponse thus far examined(Myers 1974 in EPA 1997).

Add ing that:

From central to peripheralneurohormonal functionsand from simple to com-plex behavioral acts thecho line rgic system plays anessential role in the capa-bility of living o rgan isms tocope w ith the de mands of

con stantly varying internaland external environm ents(Russell 1981 in EPA 1997).

Forty years o f animal studieshave produced a w ealth of peer-

reviewed literature on OP toxic-ity. Much of this w ork focu seson observable cholinesterase re-lated symp toms (nau sea, vomit-ing, blurred vision , con vulsion s,irregular heart beat, and evendeath) but there are many as-pects of OP toxicity reported inthe literature that rem ain less we llunders tood, and perhaps are of greater concern. Amo ng these

are the facts that:

Fe ta l a n d n e o n ata l a n im a lsare often more sensitivethan adults to the toxic ef-fects of O P exp osu re. Thisvulnerability includes in-creased sen sitivity to cho -linesterase effects and otherpotentially more seriousbrain an d n ervous system

damage.

O P exp o su re ca n p ro d ucelong term be havioral andfunctional dam age to thenervous system in the ab -sence of observable signs oftoxicity, and with little cor-relation with ChE levels.


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O Ps p ro d uce a ra nge o f toxic effects on differentregions of the brain in theabsence of overt effects (in-creased brain we ight or

size).

Infant Sensitivity

The ne rvous system in the d e-velop ing h um an is incom pleteand growing rapidly at birth.Cortical migration and neuronproliferation are complete at 5and 12 months of age respec-tively, while mylination is only 50

percent complete at 18 monthsafter birth. Seve nty-five p erce ntof brain growth occurs during thefirst tw o years, the rem aining 25pe rcent is not com pleted un tiladu ltho od . Brain size in thenewborn is proportionatelygreater than in adults . The new -born brain weighs one third ofan ad ult brain, wh ile the n ew -born w eighs only 4 percent as

much as the average adult(Snodgras 1992 in ILSI 1997).

The b lood brain barrier, wh ichrestricts the pe ne tration o f toxi-cants to the brain is not fully de -veloped in humans until aboutone year of age. It is not know nwh en the barrier beco me s fullyfunction al. Conn ection s in thevisual system are not fully

achieved until three or four yearsof age (Schlicter 1996).

Not surprisingly, experimentalstudies and clinical observation shave demonstrated that the cen-tral nervous system o f the hum aninfant is mo re sen sitive to thetoxic effects of h eavy m etals,

ethano l, retinoids, and neu roac-tive dru gs (Schlicter 1996, NRC1993, EWG 1993). Furth er, it iswe ll docume nted that functionalimpairment of the nervous sys-

tem can o ccur after exposuresthat produce no overt neurologictoxicity, no gross morphologicchanges in the brain, and n oovert toxicity to the mother(NRC 1991, NRC 1993). Thebest example of this is lead,wh ich causes long term loss ofintelligence when young chil-dren are e xpo sed to levels thatare non -toxic to the ad ult. In

several cases for currently usedpe sticides, the doses subse-quently found to affect func-tional development in test ani-mals were lower than the dosesidentified as no-effect levels inlong term animal studies used bythe EPA for regulation (Schlicter1996).

In 1993, the National Re-

search Council described thesituation this way:

The data strongly suggestthat exposure to neuro-toxic com po und s at levelsbelieved to be safe foradults could result in per-manent loss of brain func-tion if it occu rred d uringthe prenatal or early child-

hood period of brain d e-velopm en t. Th is inform a-tion is particularly relevantto dietary exposure to p es-ticides, since policies thatestablished safe levels ofexposure to neurotoxicp esticides for adu lts cou ldnot be assumed to ad-

T he data stronglysuggest that exposureto neurotoxiccompounds at levelsbelieved to be safe for

adults could result inperm anent lo ss ofbrain function if itoccurred during theprenatal or ear lychildhood period ofbrain development.

N ational Re searchCounci l, 199 3


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equately protect a childless than four years ofage. (NRC 1993 p. 61)

OPs are gene rally mo re

acutely toxic to young animals.Weanling rats (23 days old) weremore susceptible than adult ratsto the acute toxicity of 14 ou t of15 OPs tested (Brode ur andDu bo is 1963 in NRC 1993). Astudy of rats at five differentages (1 day, 12 to 13 days, 23 to24 days, 35 to 40 d ays and 63days), show ed a de creasing sus-ceptibility to parathion and me-

thyl parathion with increasingage (Benke and Murph y 1975 inNRC 1993). O ne -day-old ratsare four times m ore sen sitive tochlorpyrifos than week-old rats,and six times more sensitivethan adu lt rats (Pope andChakrabo rti 1992, Whitne y1995). And accord ing to theseautho rs, it is conce ivable, giventhis steep dose-respon se curve,

that ...even lower concentra-tion s of chlorpyrifos m ay betoxic to the fetus (Whitney 1995p. 58).

Many other studies also showthat organophosphates oftenhave a grea ter toxic effect (asmaller d ose is equ ally toxic)whe n e xposure occurs beforebirth or n eon atally as com pared

to adult expo sure (Mend oza1977, Gupta et al. 1985, Gaineset al. 1986, Pope et al. 1992,Pop e & Chakrabo rti 1992,Campbell 1997, Song 1997,Schlicter 1996, Chakraborti et al.1993, Chan da et al. 1996). In-creased vulnerab ility is no t lim-ited to ch oline sterase e ffects.

One recent study has shown thatbehavioral abnormalities couldbe produced in juvenile rats (17days old) with one fifth the doseof chlorpyrifos required to pro-

duce the same result in adult rats(Moser et al. 1995). O ther wo rkhas shown that susceptibility tocell de ath in d ifferent regions o fthe brain from chlorp yrifos ex-posure w as h ighly depe ndent onthe day o f gestation on wh ichexpo sure occurs (Camp bell et al.1997, Whitney et al. 1995).

Studies have also sho wn that

infant an imals often h ave lessdeveloped OP detoxificationmechanisms comp ared to o ldermembers of the same species(Green 1990, Murphy 1982).Tests condu cted by chem icalcompanies on hu man volunteershave shown that hum ans sharesuscep tibility to O Ps with oth ermamm als , and hum an OP p oi-soning incidents have show n

higher susceptibility by infantsand young than adults (Diggoryet al. 1977 in NRC 1993).

Long term functional damageand behav ioral effects in theabsence of over t toxicity

OP insecticides can p roducebe havioral and fun ction al deficitsat doses that cause no overt signs

of toxicity and absent any corre-lation w ith ChE leve ls. A rece ntreview of the scientific literatureon OP toxicity provides m anyexamples of th is phe nom enon(EPA 1997), includ ing a p ap er b yWolthuis and Vanwersch (1984)which concluded that exposureto low doses of cholinesterase

O P insecticides canproduce behavioraland functional deficitsat d oses that cau se noovert signs of toxicity

and ab sent anycorrelat ion with ChElevels.


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inhibitors may cau se acute be-havioral effects w itho ut o vertsymptoms, and without distur-bance of the physical fitness ofthe subject. A mo re recent pap er

by Wo lthius e t. al (1994) co n-cluded that, All four of the testmaterials affected performanceon behavioral testing in the ab-sen ce of clinical signs... In add i-tion, blood cholinesterase levelsdid not correlate with behavioraleffects. The autho rs add that thedoses administered are so lowand the CNS effects are so un-characteristic of the classical in-

toxication p icture that thesesub tle incapa citating effects m aygo undetected (Wolthius et. al1994 in EPA 1997 p. 34).

EPA analysis of a study byDe si et al. (1974) con cludes tha tBehavioral effects and braincholinesterase inhibition wereoccurring in this study at doseswh ich d id not m easurably inhibit

plasma ChE or erythrocyteChE... (EPA 1997 p 54). Severalstudies by Kurtz (1976 and 1977)found behavioral effects in theabse nce of clinical signs a fterexp osure to the w idely used in-secticide malathion . In the laterstudy, test animals showed sig-nificantly impa ired avoidan cebehavior while cholinesteraselevels remained at 90 percent of

baseline levels (EPA 1997).

Add itional studies o nmalathion reached the same re-sult. It is con clud ed tha t thesensitive functional tests havesupp lied eviden ce that m alathionmay affect the more sophisticatedfunctions of the body, or at least

it exerts a load on and exhau stsadaptability of the organisms.When the con ventional toxico-logical exam ination s yielde dne gative results, the

neurotoxicological tests demon-strated alterations in mammals(De si et al. 1976). A stud y byNagymajtenyi et al. (1988) ofdimethoate, dichlorvos and me -thyl parathion found that ad-ministration of relatively smalldoses could p roduce the samekinds of effects as administrationof large dose s. In the case ofEEG variables these data suggest

CNS dysfunction from repeatedlow dosages of cholinesterase-inhibiting com po un ds. EPAstaff fou nd this study to be...another example of study inwh ich organoph osphates causedfunctional effects in the nervoussystems at doses w hich did notyield clinical signs (EPA 1997 p.86).

Recen t lab w ork ha s revealedbrain ce ll loss in yo un g ratsgiven doses of OPs that did notaffect growth or survival oftho se individua l rats: Belowthe thre shold for system ic toxic-ity, ch lorpyrifos ne verthelessdam ages the developing brainwith little or no body or braingrowth imp airmen t (Camp bellet al. 1997). Previou s w ork had

suggested this effect, At doseswe ll below tho se that cause celldeath or standard signs of sys-temic toxicity such as w eightloss or brain weight deficits, thedevelopment of the brain maybe comp romised by chlorpyrifosexposure (Whitney et al. 1995).

Recent lab w ork hasrevealed b rain cell lo ssin young rats givendoses of O Ps that didnot affect grow th or

survival of thoseindividual rats.


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Fetal animals also can beharmed b y OPs in the absenceof any observable effect on themo ther. Whitney et al. (1995)also found that low doses o f

chlorpyrifos target the develop-ing brain during the critical pe-riod when cell division is occur-ring. Whe n p regna nt rats w eregiven low level repea ted do es ofOPs, researchers have observedaltered ne rve d evelopm ent inthe offspring causing neuro-chemical and neurobehavioralchanges in developing rats,w itho ut visible signs of ma ternal

toxicity (Gupta et al. 1985, Muto1992, Chanda a nd Pop e 1996 ).In one e xperiment, mother ratsdosed with chlorpyrifos o n ges-tational days 9 through 16showed no ill effects while theiroffspring had beh avioral prob-lems including the inability torecognize the edge of a tablebefore falling off and difficultyrighting them selves wh en placed

on their backs on po stnatal daythree (Chan da an d Pop e 1996).A report from Geller et al. (1985)reve aled similar d ifficulties inavoidance behavior in rats ex-posed to 0.046 mg/kg somanevery three days for threeweeks .

Tolerance to O Ps

It is generally accepted thatanimals build up a tolerance tothe ChE inhibiting effects of OPsafter repeated subacute expo-sures. It is no t as well ap p reci-ated, how ever, that O P toleranceis a comp lex phe nome non thatmay have more to do w ith com-pe nsation beh avior, than with

the actual ability to detoxify ortolerate increasing doses of cho-line sterase inh ibitors (Bushn ell1991). In a study with the com-po und DFP, 21 days of exp osure

at 0.2 mg/ kg/day p roduced nocholinergic symptom s or bo dywe ight change s. ChE dep ressionand dow nregulation, an indicatorof OP tolerance, wa s measured inthe test anima ls. Notably, thetolerant animals were not able tofully regain the ability to performnorma lly during the repe ateddo sing w ith D FP in sp ite o f evi-dence that the animals were com-

pensating for normal cholinest-erase effects (EPA 1997 p. 77).

Subsequent work by Bushnellet al. (1994) w ith the w idely usedO P ch lorpyrifos (CPF) con firme dthis effect. He re the au thors con -clud ed that: Rep eated dosingwith CPF induced long-term inhi-bition of ChE activity; clinical,neurochemical, and pharmaco-

logical indication s o f toleran ce tothe effects of this inhibition; andpersistent impairment of cogni-tive and mo tor function . The factthat the be havioral deficits de vel-oped slowly and did not fade asother signs of tolerance eme rgedindicates that tolerance to this OPdid not extend to all functions ofthe ne rvous system , and may infact exert a cost to some aspects

of central nervous system func-tion.

Indeed, according to the EPA,cho line sterase inhibition at su b-clinical levels potentially alters aplethora of neurologic phenom-ena that may go un iden tified un-til the individual is challenged in

Fetal animals also canbe harmed by O Ps inthe absence of anyobservable effect onthe mother.


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some way (EPA 1997 p. 76).And a s conclude d by Annau(1992) It is still no t clear w ha tlevel of exp osure (to O Ps ) doesnot result in latent toxicity (Pa-

renthesis added).

The Brain

The unpredictability of theselatent behavioral and functionaleffects reflect the com plexity ofthe central and pe riph eral ner-vous systems and the con tinuingevolution o f scien tific un de r-stand ing abo ut the w orkings and

interactions of the brain and re-lated organs. Ho w ever, the vary-ing effects that OPs e xert on dif-ferent regions of the brain doprovide som e insight into w hythe toxic effects of OPs are morecomp licated than simple cho-linesterase depression.

Hamm ond et al. (1996) foundsubstantially different levels of

ChE inhibition in different re-gions of the brain after exposureto chlorpyrifos. According to theauthors, Local variations in ace-tylcholinesterase turnover couldlead to differential inhibition indifferent parts of the brain, espe-cially during chron ic pe sticideexp osure o r during recovery fromacute exposure (EPA 1997 p.36). On e conseq uen ce of this

variable ChE de p ression is theinability of currently used tests tomeasure brain ChE levels (Desi etal. 1974). According the EPAscientists The variable region byregion ch oline sterase inhibitionin the brain suggests that moreprofound cholinesterase inhibi-tion may be occurring in certain

regions than w ould be ap parentin a single brain cho line steraseassay (EPA 1997 p. 54).

Studies have shown that low

do ses of chlorp yrifos target thedeveloping brain but producedifferent effects in different brainregions (Cam pb ell et al. 1997,Wh itne y et al. 1995). Accordingto the au thors, low doses o fchlorpyrifos target the develop-ing brain d uring the critical pe -riod when cell division is occur-ring (Wh itne y et al. 1995). Theeffect of chlorpyrifos in different

regions o f the brain, ho we ver,changes w ith the age o f the ani-mal and the corresponding de-velopmental window of vulner-ability. Comp ared to adm inistra-tion at 1 to 4 days o f age, Whe nchlorpyrifos was administered atdays 11-14 the ma jor target forcell loss shifted from thebrainstem to the forebrain, andin this case, effects (reduction in

forebrain cell num ber) w ereseen at do ses that did not com-promise growth or survival(Camp be ll et al. 1997 p. 179).

Chlorp yrifos causes brain ce lldam age an d interferes w ith DNAsynthesis in young animals withno signs of cholinesterase de-pre ssion or other toxicity. These

effects would no t be detected bythe tests required by the EPAwh ich on ly measure b rainwe ight and observe on ly grosslesions; in spite of the severebrain ce ll loss in the brainstem,brainstem growth was main-tained by en largemen t of othercells (Cam p be ll 1997). Accord-

Low doses ofchlorpyr ifos target thedeveloping brainduring the criticalperiod when cel l

division is occurring.

Chlo rpyrifos causesbrain cel l damage and

inter feres w i th D N Asynth esis in you nganim als w ith no signsof cholinesterasedepression or othertoxicity. These effectsw ould not be detectedby the tests requiredby the EPA w hich onlym easure brain w eightand observe only gross

lesions.


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ing to the authors, these cellulardeficits could lead to behavioralabnormalities later in life, a con-clusion that may p rovide someinsight to the be havioral effects

that have been reported in theliterature, in the absence of overttoxic signs. Furthe r it ap pe arsthat this type o f cell dam age inthe de velop ing an imal is notlimited to the central nervoussystem, but involves a morewidespread disruption of normalcell developm ent that include sthe heart and perhaps other or-gans (Song et al. 1997).

Conclusions

There is consistent and com-pe lling e viden ce in the p eer-reviewed literature that the fetus,infant and you ng child are mo revulnerable to a wide variety oftoxic effects caused by organo-ph osp hate insecticides. Theseeffects include increased sensi-

tivity to cholinesterase effects asw ell as increa sed vulnerab ility toa variety of toxic effects on thenervous system that occur dur-ing critical pe riod s of p rena tal,neo natal, and p ostneon atal braindevelopment .

None of the O Ps widelyfoun d in the food supp ly havebee n tested for their develop-

men tal neu rotoxicity (one OP,chlorpyrifos, is currently beingtested), nor are there plans totest the OPs for their develop-mental neurotoxicity (SAP 1996,SAP 1997). This data ga p is criti-cal because the stand ard batteryof toxicity tests do es n ot reve alany significant age related neu-

rotoxicity, nor are animals exam-ined for long term behavioral orfun ction al effects un less grossbrain o r nervous system abn or-malities occur in the develop-

mental and reproductive toxicitystudies. Inde ed , the standardbattery of toxicity tests wo uld n otdetect such well known develop-men tal neu rotoxins as lead,PCBs, an d me rcury. EPA Assis-tant Administrator for Pre vention,Pesticides, and Toxic Sub stances,Dr. Lynn Goldman concurs: Weagree that the standard p rotocolsfor d evelop me ntal toxicity studies

and reproductive toxicity studiesdo not p rovide mu ch informationon the effect of neurotoxic pesti-cides on the pe rforman ce of thenervous o r imm une system s indeveloping animals. (Goldman1997).

Unlike data generated underEPA protocols, the peer reviewedliterature an alyzed h ere sho ws a

consistent and rep eated p atternof behavioral and functional defi-cits from low level OP exposurein the absence of any overt toxiceffects, usually with no correla-tion to ChE levels, and in som ecases in the absence of significantcholinesterase dep ression.

Current regulation of OPs isbased almost exclusively on ChE

effects. The typically grea ter sen -sitivity of young animals to theseeffects alone argues for increasedprotection for children from OPs,and in and of itself supports theFQPA requiremen t for an add i-tion al ten-fold level of p rotectionin the absence of reliable data tothe con trary. There is mo un ting

The re is consistent andcompelling evidencein the peer-review edliterature that thefetus, infant and

young child are m orevulnerable to a w idevariety of toxic effectscaused byorganophosphateinsecticides.

Both curr ent studiesand the regulationsthey support do not

account for thesetoxic effects.


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eviden ce, how ever, that OPs aretoxic to the d eveloping brain andnervous system at very low levelsof expo sure. Again, both currentstudies and the regulations they

supp ort do no t accoun t for thesetoxic effects. Admittedly, ma nyof the mo re subtle an d long termneu rodevelopm ental effects

emerging in the literature todaymay no t be ripe for use as regu-latory en dp oints. This grow ingbody of evidence, however,plainly sup po rts the ne ed for

greater protection from OPs forinfants and the developing fetusand embryo.


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Children Included V alid EatingA ge I n CSFI I Survey D ays

6 -1 2 m o . 2 7 4 5 7 2

1 8 4 2 1 , 7 3 22 8 6 8 1 , 7 6 83 7 2 6 1 , 4 4 84 7 0 1 1 , 4 1 05 6 7 1 1 , 3 7 2

TO TA L 4 ,0 8 2 8 ,3 0 2

D ata Sources and M ethodology

Chapter Three

D ata Sources

All data used in this risk as-sessment are from federal gov-ernme nt sources. Food con-sump tion data are from theUSDA, pesticide residue data a re

from both the USDA and theFDA, and toxicity data are fromthe EPA.

Food Consum ption D ata

The food consumption dataused in this analysis are from theUSDA Continuing Survey of FoodIntakes by Individuals (CSFII) forthe years, 1989, 1990, 1991, 1994

and 1995, the most recent yearsfor wh ich data are available. Nodata were collected in 1992 and1993. The CSFII co ntains 3,695coded foods and beverages re-po rted a s eaten by the surveypo pu lation ranging from blue-berry pie to scrambled e ggs, po -tato chips to m int julep s. A totalof 4,082 children betwe en onemo nth and five years of age w ere

surveyed in the years 1989-91and 1994-95 (Table 3). These4,082 children provided one tothree days o f valid inform ationeach, for a total of 8,302 valideating days.

Survey p articipants are askedto complete a diary containing

the amo unt (by we ight) of eachfood eaten at each m eal duringthe three nonconsecutive days ofthe survey, and the w eight, sexand date of birth of the pe rsoncon sum ing that food. The infor-mation in the diaries w as con-

firmed by telepho ne interview .These data allow age groupana lyses, as we ll as estima tes offood consumption on a per kilo-gram of body weight per day ba-sis, for e ach individu al in the da-tabase.

The CSFII is a weighted, strati-fied sam p le of individu als that isdesigned to provide a represen ta-

tive picture of the dietary patternsof the U.S. p op ulation . Risk as-

Table 3. Ch ildrens food consum ption data used in thisanalysis.

Sourc e : U SD A C on t inu in g Surv ey o f Food In tak e by I nd i v idu a ls. Su rv ey Years: 1 9 8 9 - 9 1 , 1 9 9 4 - 9 5 .


27/54


N u m b e r ofN um ber of foods sam ples

D atabase Source D ates used in analysis used in analysis A ttr ibutes

To tal D iet Stu d y FD A 1 9 9 1 -9 6 9 0 1 ,4 5 9 co o ked an d p rep ared fo o d

Pesti c i d e D ata Pro gram U SD A 1 9 9 2 -9 5 1 4 2 5 ,8 8 6 w ash ed an d p eel ed *Pesti c i d e M on i to r in g D atab ase FD A 1 9 9 2 -9 6 6 8 2 3 ,2 3 8 raw co m m o d i t i es/red u c ti o n

factors appl ied (see table 5)

TO TA L 1 7 2 * * 5 0 ,5 8 3

sessments and estimates of thenumber of children exceedingspe cific risk stand ards an d safetymargins are based on EWGs as-sessment of the significance ofthe samp le w eights supp lied b yUSDA.

Pesticides in the Food Supply

Data on pesticides in the food

supply are collected by the USDAand the FDA. There are threema jor p rograms: the USDA Pesti-cide Data Program, the FDA Pes-ticide Surveillance and Monitor-ing Program and the FDA TotalDiet Study (Table 4). Each has aspecific p urpo se, and its ownstrengths and weaknesses.

U SD A/ Pest icide D ata Program.

The USDA Pesticide Data Pro-gram (PDP) was started in 1991specifically to monitor pesticidelevels in fruits and vegetab lesmost comm only consumed bychildren. The purpo se of theprogram was to supp lemen t theFDA surveillance d ata w ith m ore

Tab le 4. Pesticid e residue da ta used in this analy sis.

* 9 0% reduc t i on f ac to r w as app l i ed t o g reen bean resu l t s fr om the PD P bec aus e they a re tested r aw b u t ea ten c o ok ed .* * T h e se 1 7 2 f o o d s w e r e l i n k e d t o 4 0 7 d i s t i n c t fo o d s i n t h e U SD A f o o d c o n s u m p t i o n d a t ab a se .

accurate and statistically rep re-sentative information on pesti-cides residues on fruits and veg-etables heavily consum ed byinfants and children . PDP typi-cally samples twelve to fourteenfoods, mostly fresh fruits andvegetab les, p er year. Sam plesare co llected to accu rately reflectthe p ercent contribution to thenational food supply for a given

crop by growing region and sea-son. Samp les are then washed,pe eled, and co red to reflect nor-mal food preparation and con-sum ption p ractice for that fruitor vegetab le. PDP residue test-ing uses powerful analyticaltechniques that can detect traceresidues in the 1 part per billionrange or less, similar to therange of detection in the Total

Diet Stud y (TDS). PDP take s400-700 samples of each croppe r year. More than 25,800 PDPsamples from the years 1992through 1995 were u sed in thisana lysis. These data w ere thedata of first choice for freshfruits and ve getables.

So u r c e : EW G , c o m p i l e d f ro m U SD A f o o d c o n s u m p t i o n d a t a 1 9 8 9 - 1 9 9 5 , U SD A a n d F D A p e st i c i d e re si d u e d a t a 1 9 9 1 - 1 9 9 6 and re ferenc e do ses (R fD s ) ob ta ined f r om EPA in January 1 998 .


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FD A Surveil lance D ata. Th eFDA Pesticide Surveillance andMonitoring Program enforcesfood tolerances e stablished bythe EPA. Because the mon itor-

ing is de signe d for regu latoryenforcement purposes, as op-posed to dietary exposure as-sessment, the data do not pro-vide a strictly statistically re p re-sentative p icture o f pe sticides inthe US food sup ply. This sho rt-com ing, how ever, is largely off-set by the sheer size of the data-base generated by the programand the fact that the program

doe s sample food from all re-gions of the country at labs lo-cated in nine different metropoli-tan areas. Betwe en 12,000 and16,000 sam p les of foo d a retested for pesticides each year,about half of which are imports.We analyzed all records fromthe FDA surveillance datab asefrom the years 1992 through1995, which contained residue

findings for 51,280 food samp les.

Our analysis used only ran-do m surveillance samp les.Compliance samples, whichare sp ecifically aimed at crop s orgrowe rs with a know n p roblemor h istory of violation s, are n otinclud ed in the ana lysis. Surve il-lance samples are typically takenat packing sheds, warehouses,

or o ther ce ntral distribu tionpo ints. They are not taken atretail po ints of sale or from gro-cery store she lves. Furthe r, thesamples are not washed orpeeled prior to testing e.g.the melon is tested with the rind,the ban ana is tested with thepe el so that the residue levels

foun d tend to overstate theamount of pesticides consumedw he n the fruit is eaten . Becau seof these b iases built into the FDAsurveillance p rotocols, data from

this program w ere used only as alast resort. And as discussed be -low, w hen they were used , a re-duction factor was applied to theresidue s foun d o n each sample, tobetter estimate actual exposure.

FD A Tota l D iet Study. The sec-ond FDA pe sticide residue mo ni-toring program is the Total DietStud y (TDS). The TDS w as started

in the early 1960s to study thepre valence of radioactive fallout inthe food supply as a result of at-mospheric nuclear weapons test-ing. Today, the p rogram tests 234differen t foo ds four times a yearfor a ho st of con taminan ts. The234 food s sampled are d eterminedto be representative of the U.S.diet. The entire samp le is p ur-chased at grocery stores four times

each year, one in each o f fourgeograph ic region of the cou ntry.This ma rket ba sket covers abroad range of both processed(bottled, can ned , frozen) and freshfoo ds including fresh fruits an dvegetables, as well as baby food,dairy prod ucts, frozen me als, freshmea ts, cereals and p ean ut butter,and p repared food s like p izza.

Prior to testing, the foods areprep ared as they normally wou ldbe in the hom e. Bananas arepe eled, tuna casserole is baked ,rice is boiled, an d the ham burgeris grilled . The prep ared food isthen analyzed for pesticides andother toxic contaminants.

W e analyzed al lrecords from the FD Asurveillance databasefrom the years 19 92through 199 5, w hich

contained residuefindings for 5 1,2 80food samples.


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Unlike the FDA surveillancedata, the TDS data are designedto provide a representative snap -shot of contaminants in the U.S.diet. The biggest shortcom ing of

these data is that the sample sizestend to small (4 samples of eachfood p er year). The strength ofthe program is that it providesreal wo rld d ata that reflect p esti-cide residues very likely encoun-tered by the average person. Inaddition, the TDS uses powerfulana lytical tech niqu es that candetect low level residues of pesti-cides in the range o f 1 part pe r

billion or less, a significant ad-vantage over the FDA surveil-lance p rogram w hich doe s notemploy such advanced technol-ogy.

After several years o f repe atedinquires, multiple Freedom ofInformation Act requ ests, andman y roun ds o f discussions withFDA staff, Environmental Work-

ing Group received TDS data forthe years 1991 throu gh 1996 inelectronic form. These six yearsof data co ntain 4,520 foo dsamp les that were an alyzed forpe sticides. To our knowledge,these data have ne ver beforebee n assemb led in e lectronicform, nor have they ever be enreleased to the public in theiren tirety in a ny form.

Toxic i ty D ata

EPA Referen ce D oses. Th ecomb ined toxicity of organo ph os-phate insecticides is measured interms o f choline sterase inhibition.The standard of safety used toprotect the pol;ulation from these

effects, is known as a referencedo se or RfD. Sp ecifically, thereference dose is the agencysdetermination of a safe dailydose of a pesticide, or in this

case, the dose of OPs that willproduce no adverse cholinest-erase effects, exp ressed in m illi-grams of pesticide per kilogramof body weight per day (mg/kgbw / day). The reference doses(RfDs), used in this rep ort arethe most recently calculated ref-erence dose values used by EPAscientists, obtained directly fromthe EPA in January 1998.

All of these reference dosesrepresent final agency decisions,exc ep t that for chlorp yrifos. At arecent me eting, the referencedose comm ittee of the Office ofPesticide Programs recom-mended that the reference dosefor chlorpyrifos have an addi-tional ten-fold safety factor, perthe requ iremen ts of the Food

Q uality Protection Act to p rotectinfants and children from pesti-cides. The reference dose com-mittee is the pesticide programcom mittee of scien tists chargedwith making recommendationsfor pe sticide safety stand ardsun de r the FQ PA. Gen erally, rec-om me ndations from the refer-ence d ose committee have beenado pted as agen cy health stan-

dards.

The ch ronic RfD w as chosenas the appropriate measure oftoxicity in this study only afterour initial analysis revealed thaton average, 88 percent of allchildren 5 and unde r were e x-posed to at least one OP each

To our know ledge, theTotal D iet Study datahave never beforebeen assem bled inelectronic form , nor

have they ever beenreleased to th e publicin their entirety in anyform.


30/54


day. Use of an acute choline st-erase RfD in a situation w he renearly 90 percent of the studypopulation is exposed each dayto the pesticides being studied,

wou ld be inapp ropriate .

The chron ic reference dose isderived from any of a num ber ofanima l toxicity tests requ ired bythe EPA. These studies rangefrom the 90-day rat stud y, to atwo-year chronic feeding study.The test animals are u sually ratsor dogs, but, for example, theRfD for chlorpyrifos is based on

data from a study cond ucted on16 adu lt male Do w chem icalem p loyee s in 1972. RfDs forpirimiphos-methyl, ethion anddiazinon are also based on hu-man data (Table 5).

Expo sur e A ssessm ent

Food Consum ption D ata.Each year of CSFII data con-

taine d from 150 to 200 ind ividu-als per age group (one -year-olds, two -year-olds etc.). Eachindividual reported from one tothree eating days that were vali-dated b y USDA. An eating daycan be thought of as all the foodreported eaten by one individualon one day. On ly eating dayswith comp lete information andpositive validation by USDA

we re used. The five years ofCSFII data used in the reportcontained a total of 8,302 valideating da ys for ch ildren age sixmo nths throu gh five years. Agegroup cohorts were constructedby combining individuals of thesame age from the five years ofCSFII data used in the analysis.

Table

5.

EPAreference

doses(RfD

)usedinthisanal

ysis.

ReferenceDose

Uncertainty

Critical

Crit

ical

NO

ELUsed

Com

p

anythat

Date

Pesticide

RfD(m

g/kg/day)

Factor

StudiesUsed

ChEE

ffect

(m

g/kgbw)

Subm

it

ted

Study

ofStudy

acephate

0.0012

100

Rat-90

day

plasm

a

0.12

Chevron

C

hem

ical

1987

azin

phosm

ethyl

0.0015

100

D

og

-1

year

RBC

0.15

chlor

pyriphos

0.0003

100*

H

um

an

-28

day

brain

0.03

D

ow

Elan

co

1972

diazinon

0.0007

30

H

um

an

plasm

a

0.02

dichlorvos

0.00017

300

D

og

-1

year

brain,RBC

,plasm

a

0.05

AM

VACC

hem

ical

1990

dim

ethoate

0.0005

100

Rat-2

year

RBC

0.05

Am

erican

Cyanam

id

1986

ethion

0.0005

100

H

um

an

plasm

a;br

ain

0.05

FM

C

1970;1988

m

alathion

0.04

100

Rat-2

year

RBC,plasm

a

4.0

M

oellera

nd

Rifder

1962

m

etham

idophos

0.001

100

Rat-8

w

eek

?

0.1

m

ethidathion

0.0015

100

D

og

-1

year

?

0.15

m

ethyl

parathion

0.00002

1,000

Rat-2

year

brain,RBC

,plasm

a

0.02

M

onsanto

1984

phosm

et

0.003

300

Rat-2

year

brain,RBC

,plasm

a

1.1

StaufferC

hem

ical

1967

pirim

phosm

ethyl

0.00008

3,000

H

um

an

-56

day

plasm

a

0.25

ICIAm

eri

casCor

p.

1974,1976

Sourc

e:EPA

,Offic

eofP

esticid

ePro

gram

s,Jan

uary1

998.

RB

C

=

redblo

odcell

ChE=

ch

olin

estera

seinhibition

RfDorR

eferen

ceD

ose=

deriv

edfromth

eN

OELin

the

c

ritical

orm

ostsen

sitiv

estud

ywhichis

then

divid

edb

ya

varia

ble

un

certain

tyfa

ctor

an

ddetermin

edtobethedai

lydoseor

ex

posure

atwhichn

oh

armsho

uld

occur

ov

er

alife

time.

A

low

erreferen

ced

ose(RfD

)m

ean

sthe

pesticid

eis

thou

g

httobem

ore

poten

t.

NOEL=

NoObserv

edA

dv

ers

eEffe

ctsL

ev

el


31/54


Survey p articip ants throu ghfive years of age reported eatingabo ut 3,695 different food s.Many of these d ifferent food s,how ever, are n early identical

version s of the same foo d. Forexamp le, orange juice drinksthat wou ld b e co nsidered differ-ent foods in the CSFII includeunsweetened orange juice, or-ange juice with sugar, orange

juice w ith calciu m , o ra n ge juicefrom co ncen trate and fresh or-ange juice. For purposes of link-ing food co nsum ption data withresidue data in this report, these

similar foods are considered thesame food. The federal pesticideresidue databases used in thisanalysis contained residue re-sults for 561 of the 3,695 foodsrepo rted eaten by children sixmo nths through five years ofage. These 561 food s accountfor 68 percent of the diet ofthese children . O f these 561food s, 407 were foun d to con-

tain detectable levels of OP in-secticides. O ur me thod formatching the specific foods re-po rted eaten, w ith residue test-ing results, is described below.

Residue D ata. The goal ofthe e xpo sure ana lysis w as toproduce the most accurate realwo rld p icture o f pesticide exp o-sure via the d iet. To achieve

that end the three residue data-bases described above wereused in the a nalysis, in the fol-lowing orde r of priority. Forfruits and vegetables eaten raw,PDP data we re used because thedata represent residues afterwashing and peeling, and be-cause samples are statistically

reliable and representative ofU.S. foo d consu mp tion . For allother non-processed foods,FDA surveillance data wereused. These data provide large

sample sizes, but generallyoverstate residues at the timeof consum ption. To accoun tfor this, a residu e re du ctionfactor of from 25 to 90 percentw as ap plied to all FDA surveil-lance data (Table 6). The re-duction factors are b ased o nactual reductions observedwhen PDP and FDA surveil-lance data for individual OP

insecticides w ere com pared onsimilar fruits and vegetables.

For processed and cookedfoods, data from the FDA TotalDiet Study w ere used. Thesmall sample sizes in the TDScreated som e con cern that TDSdata m ight overstate exp osureto some O Ps. For examp le, thesix years of TDS data provide

to EWG contained only 16samp les of whe at bread, but allof them we re p ositive for OPresidues. Using the se 16samp les to rep resent the en tireU.S. wh eat bread supp ly mightoverstate O P exp osure viawh eat bread . On the o therhan d the residues in theseprod ucts, wh ile ubiquitous,w ere gene rally at low levels,

and not likely by themselves topresent great risk to any con-sum ing ind ividual.

To test the validity of thebread prod uct residue findings,we examined OP res idue datain all of the more than 600samples of processed wheat

The goal of theexposure analysis wasto produce the m ostaccurate real w orldpicture of pesticide

exposure via th e diet.


32/54


Table 6 . Pesticide residue reductio ns used in EW G analysis.

9 5 % r e du c ti onH eavy pee l ed f r u i ts and vege t ab l es

C or nPeanuts, in shel lL e m o n

L i m eTanger ineW a te rm e l o n

H o n e y d ew M e lo nC an t a l oupe

P la in ta inK i w i Fr u i t

A v o c a d oM a n g oPapaya

P i neapp l e

9 0 % r e du c ti onSp i nach - l i ke c r ops (r aw t o c ook ed )

R aw C o l l a r dsM us ta r d G r eens

St r i ng Beans, coo kedG reen Peas, cook ed

8 5 % r e du c ti on

Le tt uce - l i ke c r ops (w ashed w / ou t e rl eaves r emo ved)

C h i co r y LeafLet tuce, Loo se LeafBoston Let tuc e

O t he r Let tuceEndive, Escarole

R ad i cch i o

G r een C abbageC h i nese C abbage

R ed C abbage

C a u l i f l o w e rBru ssels Spro uts

7 5 % r e du c ti onJu i c e con cent ra te uncer ta in tyAp ple Ju i c e

A p p l e C i d e rO range Ju i c e

O r ange Ju i ce ( baby f ood )G rape Ju i c e

G r ape Ju i ce ( baby f ood )


Car ro t / root vegetab le compar i sonO n i o n s

Sw eet Pota toesSugar Beets

Red BeetsT u r n i p sRadishes


C or e and p i t fr u i t com par i son(com par ed app l es and p eaches:

FD A t o P D P )A p r i c o t s

D r i ed A p r i c o tsAp r i co t PastePeach

PearCher r i es

N ec t ar i nesPearP l u m s

G r ape com par i son ( FD A t o P D P )B l ackbe r r i es

B lueber r i es

Cranber r i esRaspber r i esSt raw ber r i es

C e l e r y -l i ke c r op s com par i son (FD At o P D P )

AsparagusLeeks

Scal l i ons

O t h er sM u s h r o o m sO l i ves , Green, B lack , S tu f fed

2 5 % r e du c ti onG r e e n b e a n c o m p a r iso n

(com par ed g r een b eans - FD A t oP D P )T omat oes

G r e e n T o m a to e sC u c u m b e r s

EggplantH o t Peppe r s

P ob l ano P epper sSer rano Peppers

G reen, Red or Sweet PeppersBanana Peppers

P est i c i de r esi dues f ound i n f r esh p r odu ce by t he FD A su r ve i l l ance p r og r am and U SD A P est i c i de D a t a Pr og r am

w er e r educed by 25 t o 9 5 pe r cen t t o mo r e accu r a te l y r e fl ec t the l eve l s l i ke l y t o be f ound i n coo ked and p r epa r ed foods.

R educ t i on f ac t o r s w e r e de ri ved by e i t he r com par i ng da t a fr om t he FD A su r ve i l l ance p r o g r am w i t h l eve l s o f O P s

r epo r t ed i n T o t a l D i e t St udy o r t he P est i c i de D a t a p r og r am .


33/54


pro du cts in the TDS. From p astato pretzels, to w heat bread andwh eat breakfast cereal, more than99 percent of more than 600samples tested for pesticides

were positive for eitherchlorpyrifos, malathion, or both.This strongly suggests that thelow level OP residue s repo rted inthe TDS for any single processedwh eat p roduct are very l ikelyrepresentative of the comm odityas a w hole. To increase thesample size for baby food, testsof baby food for pesticides com-missioned by EWG in 1995 were

added to TDS data from FDA.The results from both TDS andEWG w ere qu ite similar.

O f the 39 OP insecticide s w itha com mo n m echan ism o f toxicity,only 13 we re detected in thefood sup ply. These 13 OP com-pou nds , in turn , were found o n407 of the 3,695 foods reportedeaten by children age five and

under in the USDA survey.

Linking Food and ResidueD a t a . More than 3,695 foo ditems were reported eaten bychildren under age five in theCSFII. For p urp ose s of p red ictingpesticide exposure, however,many of these 3,695 foods can beconsidered the same food . Forexample, it is reasonable to as-

sume that cooked carrots withfat, cooked carrots without fat,and cooke d carrots (fat unspe ci-fied), are the same in terms ofpe sticide residu es. Many othe rdecisions were not that straightforward. Links between foodsrepo rted e aten, and residue find-ings were made as described be-

low. As a gene ral rule foodswe re l inked with residue valuesonly when a direct match be-tween the two foods was avail-able. Any deviation from this

rule is described below .

For fruits and vegetab leseaten raw, food consumptionvalues were matched first to datafrom PDP, whe n a vailable, andthen with FDA surveillance datawith a residue reduction factorap plied. Frozen fruits and veg-etables (not canned) were as-sumed to have the same residue

levels as fresh fruits and veg-etables and the same residuevalues w ere app lied . For fruitsand vegetables eaten cooked,either from cann ed or fresh veg-etables, residue values from thetotal diet study (TDS) were used.

For all other p rocessed andcooked foods that were reportedin the CSFII, TDS data were

used w hen a d irect match wasavailable. For thou sand s of spe -cific foods reported eaten by thepo pu lation studied cherries

jub ile e , p ep p e ro n i p izza, a ll so ftdrinks no direct matcheswere available in the residuefiles. These foo ds w ere notused in the an alysis. For ex-amp le, we did not attemp t tomatch the pep peroni p izza con-

sump tion data with OP residuedata from ch eese p izza, becauseof uncertainty abou t the e xactweight ratio of the foods thatconstitute each respective pizza.Likew ise w e did no t matchcherry pie residues with cherries

jub ile e co nsu m p tio n data , andso on for thousand s of food s

As a general ru le foodsw ere l inked wi thresidue values onlyw hen a d i rect matchbetween the two foods

was available.


34/54


w ith no direct ma tch. Withsandwiches, consumption datawas m atched w ith residue dataonly wh en the sandw ich con-sump tion data was rep orted in

its com po nen t parts thatmatched the residue data. Forexample, when a p eanut but terand jelly sandw ich w as repo rtedas X grams of bread, X grams ofpe anu t butter and X grams of

jelly, th ese con su m p tio n va lu eswere matched with correspon d-ing test results from the TDS.When the sandwich was simplyreport as a peanut butter and

jelly sa nd w ich , it w as n o t u se d .

The on e techn ical excep tionto this rule w as with w heatproducts in the form of pastaand bread . In this case residuedata were available for whitebread, whe at bread , macaroniand sp aghe tti. Children age fiveand under, how ever, reportedeating m any types of pasta (spa-

ghe tti, ma caron i, lasagnanoo dles etc.) and man y differenttypes of bread (French bread,Italian bread, pita bread etc.).In this case, any wh eat basedbread or pasta was matchedwith the residue values from themost closely matched wheatbased b read or p asta prod ucts inthe TDS.

The M onte Car lo . The expo-sure a ssessmen t is a Monte Carlostyle probability distributionanalysis designed to simulatereal world dietary exposure toOP pe sticides u sing the bestavailable data. The analysis w asmo deled after that used by theNation al Resea rch Cou ncil Com -

mittee on Pesticides in the Diets ofInfants and Children (NRC 1993pp. 297 through 307).

Dietary exposure to O Ps was

analyzed in 24 hour units to matchthe toxicity of OPs which are ac-tive for a least 24 hou rs after theyare consum ed. For examp le, anOP eaten at breakfast, will remainactive in the body in the afternoonand can be added , for purposes of risk assessme nt, to an OP eaten atdinner.

The program w as run o n a

Power Mac 8100 using FoxProsoftwa re. A distribu tion of dietaryOP e xposure w as simu lated foreach age group year (one-year-olds, two -year olds etc.) The dis-tribution was created by instruct-ing the computer to identify avalid individu al eating da y in thedatabase (pe rson one, day one)and to match each food eaten bythat individual on that day with a

randomly selected residue resultfrom all the sam p les for that foodin the residue database d escribedabo ve. Total daily exp osu re toeach of the thirteen individual OPsin the residue files was then calcu-lated and converted to a mg/kgexposure value for each OP con-sumed, depending on the amountof the food consumed, theresidue (s) foun d on the samp le

that was selected (zeros we re in-cluded as reported in the data),and the w eight of the child.

For exam ple, if a ch ild a te 100grams (a little under four ounces)of green bean s and the greenbean sample, randomly chosenfrom the residue database, had 1

The analysis w asm odeled after thatused by the N ationalAcademy of ScienceCom mit tee on

Pesticides in the D ietsof I nfants andChildren.


35/54


part per mill ion (ppm = mg/kg) ofacephate, the program would cal-culate that 1 mg/kg ace ph ate x100 grams of beans = 0.1 mg ofacep hate on those beans. If the

child weighed 10 kg, the dose o facephate that child got from thosegreen beans w ould be 0 .1 mg/ 10kg = 0.01 mg/kg b ody w eightacephate .

For each of the valid eatingdays available for each age year,this proce ss was rep eated 2,000times, to produce a distribution ofthree to four m illion individu al

exposure days, per age group, foreach of the O P

overexposed || organophosphate insecticides in children's food

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