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RESEARC H REPORTIN Q SERIE S

Researc h report s ofth e Offic e o f Researc h an d Development , U.S

. Environmenta l Protectio n Agency , hav e bee n groupe d int o fiv e series

. Thes e fiv e broa d categorie s wer

e establishe d t o facilitat e furthe rdevelopmen t an d applicatio n o f environmenta l technology

. Eliminatio n o f traditiona l groupin g wa s consciousl y planne d t o foste rtechnolog ytransfe ran d a maximu m interfac e i n relate d fields

. Th e fiv e serie s are : • •? *-•'" " 1

. Environmenta l Healt h Effects Researc h 2

. Environmenta l Protectio n Technolog y 3

. Ecologica l Researc h 4

. Environmenta l Monitorin g 5

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t has bee n assigne d t o th e ECOLOGICA L RESEARC H series

. Thi s serie s describe s researc h o n th e effect s o f pollutio n o n humans , plan t an d anima l species , an d materials

. Problem s ar e assesse d fo rthei rlong

- an d short-ter m influences

. Investigation s includ e formation , transport , an d pathwa ystudie s t o determin e th e fat e o

f pollutant s an d thei reffects

. Thi s wor k provide s th e technica l basi s fo rsettin g standard s t o minimiz e undesirabl e change s i n livin g organism s i n th e aquatic , terrestrial , an d atmospheri c environments

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### EPA-600/3-77-00 9 Januar y 197 7

TH E SHORT-TERM

EFFECT S O F LEAD ON DOMESTI C AN D WIL D ANIMAL S

b y

R . P . Bott s Corvalli s Environmenta l Researc hLaborator y

Corvallis , Orego n9733 0

CORVALLI S ENVIRONMENTAL RESEARC H LABORATORY OFFIC E O F RESEARC H AN D DEVELOPMEN T U.S . ENVIRONMENTAL PROTECTION AGENC Y CORVALLIS , OREGON

9733 0

ij**m'^^.'.yj&p^ ^P. 5

T T * T"STffr wv "' " '

DISCLAIME R

Thi s repor t ha s bee nreviewe db y th e Corvalli s Environmenta l Researc h Laboratory , U.S . Environmenta l Protectio nAgency , an dapprove dfo r publication . Mentio no f trad e name s o r commercia l product s doe s no t constitut e endorsemen t o r recommendatio nfo r use .



### i iP. 6 •T^FT^rrflT f

FOREWOR D

Effectiv e regulator y

and enforcemen t action s b y th e Environmenta l Protectio nAgenc y

woul d b e virtuall y

impossibl e withou t soundscientifi c dat a o n pollutant s an d thei r impac t on environmenta l stabilit y and huma n health . Responsibilit y fo r buildin g thi s dat a bas e ha s bee nassigne dt o EPA' s Offic e o f Researc hand Developmen t an d it s 1 5 majo r fiel dinstalla tions , on e o f whic hi s th e Corvalli s Environmenta l Researc hLaborator y (CERL) . Th e primar y

missio no f th e Corvalli s Laborator y i s researc hon th e effect s o f environmenta l pollutant s on terrestrial , freshwater , an d marin e ecosystems ; th e behavior , effect s an d contro l o f pollutant s i n lak e systems ; an d th e developmen t o f predictiv e model s on th e movemen t o f pollutant s i n th e biosphere . Thi s repor t present s a discussio no n th e exten t o f lea dfoundi n wil d an d domesti c animal s an d some o f th e shor t ter m effect s o f thi s toxi c sub stance .

A.F . Bartsc h Director , CER L



## •r ni\WmWtt'Uy/SB!R ' ^'" ^•^Tmmrmw P. 7

ABSTRAC T

Smal l quantitie s o f lead , a ubiquitou s and toxi c element , ma y b e found i npracticall y

al l specie s o f plant s and animals . Th e lis t o f animals , bot h domesti c and wild , reportedl y intoxicate db

y lea di s impressive . Th e source s o f lea d poisonin g var y wit hspecie s o f animals . Lea dbas e paints , use d moto r oils , spen t leadsho t an dpasture s contaminate db y lead smelter s seemingl y

hav e bee nmos t ofte nincriminated . Th e lesion s associate d wit hlea dintoxicatio nma y var y widel y bot h withi nand betwee nspecie s o f animals . Lesion s andsymptom s o f th e centra l nervou s system

ar e th e mos t prominent . Toxi c level s fo r variou s specie s a s reporte di nth e literatur e var y widel y and seemingl y

a singl e toxi c dos e fo r eac hspecies , a s yet , ha s no t bee ndefinitel y

established . Th e diagnosi s and treatmen t o f lea dintoxicatio nma y become laboriou s and tim e consuming . Mos t symptom s reporte dinvolv e centra l nervou s syste m dearrangement . Treatmen t o f mos t clinica l case s i s disappointin g generall y becaus e o f th e acut e natur e o f leadpoisoning .



### \ v

### CONTENT S P. 8



### Sectio n Pag e

I . Conclusion s 1 II . Introductio n2 III . Source s o f Lea dandth e Epizootiolog y o f Lea dToxicosi s 4 IV . Metabolis m

o f Lea d7 V . Lesion s Associate dwit hLea dIntoxicatio n1 1 VI . Othe r Functiona l Effect s Associate dwit hLead Poisonin g . 1 4 VII . Toxi c Level s o f Leadfo r Variou s Specie s o f Animal s 1 6 VIII . Signs , Symptom s an dDiagnosi s 1 9 IX . Clinica l Patholog y andChemica l Analysi s 2 1 X . Treatmen t 2 2 XI . Reference s 2 3P. 9 TTnTMTflTr rr• "

• • - - n

Sectio nI

CONCLUSION S

Fro m dat a reporte d i nth e literatur e crud e estimate s o f th e occurrenc e o f lea d poisonin g ma y be derived . Approximatel y 150,00 0 cattl e ar e annuall y expose d t o toxi c level s o f leadand 20,00 0 acut e case s occu r pe r year . O f these , 15,00 0 animal s succum bt o leadpoisoning . I naddition , i t i s estimat ed tha t 1,000,00 0 migrator y waterfow l succum

bt o leadpoisonin g du e t o consumin g spen t lead shot . Th e metabolis m

o f lea d compound s i s ver y complicate dandvariabl e bot h withi nan

d betwee nspecies . Fo r mos t mammal s includin g ma n1-5 % o f th e lea d take norall y

wil l b e absorbed . On e ma y estimat e fo r ruminant s tha t 83.6 % i s excrete d throug hth e feces ; 14.8 % throug hth e urine , an d1.6 % throug hth e milk . Lead , onc e take ninternall y i s retaine db

y th e body ; particularly , th e bone s tenaciousl y retai nlea d and ma y accoun t fo r a s muc ha s 80 % o f th e tota l bod

y burden . Th e exac t mechanism s givin g ris e t o th e pathologica l lesion s associate d wit hlead poisonin g hav e no t bee nclarified . Thi s i s particularl y tru e fo r chroni c encephalopathy and nephropathy . Severa l enzyme s ar e know nt o be inhibite d b

y lead and amon g thi s grou par e severa l enzyme s show no r suspecte d o f bein g involve d i nrena l tubula r transport . Eve nwit hth e voluminou s literatur e concernin g lead , toxi c level s fo r variou s specie s o f animal s hav e no t bee nprecisel y determined , no r i s ther e genera l agreemen t onwha t constitute s a saf e leve l o f intak e fo r extende d period s o f time . Generally , th e treatmen t o f leadpoisonin g i s disappointin g becaus e o f th e acut e natur e o f mos t clinica l cases . Thu s mor e emphasi s shoul db e place d onpreventiv e rathe r tha ntherapeuti c program s t o avoi dth e losse s du e t o lead poisoning .""T^ T TrT"P*1JT|p F '• ^~' ^ M O ^ ^ ^

Sectio nI I

INTRODUCTION

Lea d i s on e o f th e oldes t metal s use d b y mankind ; Roman s and medieva l Briton s constructe d lea d wate r pipe s (1) . Usag e ha s expande dunti l toda y th e tota l annua l U.S . consumptio ni n 196 8 wa s 1,328,97 0 ton s (2) . Approxi matel y 184,31 6 ton s annuall y ar e emitte dt o th e atmospher e fro m source s suc h a s combustio no f gasoline , fue l oil , and coa l i n additio nt o severa l othe r industria l sources . Th e mos t abundan t lead or e i s Galen a (PbS ) (1) . Approxi matel y 3 2 percen t o f th e U.S . consumptio ni s obtaine dfro m primar y smelters , 3 8 percen t fro

m secondar y

recovery , an

d 3 0 percen t fro

m import s (2) . Lea d i s a n ubiquitou s an d toxi c element . Smal l quantitie s ca n b e found i npracticall y

al l livin g tissue s o f plant s an d animals . Soils , limestone , sandstone , shal e an

d igneou s rock s contai nquantitie s varyin g fro m 7 t o 2 0 pp m (3) . Muc hha s bee nwritte nabou t lead , an d thousand s o f case s o f lea d poisonin g hav e bee nreporte d in bot hth e huma nan d veterinar y

medica l litera ture . Th e specie s o f animal s tha t hav e eithe r die do r bee nobviousl y il l fro m increase d lea d intak e include :
A . Farm

livestoc k an

d pet s 

### 1 . 2 . 3 . 4 . 5 .

Wil d 

### 1 . 2 . 3 . 4 . 5 . 6 . 7 . Horse s Cattl e Swin e Dog s Shee p (thi s review naturall y

occurin g animal s Duck s Gees e Andea nCondo r Dove s Quai l Pheasant s Falco n faile dt o

lead fin

dany poisoning) . report s invo l vin gP.1 1

• r r*' ; -ff^ i f'^n*!"rr*"' r



### Zo o animal s 1 . 2 . 3 . 4 . 5 . 6 . 7 . Non-huma n Leopard s Australia n Parrot s Pola r bea r Lorikeet s Ferret s primate s

frui t bat s

Mos t o f th e reporte dincident s o f poisonin g involve dsmal l number s o f animals . However , contaminatio no f vegetatio nb y industria l operations(4 - 13 ) ofte nresult s i ndeat ht o severa l animal s a t on e time . Becaus e leadi s th e mos t commo naccidenta l poiso no f far m animal s (14) , i t i s o f considerabl e economi c importanc e t o agriculture .Sectio nII I

SOURC E O F LEA

D AN D TH E EPIZOOTIOLOG YAND LEA D TOXICOSI S

Th e diagnosi s o f lea d poisonin g i s no t precis e inal l cases . Fo r thi s reason , knowledg e o f th e epizootiology o f lea dpoisonin g ca nhel pinarriv in g a t a definitiv e diagnosis , i nadditio nt o determinin g th e occurrenc e o f th e diseas e and definin g th e circumstance s o f exposure . EPIZOOTIOLOG Y Althoug hdefinit e estimate s o f th e incidence , morbidit y an dmortalit y i ndomesti c an

d wil d animal s i s lacking , th e literatur e contain s som e informatio nconcernin g th e epizootiolog y o f leadpoisoning . Report s ofte n stat e tha t th e morbidit y i s lo w an dth e mortalit y

o r cas e fatalit y

rat e i s hig h(14 , 15) . Lea d poisonin g i s diagnose dmor e frequentl y i ncattl e an

d dog s tha nothe r specie s (14) . Fo r cattle , th e incidenc e o f leadpoisonin g ha s bee nestimate da s approximatel y

16 7 case s pe r yea r pe r 1,000,00 0 animal s (2) . However , severa l tenuou s assumption s wer e mad e inorde r t o deriv e thi s estimate . Th e propor tiona l mortalit y

fo r lea d poisonin g (e.g. , no . o f animal s dyin g o f lead poisonin g pe r al l anima l deaths ) i ncattl e i s estimate dt o be 1. 7 percen t fo r calve s an

d 4. 5 percen t fo r olde r cattl e (16) . Th e morbidit y o f animal s exposure d t o toxi c level s o f lea d i s estimate dt o b e 11-1 5 percen t an

dthe cas e fatalit y

rat e i s 55-8 5 percen t (17) . Two possibl e explanation s ar e offere d t o explai nth e abov e estimates . Either , fe w animals--only

th e mos t seriou s cases—ar e presente dt o diagnosti c laboratorie s o r fe w expose d animal s receiv e dose s o f sufficien t magnitud e t o caus e illness . I f on e can accep t th e incidenc e o f lead poisonin g t o b e approximately

0.01 6 percen t (2 ) pe r yea r an

d th e morbidit y

o f animal s expose dt o toxi c leadlevel s t o b e 11 - 1 5 percen t (17) , the non e ma y conclud e tha t th e rati o o f expose dt o unexpose d cattl e i s 1:60 0 t o 1:900 . Wit ha tota l 196 9 cattl e populatio no f 123,748,00 0 i nth e U.S. , on e ca nestimat e tha t betwee n137,00 0 an d190,00 0 cattl e ar e annuall y expose d t o toxi c level s o f lead an dtha t 20,00 0 case s o f lea d poisonin g occu r pe r year . Lea d intoxicatio nha s a definit e seasona l trendfo r cattl e (17) , dogs(19 ) an d huma nbeing s (2) . Durin g a fiv e yea r perio d(1965-1970) , 4 1 percen t o f th e bovin e case s o f a larg e diagnosti c cente r occurre ddurin g April , Ma y an d Jun e (17) . Incontrast , lea d poisonin g indog s mor e ofte ni s diagnose d i n summe r an

d fal l (19) . Th e seasona l trend fo r cattle , a t leas t inIowa , coincide s wit hth e time whe ncattl e ar e release dt o sprin g pasture s (17) .P.1 3

Ver y littl e informatio ni s availabl e o nthe ag e distributio no f lea d poisoning . Fo r dogs , poisonin g apparentl y occur s mor e frequentl y i nyounge r animals , possibl y

becaus e o f thei r indiscriminat e chewin g habit s (2 , 19) . Th e incidenc e o f lea d poisonin g i s unknow nfo r practicall y

al l specie s o f wil d animals . However , a nestimate d on e millio nducks , gees e an dswan s di e annuall y

i nth e U.S . o f lea d poisonin g (20) . Th e source s o f lea d poisonin g ar e varie d an dofte ndependo nsuc h factor s a s th e characteristic s o f th e anima l an dit s peculia r husbandr y considerations . Consumptio no f spen t lead sho t fo r wildlif e specie s suc ha s ducks , geese , swans , mournin g doves , pheasants , condo r an dfalcon s mos t ofte nha s bee nincriminate d (21-25 ) a s th e sourc e o f leadpoisoning . Th e consumptio no f flaking-pain t containin g leadi s a commo nsourc e fo r zo o animal s (26-28) . Fo r domesti c an d pe t animals , th e source s o f leadpoisonin g ar e mor e variable . I non e stud y (17 ) th e source s o f lea dincriminate dfo r cattl e wer e pain t (2 9 percent) , oi l (2 5 percent) , unknow n(2 4 percent ) junkpile s (1 1 percent ) greas e ( 6 percent ) an dbatterie s ( 5 percent) . Tabl e 1 list s th e mos t ofte nquote d source s o f lea db y specie s (4,5,6,7,8,9,10,17 , 29-33) . Tabl e 1 . Source s o f Lea dPoisonin g fo r Variou s Specie s
o f Livestoc k

Specie s Source s

Cattl e

Horse s Swin e
Do g Lea d bas e paint , use dmoto r oil , grease , use d batteries , junkpile s containin g lead , putty , roofin g material , linoleu m contaminate dwater , contaminate d fee d contaminate dpasture s fro m leadsmelter s Contaminate d pasture s fro m leadsmelter s

Lea d bas e pain t Paint , linoleum , sho t gunslugs , curtai n weights , plaste r

Som e o f thes e divers e source s ar e mor e poten t 1 nterm s o f thei r lea d content . Greas e ma y

contai na s muc ha s 450,00 0 pp m (17 ) an doi l a s muc ha s 50 0 pp m (34) . Horse s an

d cattl e hav e die d grazin g o ncontaminate dpasture s tha t containe d a s muc ha s 2,00 0 pp m (35 ) o f lead .Th e epizootiolog y o f lea dpoisonin g ma y b e briefl y

summarized : 1 . Fo r Far

m Animal s

a . Th e diseas e occur s mor e ofte ninspring . b . Th e morbidit y

i s lo w an dmortalit y

high . c . Th e source s mos t ofte nincriminate dinclud e paint , use d oil , grease , anddiscarde dbatteries . 2 . Fo r Dog s

a . Th e diseas e occur s mor e ofte ninsumme r an dfall . b . Mos t ofte ni t i s a diseas e o f youn g dogs . c . Severa l source s hav e bee nsuggested . 3 . Fo r Wildlif e

a . Consumptio no f spen t lea dsho t i s th e primar y source . b . Approximatel y

1,000,00 0 migrator y bird s ar e los t annually . 4 . Fo r Zo o Animal s

a . Lea dbas e pain t consume dafter i t ha s flake dfro m cage s an denclosure s i s th e primar y source . Obviously , th e salien t feature s o f a program t o reduc e th e occurrenc e o f lea dpoisonin g woul dinvolve : 1 . Onth e farm , implemen t clea nhusbandr y practices . I

nparticula r

a . Don' t drai nth e oi l fro m moto r vehicle s inpastures . b . Don' t discar dbatteries , pain t buckets , o r use dgreas e can s i npastures . c . Erec t fence s t o kee panimal s ou t o f ol djun k pile s 2 . Wit hnon-lea dpaint , thoroughl y clea nan

drepain t al l cage s fo r animals . 3 . Fo r wildlife , a preventiv e program (being implemented)(2 ) involve s developin g a substitut e fo r lea dshot .P.1 5

Sectio nI

V

METABOLIS M

O F LEA D

ABSORPTIO N Th e absorptio no f lea d compound s i s quit e comple xan dinvolve s thre e differen t routes : inhalation , ingestion , andabsorptio nthroug hth e skin . O f thes e inhalatio ni s mos t efficient , an dski nabsorptio ni s th e leas t efficient . Fo r man , 14-4 5 percen t o f inhale dleadi s retained , wherea s onl y 5-1 5 percen t o f tha t ingeste d i s retaine d (36) . Factor s tha t ma y modif y retentio no f lead particulate s i nth e lung s ar e th e particl e size , mucou s flow , ciliar y

action , an

d th e alveola r clearanc e rat e (36) . Th e percen t retaine d b y ingestio no r th e digestiv e coefficien t i s compute d b

y determinin g th e ratio—th e portio nretained/portio nconsumed . Th e digestiv e coefficien t o f lea d varie s widel y betwee nspecie s fro

m 5-1 5 percen t i nma n(36 ) t o a s littl e a s 1- 3 percen t incattl e an don e percen t i

nrabbit s (37) . Fo r many

toxi c metals , th e rat e o f absorptio ndepend s onsuc hfactor s a s th e chemica l for

m o f th e lead , th e ag e o f th e animal , th e p H o f th e gastro-intestina l tract , th e gu t transien t time , th e gu t microflora , an dth e presenc e o r absenc e o f othe r metals . Fo r exampl e reducin g th e calciu m leve l i nth e die t ma y

increas e th e leadabsorptio ni nrat s (38) . I

ncontras t vitami nD ha s a revers e effec t (39) . Furthermor e leadabsorptio nb v th e gastro-intestina l trac t i s greate r i nyoung tha ninol drat s (40,41) . TRANSPORT , DISTRIBUTIO N AND EXCRETION

Onc e lea d i s absorbed , i t enter s int o a stat e o f exchang e betwee n tissue s and th e blood . Th e variou s organ s retai ndifferen t amount s o f lead . Transport , distributio nand excretio no f leadma y be bes t conceptualize d a s a serie s o f compartment s interconnecte d wit hon e anothe r vi a th e bloo d (Figur e 1) .Fig . 1 : Hypothetica l Transpor t o f Lea d

Sof t Tissue s Bon e

Eac hcompartmen t receive s an dwil l retai nlea dfro m th e blood . Th e retentio ntime o f th e lead depend s o nit s biologica l half-time t*|/2 , whic h i ntur ndepend s upo nth e strengt ho f th e bon dbetwee nleadan

dth e bindin g tissue . I f th e transfe r fro

m a tissu e ca nb e assume dt o b e a first-orde r decay , th e t1/ 2 i s th e time require dfo r 1/ 2 o f th e presen t burde no f lead t o b e transferre d fro m th e tissu e t o th e blood . Inmany biologica l systems , th e transfe r o f materia l betwee ncompartment s ca nb e simulate db y assumin g a firs t orde r deca y

(42,43) . The nth e transfe r rat e depend s onl y onth e concen tratio ni nth e originatin g compartmen t an dth e transfe r coefficien t fo r tha t compartment . Th e transfe r coefficient , k , i s relate dt o ti/ 2 b y th e equa tion :

k 

## ..-M? l

x l/ 2

On e ca nappreciat e tha t th e concentration s i nth e variou s organ s wil l chang e wit htime afte r a singl e dos e o f leadi s absorbe dan dtha t thes e concentration s wil l depen d partl y upo nth e t-j/2 - Sinc e bloo d i s th e mediu m tha t transport s lead , rol e i nth e metabolis m o f lead . Base d o ntrace r stu d we t chemica l analysi s o f tissue s an d bloo dfro

m shee p tha t bloo d contain s mor e tha non e compartment . Resu l indicat e a t leas t thre e compartments . Some sugges t ( re d bloo d eel 1 s (RBCs) , specifi c metalloproteins , p l molecula r weigh t plasm a proteins . Th e transfe r rat e th e ti/ 2 i s longer ) fo r "RBCs tha nfo r plasma r *o r sera ; part , th e concentratio nwoul d be greate r i nth e RBC s Fort y an d one-hal f hour s afte r receivin g a nora l dos e •plasm a rati o wa s 12 2 i na cal f (46) . Incontrast , t h t o b e 1 1 i nsheep , 4 0 hour s afte r .a nintravenou s dos e i t assume s animportan t

ie s (44 ) inth e do g an d (45) , on e ma y

conclud e t s reporte di ndog s (44 ) 36 ) fou r compartments : asm a protein s andlo

w i s muc hslowe r (tha t i s thus , fo r th e mos t tha ninth e plasma . o f lead , th e RB C t o i s rati o wa s estimate d (45) . Thi s latte rP.1 7



### dat a (45 ) sho

w tha t th e tj/ 2 1 s longe r fo r RBC s tha nfo r serum , andconse quently , th e fractio nboundt o seru m woul db e transferre dmor e readil y t o othe r tissues . Severa l factor s tha t combin e t o maintai nth e leve l o f lead i nth e bloo dInclud e th e Initia l dos e o f lead , th e t|/ 2 o f th e compartment s inth e blood , andth e tj/ 2 o f th e variou s compartment s perfuse db y th e blood . Fro

m th e result s reporte d1ndog s (44 ) afte r 2 0 day s th e leve l inth e bloodfel l t o a nestimate d5. 8 percen t o f th e leve l a t th e tim e o f Injectio n and , afte r a nadditiona l 26 0 days , furthe r fel l t o approximatel y 2. 5 percent . Thi s fac t demonstrate s th e persistenc e o f lea donc e 1 t 1 s take nInternally . Th e distributio no f lead1nth e variou s tissue s a t an y on e time afte r a dos e o f lea ddepend s o nth e perfusio no f th e tissue , th e fractio ni nth e bloo dtha t I s diffusable , an dth e ti/ 2 o f th e perfuse dtissues . Concentra tio no f lea d1ndifferen t tissue s demonstrat e remarkabl e variations . Gen erally , lea d1 s concentrate d1 nbone , Uve r an dkidne y tissues—concentra tion s a s muc ha s 10 0 time s greate r tha ni nplasm a o r muscle . Ina cal f analyze d42. 5 hour s afte r Injectio nwit hlead , 3 4 percen t o f th e tota l body burde nwa s foundinth e Uver , 3 3 percen t inth e bone , an d2 1 percen t inth e blood(46) . Inrabbit s 9 6 hour s afte r Injection , 2 1 percen t o f th e leadwa s found1 nth e Uver , 7 0 percen t inth e bone , an don e percen t i nth e bloo d(45) . Th e kidne y

concentrate s leadbut , becaus e o f th e relativ e weight , contain s appreciabl y

les s o f th e tota l bod y burden . A

publicatio nreporte ddat a fo r a cal f tha t consume da dall y averag e o f 0. 1 m

g o f leadfo r 16 9 day s (47) . I f on e assume s tota l body ratio s o f .0 4 fo r blood , .0 4 fo r bone , an d.0 3 fo r liver , on e ca nestimat e tha t approximatel y 80 % o f the tota l bod

y burde ni s locate d1 nbon e an

d5 percen t i nth e Uver . A t lo w Intak e level s an

dafte r a sufficien t lengt ho f time , a nequilibriu m 1 s reache dwher e excretio nequal s intake . The nth e concentration s i nth e variou s compartment s d o no t change , an dtha t compartment s (bon e fo r lead ) wit hth e longes t t-j/ 2 wil l contai na n appreciabl e amoun t o f th e tota l bod y burden . Th e t-\/o

^ o r 

### bon e i

ndog s wa s estimate dt o b e 750 0 day s (48) . Incontras t a U/o o r bloodwa s estimate dt o b e 3. 5 days(42) . Lea dabsorbe db

y th e gastrointestina l trac t ca nbe excrete dvi a fou r routes : (1 ) glandula r excretio nan depithelia l sheddin g o f th e gastro intestina l tract , (2 ) bilia r excretion , (3 ) urinar y excretion , an

d(4 ) mammar y glandula r excretio n(36) . Th e relativ e importanc e o f thes e route s i s unknow nfo r many

animals . Afte r intravenou s injectio no f lead , th e rati o o f th e feca l (i.e. , th e su m o f th e glandula r excretio nan depithelia l shedding ) t o tota l excretio nca n b e computed. Inth e do g thi s rati o i s approximatel y 0.6 5 (44) ; inshee pove r a 1 0 da y collectio nperio dth e rati o wa s 0.8 4 (36) . Th e discrepancie s betwee n thi s rati o fo r dog s an dshee pma y

b e du e t o th e fac t tha t th e dos e o f lead receive db

y th e do g (44 ) wa s muc hles s ona pe r weigh t basi s tha ntha t re ceive db y th e shee p(37 ) o r du e t o difference s inth e metabolis m o f lead . Toxi c dose s o f leadma y chang e excretor y

function s an

dresul t i nchange s o f excretor y

pathways . Fo r example , whe ncadmiu m cause s rena l damage , cadmiu m excretio nincrease s (36) .""TTfr'jtr^' '



### Mammar y glandexcretio ni s muc hles s tha nurinar y excretion . Fro

m dat a collecte d6 day s inon e cow (46) , the mammar y

glandexcretio nwa s 1 0 percen t o f th e valu e fo r urinar y excretion . Combinin g the dat a fro m shee p(37 ) an

d cow (46) , on e ca ncomput e a crud e excretio nratio : feca l excretion—83. 6 percent ; urinar y excretion—14. 8 percent ; an

d mammar y

excretion—1. 6 percent .

1 0P.1 9 •r"TY"v"'^jfir'

r '-

Sectio nV

LESION S ASSOCIATE D WITH LEAD INTOXICATION

Th e functiona l an

d pathologica l effect s quote din th e literatur e ar e quit e irregula r an

d variabl e fo r ma n an d variou s specie s o f animals . ANEMI A Whe nth e synthesi s o f RBC s an d thei r component s i s decrease danemi a occurs . In mos t case s o f lead intoxication , anemi a i s no t a predominatin g clinical.sign ; however , th e toxi c effect s o f leadhav e motivate dresearc ht o understan d porphyri nmetabolis m whic hi s controlle d b y severa l enzyme s (49) . Th e lis t o f enzyme s tha t lead inhibit s o r enhance s i s impressive . Many o f thes e effect s ar e demonstrabl e in vitr o only , an d i n som e instances , a t concentration s tha t neve r have bee nobserve di n clinicall y il l individual s (49) . Heme synthesi s ma y b e briefl y

outline da s (2) :
ALA synthetas e (ALAS ) Succiny l Co

A + Glycin e ^ 6

_ amin 0 levulini c (] ) aci d (ALA )

AL A dehydras e . . AL A • porphobilinoge n(PBG ) ( 2 ' PB G• • uroporphybinoge nII I (UR O III ) (3 )

urogenas e UR O II I • coproporphybilinoge nII I (coproIII ) (4 )

coprogenas e Copr o II I • protoporphyri nI X(prot o IX ) (5 )

Hem e synthetas e Prot o I X— : • Hem e (6 ) Step s (1) , (2) , ( 3 o r 4) , (5 ) and (6 ) hav e bee ndemonstrate dt o b e inhibite d b

y lea d (2 , 49) . Over t clinica l lea d poisonin g i s accompanie d b y increase d AL A

an d coproporphyri ni n th e urin e and bloo d(50) . I n vitr o studie s sugges t tha t step s (2 ) an d (5 ) ar e mos t sensitiv e toHTea d inhibitio n(47) . Depresse d AL A dehydras e activit y

in erythrocyte s and



### 1 1

««ua^.yj:UHia^ ^elevate d urin e an d seru m AL A hav e bee nobserve d incattl e chronicall y poisone d (51) . Inadditio nt o inhibitin g hem e synthesi s lead apparentl y suppresse s globuli nsynthesi s (49) . Othe r anemia-relate d abnormalitie s tha t hav e bee nobserve d i nma nan d animals include : 1 . Shortene d surviva l o f RBC s (52 ) 2 . Reticulocytosi s (2,33,53 ) 3 . Decrease d hemoglobi n(53 , 54 , 55 ) 4 . Basophili c stipplin g o f RBC s (2 ) 5 . Siderocytosi s (54 ) 6 . Increase d osmoti c and mechanica l fragilit y (2,49 ) 7 . Los s o f intracellula r K + ion s (49 ) 8 . Immatur e form s o f RBC s ingenera l circulatio n(33 ) 9 . Erythroi d hyperplasi a o f th e bon e marrow (54 ) 10 . Mitosis o f erythrocyte s inth e periphera l blood infowl (22,56) . Basophili c stippling , ofte nmentione d a s a sympto m o f lead poisoning , i s du e t o accumulation s o f cytoplas m and nuclea r fragment s alon g wit hnon hem e ironindevelopin g erythrocyte s (2) . Ingeneral , th e anemi a associate d wit hlea d poisonin g i s no t sever e an d i s difficul t t o distinguis hfro m anemi a du e t o othe r causes . NEPHROPATH Y

Inman , rena l insufficienc y i s a lat e sequel a o f lead poisonin g (1,2,54) . Th e pathogenesi s o f rena l insufficienc y i s no t clearl y

define d (2 ) an

d apparentl y

occur s inthos e individual s wh o ar e expose d t o lead ove r long period s o f time (1,2,54) . Lead-induce d rena l insufficienc y i s characterize d b y glycosui a an

d hyper-amin o aciduri a (2 , 54).I nadditio nt o amin o aciduri a an d glycosuri a extreme exposur e ca ncaus e hypophosphatemi a and hyperphospha turi a (Fancon i syndrome ) (2) . Uri c aci d excretio nsometime s i s reduce d causin g saturin e gou t (2) . Mos t clinica l finding s poin t t o rena l tubula r dysfunction . Electro n microscopi c an

d biochemica l studie s demonstrat e alteration s inmitochondria l structure s an

d cellula r oxidatio nprocesse s (58,59) . Th e enzymes , alkalin e phosphatase , carboni c anhydrase , ATPases , an d cytochrome oxidas e al l inhib ited b y lea d (49)—ar e know

no r suspecte d o f being involve d i nrena l tubula r transpor t mechanism s (60) . Th e mos t consisten t lesio nassociate d wit hlea d poisonin g i s intranuclea r inclusio nbodie s o f th e proxima l tubules . Thes e inclusions , believe d t o b e lead protei ncomple x(61) , ar e reporte d invariou s specie s o f mammal s an d bird s dyin g o f lead poisonin g (22,56,62,63,64) . Althoug hcloudy

swellin g an

d degenerativ e changes o f th e tubule s ca nb e observed , thos e condition s ar e usuall y mil d an d inconspicuou s (15,65) .



### 1 2P.2 1

I nsummary , th e significanc e o f rena l insufficienc y inleadpoisonin g o f domesti c animal s i s unknow nan d ha s no t bee ndescribed , probabl y becaus e domesti c animal s ar e no t expose d t o leadlon g enoug hfo r rena l insufficienc y t o b e observed . NERVOU S SYSTE M Symptom s o f centra l nervou s syste m dearrangemen t predominat e inmos t diagnose d case s o f lea d poisoning . I nma nacut e encephalopathy du e t o lea d intoxicatio ni s characterize d b y rapi d onse t o f seizures , ofte nfollowe db y coma . Inacut e encephalopathy (2 ) vascula r injur y i s th e lesio nmos t ofte n associate d wit hedem

a o f th e brain . I ncontrast , patient s wit hchroni c encephalopathy

develo p progressiv e menta l deterioratio nwit hlos s o f moto r contro l (2) . Th e etiolog y o f chroni c encephalopathy i s no t clea r an

dma y b e du e t o severa l othe r factors . Encephalopathy

dominate s i nmos t diagnose dcase s o f lea dpoisonin g in domesti c animals . Apparently , a s i nman , vascula r injur y i s th e initiatin g lesio n(55) . Incattle , brai nlesion s progres s fro m a prominenc e o f endo thelia l cell s o f th e capillarie s t o th e developmen t o f edem a foc i an

dneuro na l degenerativ e changes . Thes e foca l lesion s develo pa lamina r patter n accompanie d b

y enlargemen t o f astrocytes . Chronicall y il l animal s develo p lesion s i nth e tip s o f th e gyri , accompanie db y capillar y

endothelia l prolif eration , astrocyti c proliferation , spongy degeneration , neurona l necrosis , cavitatio ndu e t o los s o f cells , an dcapillar y

proliferatio ninthes e areas . I ndogs , th e reporte d lesion s ar e simila r t o thos e i ncattl e (66) . Damag e t o th e smal l vessel s includ e necroti c endothelium , usuall y associate d wit hlamina r necrosi s i nth e cerebra l cortex . Gliosi s an dcapillar y

prolif eratio nar e observe d i nth e chronicall y ill . I

npe r acut e cases , significan t lesion s ma y

no t b e observe d (67) . Lesion s o f th e centra l nervou s syste m ar e no t sever e i

nbirds . Chicken s tolerat e relativel y

highdose s o f lead(68) , an dCN S lesion s ar e no t wel l define d inth e literature . Gees e experienc e cerebra l edem a wit hseriou s flui d accumulatio ni nth e space s o f Virchow-Rubi n(69) . However , routin e stainin g procedure s faile d t o demonstrat e any significan t lesion s inpoisone d duck s (22) . PERIPHERAL NEUROPATH Y

I nman , periphera l neuropathy i s observe d an

dcharacterize db

y moto r involve men t wit hn o sensor y nerv e aberrations . Chronicall y poisone dexperimenta l animal s develo p segmenta l demyelinatio no f som e nerv e fiber s (2) . Electro physiologica l studie s o f poisone dbaboon s reveale dn o abnormalitie s o f nerv e conductio n(70) . Horse s wit hleadpoisonin g exhibi t sign s o f sever e inspira tor y dyspne a (4) , possibl y havin g th e sam

e histologica l basi s a s periphera l neuropathy

observe d i nma n(15) .



### 1 3P.2 2

Sectio nV I

OTHE RFUNCTIONAL EFFECT S ASSOCIATE D WIT H LEA D POISIONING

Numerou s organ-system s reportedl y (2 ) impaire db

y leadintoxicatio n include : 1 . Decrease d iodin e uptak e 2 . Decrease d gonadotrophi c hormone s 3 . Abnorma l functio no f th e pituitary-adrena l axi s 4 . Myopathy

o f skeleta l muscle s 5 . Cardia c arrhythmia s 6 . Decrease d fertilit y 7 . Abnorma l seru

m albumin s an

d seru m globuli nlevel s (54 ) 8 . Elevate d seru

m cholestero l level s (54 )

A s i nman , a variet y

o f abnormalitie s have bee nreporte dindomesti c an d experimenta l animals . Apparentl y lea d i s immuno-suppressiv e evidence d b y reduce d lysozyme indog s poisone d wit hlead(54) . Lea ddecrease s th e resistanc e o f mic e t o Salmonell a typhimuriu m (71) , inadditio nt o decreasin g th e numbe r o f spleni c cell s producin g bot hIg m an dIg Gantibodie s (72) . Lead poisonin g inth e do g produce s acidophili c intranuclea r inclusio nbodie s i n th e liver . Live r functio ntest s reporte d indog s (73 ) an dcattl e (55 ) occa sionall y indicat e elevate d level s o f som e enzyme s (e.g. , seru m glutami c oxalaceti c transaminase , seru m pyruvi c transaminase , an dornithin e an

d carbamy l transferase) . Th e gastroenteritis associate dwit hlead intoxicatio nvarie s fro m n o lesion s i ncattl e (15 ) t o sever e lesion s inshee p(29) . On e do g experience da perforate d gastri c ulce r wit hlead poisonin g (74) . Inanothe r report , 2 4 percen t o f poisone d cattl e ha dsome for

m o f gastroenteriti s (17) . Abnorma l change s i nbon y tissu e hav e bee nreporte di nhorse s sufferin g fro m lead poisonin g (63) . Thei r lesion s include dedematou s synovia l mem branes , erosio no f join t surfaces , an d exostosis . Radiograph s o f experi menta l poisone d dog s demonstrate d radio-opaqu e line s o f th e dista l radi i and thoraci c spine s (73) . On e stud y o f th e interaction s o f lead , zinc , cadmiu m i npigs(75 ) reporte d radio-opaqu e line s i nth e metaphysis . Othe r change s associate d wit hlea d poisonin g includ e chromosome damag e (76) , abortio n (76,77) , reduce d fertilit y (76) , an

dendocardia l an

depicardia l hemorrhage s (16) . Th e relativ e frequenc y o f th e lesion s an

dreporte dfunctiona l effect s ar e unknow

nan d probabl y

var y widel y eve nwithi nspecies . On e repor t (17 )



### 1 4- -a—r »'»ff rffif W

"



### list s th e frequenc y

o f gros s lesion s in cattl e as : gastroenteriti s (2 4 percent) , petechiatio no f th e epicardiu m an dmyocardiu

m (2 1 percent) , pulmo nar y congestio n(1 6 percent) , an ddegenerativ e change s o f th e kidney s (1 6 percent) . Othe r lesion s wit hreporte dfrequencie s o f les s tha n1 0 percen t are : fatt y

liver , pal e muscles ; petechiatio no f subcutaneou s tissue , thymus , an dtrachea ; cystitis ; opaqu e cornea ; ocula r hemorrhage ; edem a andhyperemi a o f th e brain ; andswolle nmesenteri c lymp hnodes . Th e lesion s reporte di n duck s an dgees e poisone dwit hleadcontras t sharpl y wit htha t reporte din mammals . In duck s th e mos t notabl e lesion s ar e atrophi c pectora l muscle s andemaciatio nwit hlos s o f fa t deposit s (22) . Othe r lesion s includ e impactio no f th e proventriculus , smal l spleen , an d vacuolization,o f hepati c cor dcells . I n additio nt o th e lesion s reporte din ducks , geese,'experienc e marke dcephali c edem a involvin g eyelids , submandibu la r region , andth e brai n(69) .

i



### 1 5P.2 4 Tf*"*)'*--*TiMT!T f * _—" !

Sectio nVI I

TOXI C LEVEL S O F LEA

D FO RVARIOU S SPECIE S O F ANIMAL S

Th e toxi c and/o r letha l level s o f lead , liste d i nTabl e 2 b y specie s o f animals , reporte d i nth e literatur e var y widely . Tabl e 2

TOXI C LEVEL S O F LEA

D (ORA L DOSE )

Specie s Referenc e Comment s Cattl e 2 9

2 9

2 9

2 9

4

3 5

Horse s 8 1

3 5 Singl e letha l dos e fo r calve s

200-40 0 mg/k g B.W . Singl e letha l doe s fo r adul t cattl e 600-80 0 mg/k g B.W . Adul t cattl e wil l tolerat e 6 mg/k g B.W./da y fo r 2- 3 year s Adul t cattl e wil l tolerat e 25 0 pp m o f lead i nratio nfo r 2- 3 year s 6mg/kg/da y

(equivalen t t o 27 5 pp m i nth e ration ) i s minima l chroni c fata l dose . 5 ou t o f 8 animal s die d grazin g pastur e containin g a media no f 51 6 pp m o f lead

5 ou t o f 1 5 animal s die d and a n additiona l 5 wer e symptomati c grazin g pastur e containin g 35 0 ppm . 1 ou t o f 6 cow s die d afte r consumin g 5 mg/k g B.W./da y

fo r 6 9 days . 2 ou t o f 2 horse s die d grazin g pasture s wit hmedia nconcentratio no f 51 6 ppm . 

### 1 6Shee p



### Do g

Poultr y 

### 7 8

5 6

7 9

7 9

2 9

2 9

7 6

8 2

6 7

6 7

6 7

7 3

8 0

8 0

5 6 2. 4 mg/kg/da y equivalen t t o 15 0 pp m in ratio ni s th e minimu

m chroni c fata l dos e (fo r 6 months )

4 ou t o f 9 animal s die d and a nadditiona l 2 wer e symptomati c whe ngrazin g pasture s fo r 4 month s containin g 200-84 0 ppm . 5 ou t o f 6 youn g horse s and 1 ou t o f 2 2 olde r animal s wer e symptomati c whe n grazin g pasture s containin g 38 , 9 0 and 24 6 ppm . 2 ou t o f 2 shee p apparentl y norma l for ' 4 5 day s consumin g 5 mg/kg/day . 2 ou t o f 2 pregnan t animal s aborte d and die d o n59t hand 106t hda y consumin g 9 mg/kg/B.W./da y 1 ou t o f 1 pregnan t shee p aborte d whe n consumin g 1 mg/k g B.W./da y fo r 5 0 days . 1 ou t o f 1 die d whe nconsumin g 8 mg/k g B.W./da y fo r 22 0 days . 1 0 ou t o f 1 0 wer e asymptomati c fo r 2 6 week s consumin g 4. 5 mg/k g B.W./da y 4 ou t o f 4 wer e symptomati c whe n consumin g 10 0 mg/k g B.W./da y fo r 3 0 days . 3 mg/k g B.W./da y

fo r 18 0 day s produce s symptom s 10-3 0 mg/k g B.W./da y

produce s symptom s fro m 13t hda y 60 0 mg/kg/da y

fo r 2 day s i s letha l Consumin g 10 0 pp

m i nth e ratio nproduce s symptom s 10 0 pp m o f PbAC i nratio nfo r 4 week s asymptomati c 100 0 pp m inth e ratio nfo r 4 week s depresse d weigh t gain s 200 0 pp m i nth e ratio nfo r 3 week s asymptomati c 

### 1 7-If W

Duck s

Fis h 5 6

6 8

2 2

8 3

8 3

1 9

Othe r aquati c lif e 1 9 500 0 pp m i nratio nfo r 3 week s produce d necrosi s o f rena l tubule s Feedin g 16 0 mg/kg/da y fo r 3 5 day s asymptomati c 1 0 ou t o f 1 0 develope d symptom s afte r consumin g eigh t # 6 lead shot . Consumin g 6 mg/k g B.W./da y fo r 13 7 day s wa s asymptomati c Consumin g 8-1 2 mg/k g B.W./da y ha d averag e surviva l time s o f 2 8 an d2 5 days . Toxi c o r letha l level s var y widel y dependin g o nth e kin

d o f wate r and lengt ho f exposure . Var y fro m 0.0 1 t o 6 3 ppm . Toxi c level s fo r daphni a an dcyclop s varie dfro

m 0.0 1 t o 12 8 ppm .

Th e fata l o r minima l toxi c dose s reporte d inth e literatur e ar e difficul t t o interpret . Fro m Tabl e 2 , assumin g a safet y facto r o f 2-3 , olde r cattl e shoul d tolerat e 2 mg/k g B.W./da y o r 80-10 0 pp

m inth e ratio nfo r 2 t o 3 years . Shee pshoul dtolerat e 1 0 mg/k g B.W./da y or , assumin g tha t shee p consume approximatel y 3 percen t o f thei r bod y weigh t pe r day , the y

shoul d tolerat e 5 0 pp m o f thei r ratio nfo r approximatel y one-hal f year . However , pregnan t shee p have aborte da t thes e level s (29) . Assumin g a hors e consume s 2. 1 percen t o f it s bod y weigh t pe r day , 1. 0 t o 1. 2 mg/k g B.W./da y

o r 40-5 0 pp

m i nth e ratio nfo r time period s o f les s tha none-hal f yea r shoul d b e tolerated . Thes e implie dsaf e level s wer e compute d b

y makin g severa l assumptions ; consequently , les s subtl e effect s coul d b e observe d a t level s o f leadintak e lowe r tha nthese .



### 1 8"WIW '

Sectio nVII I

SIGNS , SYMPTOM S AND DIAGNOSI S

Th e diagnosi s o f lead poisonin g depend s o nidentifyin g thes e factor s (14) : 1 . Opportunit y fo r exposur e an

d th e sources . 2 . Symptom s compatibl e wit hlead poisoning . 3 . Concentration s o f lead i nfluids , tissues , andorgan s o f intoxi cate d animal s and concentration s o f lead i nth e source . 4 . Gros s and microscopi c lesion s compatibl e wit hleadpoisoning . I nsom e extrem e instances , tes t animal s ma y hav e t o be expose dt o th e sourc e t o determin e effect s o f tha t particula r lead concentration . SIGN S AN D SYMPTOM S Th e gros s symptom s observe d inleadpoisonin g o f domesti c animal s resul t fro

m disturbance s o f th e gastrointestina l trac t an dcentra l nervou s system . Mos t case s o f intoxicatio nar e acut e o r subacute ; consequently , th e cours e o f th e diseas e wil l b e short , abou t 2- 3 day s (14) . Cattl e Experimenta l evidenc e collecte di nyoun g calve s indicate s tha t 2- 3 day s afte r exposur e symptom s wil l b e observed ; however , thi s tim e interva l i s modifie d b

y initia l dos e (24) . Infata l cases , th e firs t symptom s observe d ma y be impressive ; uncontrolle d vocalization , extreme ataxia , nystagmus , excessiv e salivation , sudde ncollapse , and deat h(29) . Generall y lac k o f appetit e wit hdiarrhe a an d constipatio nwil l b e observed . Insom e instance s marke d anemi a 1 s observed . Th e frequenc y

o f som e symptom s fo r cattl e hav e bee nreporte da s (17) : 

### 1 . 2 . 3 . 4 . 5 . 6 . 7 . 8 . Blindnes s Excessiv e salivatio n Muscula r twitchin g Hyperirritabilit y Convulsio n Depressio n Grindin g teet h Ataxi a 

### 51 % 45% 33% 33% 32% 32% 24% 18%

1 9* W1* 7 If " • T " ^ "MITJWTT :



### 9 . Circlin g 16 % 10 . Bellowin g 13 % 11 . Diarrhe a 10 % 12 . Pushin g agains t object s 10 %

SHEE P Generally , th e symptom s o f shee pcontras t wit hthos e seenincattle ; rathe r tha nexcitement , depressio nofte n1 s reporte d(30) . Progressiv e anorexia , inadditio nt o constipatio nan ddiarrhe a (29) , lethargy an dataxi a ar e typica l symptoms . HORSE S Inspirator y

dyspnea , "roaring " afte r exercise , i s th e mos t ofte n reporte dsympto

m o f horse s (4,84) . Pharyngea l paralysi s wit hregurgitatio n als o occurs , an

dsever e case s evidenc e ataxia , paralysis , an dcloni c convul sion s (84) . DOG S Symptom s fo r dog s ar e simila r t o thos e reporte dfo r cattl e including excessiv e salivation , uncontrolle djaw movements , hyperesthesi a o f th e ski n andrecumbenc y

wit hpeda l movement s (67) . Onse t ma y be ver y rapi dwit h apparen t recover y

fro m anacut e episod e followin g b y vomitin g (67) . Pharyn gea l paralysi s als o i s reporte d(30) . DUCK S AND GEES E
Sever e weigh t loss , marke dweakness , an datroph y o f pectora l muscle s ar e usuall y

reporte dinduck s an

dgees e (22,69) . Cephali c edem a an dcharac teristi c highpitche dvocalization s ingeese , contras t wit htha t reporte di n duck s (69) . FIS H Fis hresidin g i nfres hwate r containin g leadion s develo pa coagulate d fil m o f mucou s ove r th e entir e body , particularl y noticeabl e ove r th e gill s (2) . Thi s conditio nfrequentl y occur s infis hexpose dt o othe r heav y metals .

2 0P.2 9 "nr-rr^ffTT "

Sectio nI X

CLWICA L PATHOLOG YAND CHEMICA L ANALYSI S

Man y o f th e clinica l pathologi c observation s note dwit hlea dpoisonin g ar e associate d wit hth e developmen t o f anemia . Cattl e experienc e hemoglobi n level s o f 5 gm/10 0 m

l and packe d cel l volume s o f 2 0 percent(55 ) a s wel l a s elevate d reticulocyt e count s (19,55) . Seru m glutami c oxalaceti c transaminas e an d seru m glutami c pyruvi c transaminas e ar e elevate d(73) ; however , i nsom e instance s thes e enzyme s ar e no t elevate d(55) . Increase dprophyrin s inth e urin e seemingl y

i s a ninconsisten t findin g (53) . Delta-amin o levulini c aci d (D.A.L.A. ) i nth e seru m an d urin e o f ma nbecome s elevate dbefor e th e appear anc e o f symptom s (2) . I ncatt1e(49 ) an

dsheep(85 ) elevate dD.A.L.A . ha s bee n reported . Stipplin g o f red bloo dcell s ofte ni s reported ; however , condi tion s othe r tha nlea d intoxicatio ncaus e stipplin g o f do g RBC s (86) . A coun t o f 1 5 o r mor e stipple d cell s pe r 10,00 0 ma y sugges t leadpoisoning . Othe r finding s reporte d i nIntoxicate d animal s include : leadline s inth e meta physe s an d epiphyse s o f th e radi i (33,63,73 ) andepithelia l cast s i nurin e sedimen t (19) . Chemica l analysi s o f fluids , tissues , an dsource s i s th e mos t frequentl y use d metho d t o suppor t th e clinica l diagnosi s o f lea d poisoning . Kidney , liver , an

d bloo d tissue s ofte nar e analyze dfo r lead content . Ten , 20 , an d 0.3 5 pp m i nth e liver , kidney , an dbloo d respectivel y

ar e level s indicativ e o f lead poisonin g (4,30) . Other s sugges t 5 0 pp m i nth e kidne y

corte xan

d1 0 pp m i nth e live r a s significan t (29) . Level s considere dsignifican t inthe do g are : bloo d (3 5 ug/10 0 ml) ; urin e (7 5 yg/liter) ; hai r (8 8 yg/gram) ; an d live r (3. 6 yg/gram)(87) . Th e antemortem

diagnosi s o f lead poisonin g indomesti c animal s probabl y i s no t a s crucia l a s fo r huma nbeings . Primaril y becaus e th e cours e o f th e diseas e i s mor e acut e an d a fe w animal s wil l hav e succumbe dbefor e th e problem become s evident . Th e differentia l diagnosi s shoul dinclud e any diseas e o f th e centra l nervou s andgastrointestina l syste m (1.7) .



### 2 1P.3 0

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### Sectio nX

TREATMEN T

Becaus e o f th e acut e natur e inmos t domesti c animals , th e treatmen t generall y

i s disappointing . Th e treatmen t regime nma y Includ e (85) : 1 Sedatio nfo r convulsiv e seizures . 2 . Smal l ora l dose s o f magnesiu m sulphate . 3 . Parentera l o r force dfeedin g 4 . Ethylenediaminetetracetat e (EDTA) . Th e recommende ddosag e o f EDTA varies . Som

e recommenda 12. 5 percen t solutio ngive na t th e rat e o f 1. 0 g/3 0 l b(13. 6 kg/day ) (84) . Th e dos e shoul db e divide dintw o dose s give nintravenousl y andvery slowly . Th e dos e ca nb e repeate dunti l symptom s improve . Other s sugges t a 1 0 percen t solutio ngive nintravenou s a t 1. 0 gm/3 0 l b(13. 6 kg)/da y limitin g th e tota l dos e t o 5 gm/3 0 l b(13.6kg ) pe r wee k suspende dfo r on e wee k afte r 7. 5 gm/3 0 1b(l3.6kg ) ha s bee ngiven . Toxi c sign s Includ e accelerate dhear t an drespir ator y rate s wit hmuscula r tremor s (84) .

2 2P.3 1 "-w^'yf^']" r

nwiif : '' - ~ • —

REFERENCE S

1 . Browning , E . Toxicit y o f Industria l Metal s (2n ded. ) Apple-Centur y -Crofts : N.Y . and London . 1969 . 2 . Lead:Ai r Lea d i n Perspective . Nationa l Academ y o f Sciences : Washingto nD.C . 1972 . pp . 330 . 3 . Bowen , H . J . M . Trac e Element s i n Biochemistry . Academi c Press : N.Y . and London . 1966 . 19 7 pp . 4 . Hammond , P . B . and Aronson , S . L . Lea dPoisonin g i n Cattl e an d Horse s i n th e Vicinit y o f a Smelter . N . Y . Acad . Sci . 111:595 - 611 . 1961 . 5 . Beijers , J . A . Loodvergiftiging . Tijschr . v . Diergeneesk . 77:587-605 . 1953 . 6 . Harbourne , J . F. , C . T . McCre a an d J . Watkinson . A

n Unusua l Outbrea k o f Lea d Poisonin g i n Calves . Vet . Rec . 83:515-517 . 1968 . 7 . Haring , C . M . and K . F . Meyer . Investigatio no f Livestoc k Condition s and Losse s i n th e Selb y Smok e Zon e U.S . Burea uMine s Bull . 98:474 - 502 . 1915 . 8 . Holm , L . W. , J . D . Wheat , E . A . Rode , an d G . Firch . Th e Treatmen t o f Chroni c Lea d Poisonin g i n Horse s wit hCalciu m Di-sodiu

m Ethylen e Diamoni o Tetracetate . Jour . Am . Vet . Med . Assoc . 123:282-388 . 1953 . 9 . Hughes , W . Lead Poisonin g i n Horse s and Cattle . Vet . J . 79:270 - 271 . 1923 . 10 . Hupka , E . Ube r Flugstaubvergiftunge ni m de r Umgebun dvo nMetalIhutten . Wein . Terarztl . Monatsschr . 42:763-775 . 1955 . 11 . Knight , H . D . and R . G . Buray . Chroni c Lea dPoisonin g i n Horses . Jour . Am . Vet , Med . Assoc . 162(9):781-786 . 1973 . 12 . Kradel , D . C , W . M . Adams , and B . S . Guss . Poisonin g and Eosino phili c Meningoencephaliti s i n Cattle- A Cas e Report . Vet . Med . 60:1045-1059 . 1965 .



### 2 3



# HH t13 . Miessner , H . Schadigun g de r Tierwei t durc hIndustri e un dTechnik . Deut . Tierarztl . Wchnschr . 39:340-345 . 1931 . 14 . Buck , W . Laborator y Toxicologi c Test s andThei r Interpretation . Jour . Am . Vet . Med . Assoc . 155(12):1928-1941 . 1969 . 15 . Jubb , K . V . F . andP . C . Kennedy . Patholog y o f Domesti c Animals , Vol . 2 , Academi c Press : N.Y . andLondon . 1963 . 16 . Todd , J.R . A

Knacker y

Surve y o f Lea dPoisoning : Incidenc e i n Cattl e i nNorther nIreland . Vet . Rec . 74(4):6-118 . 1962 . 17 . Leary , S . L. , W . B . Buck , W . E . Lloy dandG . D . Osweiler . Epide miolog y o f Lea dPoisonin g i nCattle . Ia . St . Vet . 3:112-117 . 1970 . 18 . Agricultural Statistics . U.S.D.A . 1969 . U.S . Governmen t Printin g Office : Washington , D.C . 19 . Zook , B . C , J . L . Carpenter , andR . M . Roberts . Lea dPoisonin g in Dogs : Occurrence , Source , Clinica l Patholog y andElectroencepah lopathy . Am . J . Vet . Res . 33(5):891-902 . 1969 . 20 . Lambou , V . andB . Lim . Hazard s o f Lea di nth e Environmen t wit h Particula r Referenc e t o th e Aquati c Environment . Federa l Water Qualit y Administration , U.S . Dept . Int . Washington , D.C . Augus t 1970 . 2 8 pp . 21 . Bagley , G . E . an dL . N . Locke . Th e Occurrenc e o f Lea di nTissue s o f Wil dAnimals . Bull . Environ . Contamin . Toxicol . 2:297-305 . 1967 . 22 . Baytes , F . Y. , D . M . Barne s an dJ . M . Higbee . Lea dToxicosi s i n Mallar dDucks . Bull . Wildlif e Dis . Assoc . 4:116-125 . 1968 . 23 . Benson , W . W . B . Pharoah , an dP . Miliei . Lea dPoisonin g i na Bir d o f Prey . Bull . Environ . Contamin . Toxicol . 11(2):105-108 . 24 . Locke , L . N. , G . E . Bagley , D . N . Frickie , andL . T . Young . Lea d Poisonin g an

dAspergillosi s i nanAndea nCondor . Jour . Am . Vet . Med . Assoc . 155(7):1052-1056 . 25 . Locke , L . N. , andG . E . Bagley . Lea dPoisonin g i na Sampl e o f Marylan dMournin g Doves . J . Wildl . Mgmt . 31:151-518 . 1967 . 26 . Bazell , R . L . Lea dPoisoning : Zo o Animal s Ma y B e Firs t Victims . Scienc e 173:130-131 . 1971 . 27 . Zook , B . C , R . M . Sauer , an dF . M . Garner . Lea dPoisonin g i n Captiv e Wil dAnimals . J . Wildlif e Disease s 3(3):264-272 . 1972 .



### 2 4"TT"T ' "•'irrnff ' r

28 . Zook . B . C , R . M . Sauer , and F . M . Garner . LeadPoisonin g i n AustralianFrui t Bats . Jour . Vet . Med . Assoc . 157(5):691-694 . 1970 . 29 . Al l croft , E . and K . L . Baxter . Lea d a s a Nutritiona l Hazar dt o Far m Livestock . V . Th e Toxicit y o f Leadt o Cattl e and Shee pand a nEvaluatio no f th e Lea d Hazar d Unde r Far m Conditions . J . Comp . Path . 60:209-218 . 30 . Buck , W . B . Lea d and Organi c Insecticide s Poisoning s i nCattle , Jour . Am . Vet . Med . Assoc . 156(10):1468-1472 . 1970 . 31 . Cristea , J . Acut e Lea d Poisonin g i nPigs . Reel . Med . Vet . 143:749 - 754 . 1967 . 32 . Hatch , R . C . an

d H . S . Funnell . Lea d Level s inTissue s and Stomac h Content s o f Poisone d Cattle : A Fiftee nYea r Survey . Can . Vet . J . 10(10):258-263 . 1969 . 33 . Zook , B . C , J . L . Carpente r and E . B . Leeds . LeadPoisonin g in Dogs . Jour . Am . Vet . Med . Assoc . 155:1329-1342 . 1969 . 34 . Slatter , D . H . Sum p Oil : A

Poten t Sourc e o f Lead . Australian vet . J . 49(9):46 . 1971 . 35 . Donovan , P . P. , P . T . Feeley , an d P . P . Canavan . Lea dContaminatio n i nMinin g Area s i nWester nIreland . II . Surve y o f Animals , Pasture , Food s and Waters . J . Sci . Fd . Agric . 20:43-45 . 1969 . 36 . Accumulatio no f Toxi c Metal s wit hSpecia l Referenc e t o Thei r Absorption , Excretio nand Biologica l Half-Times—Addendum , Environ . Physiol . Biochem . 3:65-107 . 1973 . 37 . Blaxter , K . L . Lea d a s a Nutritiona l Hazar di nLivestock . II . Th e Absorptio nan

d Excretio no f Lea d b y Shee pan

d Rabbits . J . Comp . Path . 60:141-159 . 1950 . 38 . Fleischman , A . I. , H . Yacowits , T . Hayton , and M . L . Bierenbaum . Effec t o f Calciu

m an d Vitami nD 3 upo nFeca l Excretio no f Some Metal s i nth e Matur e Mal e Rat e Fe d a Hig hFa t Cholestero l Diet . J . Natur . 95:19-22 . 1968 . 39 . Byers , R . K . Lea d Poisoning . Pediatric s 23:585-603 . 1959 . 40 . Kostial , K. , I . Simonovi c and M . Pisonic . Lea dAbsorptio nfro m th e Intestin e i nNewbor nRats . Nature . 233-564 . 1971 . 41 . Six , K . M . an

d R . A . Goyer . Experimenta l Enhancemen t o f Lead Toxicit y b y Low Dietar y Calcium . J . Lab . Clin . Med . 76(6):933 - 942 . 1970 .



### 2 5



### mmmmmmismmaWPr''P.3 4

F T T , • •-^T T rr""* "

42 . Jacquez , J . A . Trace r Kinetic s inPrinciple s o f Nuclea r Medicine . (H . N . Wagner , Jr . ed. ) W . B . Saunder s Co. , Philadelphia . 1968 . 43 . Rescigno , A . an

d G . Segre . Dru g andTrace r Kinetics . Blaisdel l Publ . Co : Waltham , Mass . Toront o andLondon . 1963 . 44 . Hursh , J . B . Retentio no f 25(l):29-35 . 1973 . 

### 21 0 Pbi nBeagl e Dogs . Healt hPhysics .

45 . Blaxter , K . L . Lea d a s a Nutritiona l Hazar dt o Far m Livestock s III . Factor s Influencin g th e Distribtuio no f Leadi nth e Tissues . J . Comp . Path . 60:177-189 . 1950 . 46 . Potter , G . D. , D Q 3 R . Mclntyre , andG . M . Vattuone . Th e Fat e Implicatio no f P bIngestio ni na Dair y Cow andCalf . Healt h Physics . 20:650-653 . 1971 . 47 . Allcroft , P . Lea d a s a Nutritiona l Hazar dinLivestock . IV . Distributio no f Lea d inth e Tissue s o f Bovine s afte r Ingestio no f Variou s Lea d Compounds . J . Comp . Path . 60:190-208 . 1950 . 48 . Fisher , H . L. , Jr . A Mode l fo r Estimatin g th e Inhalatio nExposur e t o Radon-22 2 an

d Daughte r Product s fro m Accumulate dLead-21 0 Bod y Burden . Healt hPhysics . 16:597-616 . 1969 . 49 . Valee , B . L . and D . D . Ulmer . Biochemica l Effect s o f Mercury , Cadmiu m an d Lead . Ann . Rev . Biochem . 41:91-128 . 1972 . 50 . Ulmer , D . D . and B . L . Vallee . Effect s o f Lea do nBiochemica l Systems . In : Trac e Substance s i nEnvironmenta l Health , Vol . II , 2nd Ed . (D . D . Hemphill , ed.) . Proceeding s o f Annua l Conferenc e a t th e Universit y

o f Missouri , Columbia , pp . 7-27 . 1968 . 51 . Kelliher , D . J. , E . P . Hilliard , D . B . R . Poole , andJ . D . Collins . Chroni c Lea d Intoxicatio ninCattle . Preliminar y Observation s on It s Effect s onErythrocyte s andonProphyri nMetabolism . Irish . Jour . Ag . Res . 12(1):61-69 . 1973 . 52 . Hernberg . S. , Nurmine nand J . Hasan . Nonrandom Shortenin g o f Re d Cel l Surviva l Time s i nMe nExpose d t o Lead . Environ . Res . 1:247 - 261 . 1967 . 53 . Christina , R . G . and L . Tryphonas . Lea dPoisonin g i nCattle : Brai nLesion s and Hematologi c Changes . Am . J . Vet . 32(2):203-216 . 1971 . 54 . DeBruin , A . Certai nBiologica l Effect s o f LeadUpo nth e Anima l Organism . Arch . Environ . Hlth . 23:249-264 . 1971 .



### 2 655 . Donawick , W . J . Chroni c Lea d Poisonin g i na Cow . Jour . Am . Vet .

Med . Assoc . 148(6):655-661 . 1966 . 56 . Simpson , CF , and B . L . Damron . Abnormalitie s o f Erythrocyte s an d Rena l Tubule s o f Chick s Poisone d wit hLead . Am . J . Vet . Res . 31(3):515-523 . 1970 . 57 . Reifenstein , E . C . Osteomalaci a andRickets . In : Principle s o f Interna l Medicine . 4t hEd . J . R . Harrison , R . D . Adams , I . L . Bennett , W . H . Renik , G . W . Thorn , and M . M . Wintrobe . McGraw-Hil l Boo k Co. , N.Y. , Toronto , andLondon . 1964 . 58 . Goyer , R . A . Th e Rena l Tubul e i nLea dPoisoning . I . Mitochondria l Swellin g an d Aminoaciduria . Lab . Invest . 19(1):71-77 . 1968 . 59 . Goyer , R . A . an

d R . Krall . Ultrastructur e Transformatio ni n Mitochondri a Islate d fro m Kidney s o f Norma l an dLead-Intoxicate d Rats . J . Cell . Bio . 41(2):393-400 . 1969 . 60 . White , A. , W . Handler , and E . L . Smith . Principle s o f Biochemistry . McGra w Hil l Boo k Co : N.Y. , St . Louis , an d Sa nFrancisco . 1973 . 61 . Goyer , R . A. , P . May , M . M . Cates , and M . R . Krigman . Lea dan d Protei nConten t o f Isolate dIntranuclea r Inclusio nBodie s fro m Kidney s o f Lead-Poisone d Rats . Lab . Invest . 22:245-271 . 62 . Campbell , K . I , N . K . T . Weaver , J . A . Taylor , an dA . A . Krumm . Biologica l Effect s i nAnimal s Chronicall y Expose dt o Lea dChloro bromid e Atmosphere s Jour . Am . Vet . Med . Assoc . 159(11):1523-1529 . 1971 . 63 . Nicholas-Schmitt , D . Brown , E . Devlin , A . A . Larsen , E . D . McCausland , and J.M . Sanville . Lea dPoisonin g i nHorses : AnEnvironmenta l Healt hHazard . Arch . Environ . Hlth . 23:185-195 . 64 . Thompson , R . G . Reliabilit y o f Acid-Fas t Inclusion s i nth e Kidney s o f Cattl e a s a nIndicatio no f Lea d Poisoning . Can . Vet . J . 13(4) : 88-89 . 1972 . 65 . Little , P . B . and D . K . Sorenson . Bovin e Polioencephalomalacia ; Infectiou s Emboli c Meningoencephaliti s andAcut e Lea dPoisonin g i n Feedlo t Cattle . Jour . Am . Vet . Med . Ass . 155(12):1892-1903 . 1969 . 66 . Zook , B . C . Th e Pathologi c Anatom y o f Lea dPoisonin g i nDogs . Vet . Path . 9(5):310-327 . 1972 . 67 . Robertson , CM . A Cas e o f Acut e Lea dPoisonin g i na Dog . Vet . Rec . 86:195-196 . 1970 .



### 2768 . Vengris , V . E . andC J . Mare . Lea dPoisonin g inChicken s an dth e Effec t o f Lea do nInterfero nandAntibod y Production . Can . J . Comp . Med . 38:328-335 . 1974 . 69 . Bagley , L . N . andL . N . Locke . Lea dPoisonin g i nCanad a Gees e in Delawar e Avia nDis . 11:601-608 . 1967 . 70 . Hopkins , A . Experimenta l Lea dPoisonin g i nth e Baboon . Br . J . Ind . Med . 27:130-140 . 1970 . 71 . Hemphill , F . E. , M . L . Kaeberl e andW . B . Buck . Lea dSuppressio n o f Mous e Resistanc e t o Salmonell a typhimurium . Science . 172:1031 - 1032 . 72 . Koller , L . D . andS . Kovacic . Decrease dAntibod y Formatio ni nMic e Expose dt o Lead . Natur e 250:149 . 1974 . 73 . Stowe , H . D. , R . A . Groyer , M . M . Krigman , M . Wilso nandM . Cates . Experimenta l Ora l Lea dToxicit y i nYoun g Dogs . Arch . Path . 95(2) : 106-116 . 1973 . 74 . Sass , B . Perforatin g Gastri c Ulce r Associate dwit hLea dPoisonin g i nth e Dog . Jour . Am . Vet . Med . Assoc . 157(1):76-78 . 1970 . 75 . Hsu , Fran k Shin-Yun . Lead , Zinc , andCalciu m Interatio ni nGrowin g Pigs , Diss . Abst . Int . B . 35(2):917-918 . 1974 . 76 . Carson , T . L. , G . A . Va nGelder , W . B . Buck , an dL . J . Hoffman . Effect s o f Lo

w Leve l Lea dIngestio ni nSheep . Clinica l Toxicology . 6(3):389-403 . 1973 . 77 . Egan , D . A . andT . O'Cuill . Opencas t Lea dMinin g Areas . A Toxi c Hazar dt o Grazin g Stock . Vet . Rec . 84:230 . 1969 . 78 . Egan , D . A . an

dT . O'Cuill . Cumulativ e LeadPoisonin g i nHorse s i n a Minin g Are a Contaminate dwit hGalena . Vet . Rec . 86:736-738 . 1970 . 79 . James , L . F. , V . A . Lazard , an dW . Binns . Effect s o f Subletha l Dose s o f CertainMineral s onPregnan t Ewe s andFeta l Development . Am . J . Vet . Res . 27(116):132-135 . 1966 . 80 . Damron , B . L. , C L . Simpson , an dR . H . Harms . Th e Effec t o f Feedin g Variou s Level s o f Lea donth e Performanc e o f Broilers , Poultr y Sci . 48(4):1507-1508 . 1969 . 81 . Shupe , J . L. , W . Binns , L . F . James , andR . F . Keeler . Lupine : A Caus e o f Crooke dCal f Disease . Jour . Am . Vet . Med . Assoc . 15(2) : 198-203 . 1967 .



### 2 8P.3 7 "~TMnTr- T y ' p- ir»rrr' "

82 . Va nGelder , G . A. , T . Carson , R . M . Smith , andW . B . Buck . Behaviora l Toxicologi c Assessmen t o f th e Neurologi c Effec t o f Lea di nSheep . Clinica l Toxicolog y

6(3):405-418 . 1973 . 83 .

84 .

85 .

86 . Coburn , D . R. , D . W . Metzler , andR . Treichler . A Study o f Absorptio n and Retentio no f Lea d i nWil d Waterfow l i nRelatio nt o Clinica l Evidenc e o f lead Poisoning . J . Wild . Manag . 15:186-192 . 1951 . Blood , D . C . and J . A . Henderson . Veterinar y Medicine , 2n

dEd . William s and Wilkin s Co. , Baltimore . 1963 . 101 3 pp . 

### Th e

Prigge , E. , and J . H . Hapke . Di e Festellunge r Eine r Experimentelle n Sub-Klinische nBlievergiftun g Be i Schafen . Deutsch e Tier . Wochen shrif t 79(19):475-476 , 481-482 . 1972 . Zook , B . C , M . C Connell , an d G . E . Gilmore . Basophili c Stipplin g o f Erythrocyte s i nDog s wit hSpecia l Referenc e t o Lea dPoisoning . Jour . Am . Vet . Med . Assoc . 157:2092-2099 . 1970 . 87 . Zook , B . C , L . Kapito , J . L . Carpenter , D . V . Cramer , andH . Schwachmann . Lea d Poisonin g i nDogs : Analysi s o f Blood , Urine , Hai r and Live r fo r Lead . Am . J . Vet . Res . 33(5):903-909 . 1972 .



### 2 9P.3 8

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. TITL E AN O SUBTITL E S

. REPOR T OAT E TH E SHORT-TERM

EFFECT S O F LEAD O N DOMESTI C AN D WIL D ANIMAL S Januar v 197 7 3

. PERFORMIN G ORGANIZATIO N COO E

7

. AUTHOR(S ) R.P

. Bott s 3

. PERFORMIN G ORGANIZATIO N REPOR T NO

.

e . PERFORMIN G ORGANIZATIO N NAM E AN O ADDRES S 10

. PROGRA M ELEMEN T NO

. Corvalli s Environmenta l Researc hLaborator y Corvallis , Orego n9733 0 1AA60 2 N.edNYtaAeWdhAfoVtob

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12

. SPONSORIN G AGENC Y NAM E AN D ADDRES S Corvalli s Environmenta l Researc hLaborator y 20 0 S.W . 35t hSt . Corvallis , Orego n9733 0 13

. TYP E O F REPOR T AN D PERIO D COVERE D in-house s literatur e review 14

. SPONSORIN G AGENC Y COD E EPA-0R D

19

. SUPPLEMENTAR Y NOTE S

16

. ABSTRAC T Smal l quantitie s o f lead , a ubiquitou s an d toxi c element , ma y b e foundi n practicall y al l specie s o f plant s an d animals . Th e lis t o f animals , bot hdomesti c an d wild , reportedl y

intoxicate d b

y lead i s impressive . Th e source s o f lead poisonin g vary wit hspecie s o f animals . Lea dbas e paints , use d moto r oils , spend lea d sho t an d pasture s contaminate db y lea dsmelter s seemingl y hav e bee nmos t ofte nincriminated . Th e lesion s associeate dwit hlea d intoxicatio nma y vary ! widel y bot hwithi nan

d betwee nspecie s o f animals . Lesion s and symptom s o f th e centrsfli nervou s system

ar e th e mos t prominent . Toxi c level s fo r variou s specie s a s reporte d i nth e literatur e var y widel y and seemingl y

a singl e toxi c dos e fo r eac hspecies , a s yet , ha s no t bee ndefinitel y established . Th e diagnosi s and treatmen t o f lead intoxicatio nma y become laboriou s and time consu m ing . Mos t sysmptoms , reporte d involv e centra l nervou s system dearrangement . Treat men t o f mos t clinica l case s i s disappointin g generall y becaus e o f th e acut e natur e o f lea d poisoning .

17

. KE Y WORD S AN D DOCUMEN T ANALYSI S DESCRIPTOR S b.IDENTIFIERS/OPE N ENDE D TERM S c . COSAT I Field/Grou

p anima l disease s lead poisonin g anima l nutritio n veterinar y

medicin e leadpoisonin g i n wil d anddomesti c animal s source s an

d effect s o f lea dpoisonin g i n animal s 02/ E 06/F J

18

. DISTRIBUTIO N STATEMEN T RELEAS E T O PUBLI C 19

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# M&m w This Report) 2 1

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. O F PAGE S

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. SECURIT Y CLAS S (Thispage) UNCLASSIFIE D 22

. PRIC E

EP A Form 2220- 1 (B-73 ) 

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