P. 1

D-3 3 perhaps , below " (CD , p . 12-95) . 3 . Effect s o nth e Cardiovascula r Syste m Symptom s consisten t wit hcardia c disease , suc ha s degenerativ e change s i nhear t muscl e (Kline , 1960) , abnorma l electrocardiogram s (ECG ) (Silve r andRodriquez-Torres , 1968 ) andincrease dcerebrovascula r mortalit y (Dingwall-Fordyc e andLane , 1963 ) hav e bee nassociate dwit hhig hhuma n lea dexposures . Cardiotoxicit yha s bee nreproduce di nexperimenta l animal s acutel yexpose dt o highconcentration s o f lead . Effect s includ e depressio ni ncontractility , increase dsusceptibilit yt o norepinephrine-induce d arrhythmia s (exaggerate di nneonates) , anddecrease dcardia c protei n phosphyrlatio n(Kopp e t al. , 1980b ; William s e t al. , 197 7 a,b) . I t appear s tha t effect s ma ypersis t i nimmatur e rat s eve nafte r cessatio no f lea dexposur e (William s e t al. , 1977b) . Chroni c administratio no f lea dresultin g i nPb B level s a s lo wa s 4 0 ug/d l cause dstructura l change s i nth e myocardiu mo f mice , andEC G abnormalitie s tha t ar e likel ydu e t o nerv e conductio ndisturbance s (Kha n e t al. , 1977 , Kop p e t al. , 198 0 a,b) . Beside s affectin g cardia c output , lo wlevel s o f lea dexposur e hav e produce dincrease dvascula r responsivenes s t o contractil e agent s suc ha s noradrenaline , andsignifican t elevation s i nsystoli c bloo dpressur e i nrat s wit hPb B level s aroun d4 0 ug/d l (an d possibl ylower ) (Webbe t al. , 1981 ; Victer ye t al. , 1982 ; Perr yand Erlanger , 1979 ; Kopp , 1980a) . Thes e change s ma yb e linke dt o reduce d energ yavailabilit ydu e t o hem e synthesi s inhibitio n(Kopp , 1980a ) o r t o altere dnerv e transmissio ncause db ychange s i ncalciumavailability (Webbe t al. , 1981) , andsugges t possibl e mechanism s b ywhic hlea dma y contribut e t o hypertensio ni nhumans .P. 2

D-3 4 Excessiv e amount s o f mobilizabl e lea dhav e bee nmeasure di npatient s wit hhypertensio n(an drena l impairmen t o f unknow ncause ) (Batuma ne t al. , 1983 ) andevidenc e o f increase dhypertensio nha s bee nfoun damon g me n occupationall yexpose dt o hig hlevel s o f lea d(Ingli s e t al. , 1978 ; Lili s e t al. , 1977) , althoug hther e hav e bee ncontrastin g finding s i n simila r population s (Riche t e t al. , 1966 ; Crame r andDahlberg , 1966;) . Lowe r level s o f exposur e a s indexe db yPb B o r urinar yP blevels , hav e bee n associate di nsom e adul t population s wit hhypertensio nprevalenc e (Beever s e t al. , 1976 ; Kromhou t andCoulande , 1984 ) andbloo dpressur e (Morea u e t al. , 1982 ; Pococ k e t al. , 1984) , bu t no t i nother s (Staesse ne t al. , 1984) . Pococ k e t al . (1984 ) considere dth e wea k (bu t statisticall ysignificant ) correlatio nbetwee nlea dexposur e andhypertensio na t level s abov e 3 7 ug/d l t o b e o f mino r importanc e give nth e lowe r Pb B level s typicall yfoun di n Britis hmen . However , anunpublishe dEP Areanalysi s o f th e groupe ddat a reporte db

yPococ k e t al . (1984 ) indicate s tha t bloo dlea di s a significan t predicto r o f bloo dpressur e i nthei r data , bot hbefor e andafte r adjustin g fo r covariates , whe na regressio no f bloo dpressur e i s performe dversu s th e lo g o f bloo dlea dfo r thei r reporte dgroup average s (U.S . EPA , 1985c) . Furthermore , th e regressio ncoefficien t indicate dtha t th e siz e o f th e effec t wa s significant , suggestin g a bloo dpressur e increas e o f 3 m mH g a s bloo dlea dincrease s fro m5 t o 1 5 ug/dl . Recen t analyse s o f NHANE S I I dat a hav e demonstrate dsignifican t association s betwee nbloo dpressur e (systoli c anddiastolic ) andPb B level s amon g male s (no t females ) age d1 2 t o 7 4 year s independen t o f other , potentiall y confoundin g variable s (e.g. , nutrition ) (Harla ne t al. , 1985) . Furthe r analyse s wer e conducte do nwhit e male s age d4 0 t o 5 9 year s t o avoi dth e collinearit ybetwee nbloo dpressur e andbloo dlea deviden t a t lowe r age s andbecaus e dat a relatin g cardiovascula r diseas e t o bloo dpressur e ar eP. 3

D-3 5 les s extensiv e fo r non-white s (Pirkl e e t al. , 1985) . Pb B level s wer e a significan t predicto r o f bloo dpressur e i nthi s subgrou p afte r includin g i nth e multipl e regressio nanalyse s al l know nfactor s previousl yestablishe d a s correlate dwit hbloo dpressur e andals o whe nth e relationshi p wa s teste d agains t ever ydietar yandserologi c variabl e measure di nth e NHANE S I I surve y(Pirkl e e t al. , 1985) . Includin g bot hcurvilinea r transformation s andinteractio nterms ha dlittl e effec t o nth e bloo dlea dcoefficient . A threshol dbelo wwhic hbloo dlea dwa s no t significantl yrelate dt o bloo d pressur e coul dno t b e foun dacros s a rang e o f adjuste dPb B levels betwee n 7 an d3 4 ug/dl . I t i s o f interes t t o not e tha t th e dose-respons e relation

ships foun db

yPirkl e e t al . (1985 ) sugges t a larg e initia l effect , levelin g of f a t highe r Pb B levels , whic hi s consisten t wit hth e biphasi c bloo d pressur e respons e t o Pb B level s foun di nrat s (Victer ye t al. , 1982 ) and whic hma yaccoun t fo r th e inconsisten t epidemiologi c finding s i npersons wit hmil dt o moderat e elevation s o f bloo dlead . Becaus e o f th e comple xinter-relationship s amon g th e multipl e environmental , dietary , medical , socio-economic , andgeneti c factors tha t influenc e bloo dpressure , al l o f whic hma yno t b e measurable , result s fro m eve nth e recen t studies tha t employe dthoroug handextensiv e analyse s andhig hqualit ydata , mus t b e interprete dcautiously . Nevertheless , th e suggeste drelationship s betwee nbloo dlea dandbloo dpressur e amon g adults , eve na t Pb B levels belo w3 0 ug/dl , shoul dcontinu e t o b e carefull ystudie d andb e considere dt o hav e potentiall yimportan t publi c healt himplication s i n term s o f increase dincidenc e o f hypertensio nandmor e serious cardiovascula r disease . Pendin g revie wo f th e mos t recen t papers i nth e criteri a document , thei r result s ar e no t reflecte di nth e assessmen t o f healt hrisk s associate d wit hdifferen t Pb B level s i ndeterminin g anacceptabl e Pb B level .P. 4

D-3 6 4 . Effect s o nth e Kidne y Lea da t hig hconcentration s i s concentrate d i nth e kidney s b yhig h affinit ybindin g protein s (whic hfor mintranuclea r inclusio nbodies ) and cause s numerou s type s o f change s i na variet yo f physiologica l processe s associate dwit hth e kidney . A t lo wdosages , lea d affect s rena l mitochondria l structur e (e.g. , swelling ) and functio n(e.g. , altere d respirator yrates , oxidativ e phosphorylatio nandsynthesi s o f heme , proteins , nuclei c acid s and vitami nD hormone ) (Goyer , 1968 ; Fowle r e t al. , 1980 , 198 1 a,b ; Silbergel de t al. , 1982 ; Rose nandChesney , 1983) . Lead' s interferenc e wit hthes e biochemica l processe s i nth e kidney , particularl yenerg y metabolism , migh t accoun t fo r th e transien t decrease s i nrena l tubula r reabsorptiv e processes , a s indicate d b yhyperaminoaciduria , glycosuria , and hyperphosphaturia , a t Pb B level s rangin g fro m4 0 t o mor e tha n10 0 ug/dl , and possibl ya s lo wa s 3 0 ug/d l (Se e CD , Section s 12.5. 2 and 12.5.3 ; p . 12-170) . Irreversibl e kidne ydamag e (e.g. , interstitia l nephritis ) appear s t o requir e prolonge dhig hexposure , wit hPb B level s probabl y exceedin g 7 0 ug/d l i nadult s althoug hlea d chelatio ni s necessar yt o detec t cumulativ e bodystore s tha t maycontribut e t o th e gradua l develop
men t o f thi s diseas e (Lili s e t al. , 1968 ; Crame r e t al. , 1974 ; Wedee ne t al. , 1979) . I t shoul db e note dtha t th e effect s o f chronic , low-leve l lea d exposur e o nrena l dysfunctio ni nchildre nhav e no t bee nadequatel y studied . Ther e i s limite devidenc e tha t elevate dlea dabsorptio ncontribute s t o rena l diseas e i nassociatio nwit hgou t and hypertensio n(Emmerson , 1973 ; Batuma ne t al. , 1981 ; Wedeen , 1982) . Th e mil d hypertensio nobserve d wit hchroni c low-leve l lea dexposur e however , ma yb e relate dt o lead' s abilit yt o directl yalte r vascula r reactivit y(Webbe t al. , 1981 ; se e Appen di xD.3 ) and anycontributio no f lead-induce drena l impairmen t t o thi sP. 5

D-3 7 disorder , a t lo wexposur e levels , remain s t o b e determined . 5 . Effect s o nReproductio nand Developmen t Lea dcompound s hav e bee nuse da s a nabortifacien t and lea d poisonin g ha s bee nshownt o b e accompanie d b yreduce d fertility , miscarriage s and stillbirth s (Oliver , 1911) . Littl e researc hha s bee ndirecte dhowever , a t whethe r subtoxi c level s affec t fertilit yo r caus e feta l injurie s i n humans . I nfemal e animals , relativel ylow-leve l lea d exposur e ha s bee n shownt o affec t puberta l progressio nand hypothalmic-pituitary-ovarian

uterin e functions , a s evidence db yovaria nabnormalitie s (Hilderbran de t al. , 1973 ; De r e t al. , 1974) , anddelay s i nvagina l openin g (Gran t e t al. , 1980 ; Kimme l e t al. , 1980 ) and firs t conceptio n(Make r e t al. , 1975) . I naddition , th e abilit yo f th e placent a t o suppor t fetuse s i s compromise di nmic e expose d t o relativel ylo wlea d level s (Maisi ne t al. , 1975 ; Jacque t e t al. , 1976) . I t i s o f particula r concer ntha t placenta l transfe r o f lea dbegin s a s earl ya s th e 12t hwee k o f gestatio nand continue s t o accumulat e i nth e fetu s throughou t pregnanc y(Barltrop , 1969 ) resultin g i ncomparabl e Pb B level s i nth e mothe r andnewbor nchil d (Alexande r and Delves , 1981 ; Rabinowit z andNeedleman , 1982) . Newbor nrodent s whos e mother s wer e expose dt o lea ddurin g pregnanc yshowe dcompromise d growt h(Reite r e t al. , 1975) , congenita l malformation s i nth e spina l cor d (Carpente r and Ferm , 1977 ; Jacque t andGerber , 1979 ) anddelaye ddevelopmen t o f th e CN S (e.g. , cortica l connections ) andit s function s (e.g. , moto r function , siz e discrimination ) (Klei ne t al. , 1978 ; Crofto ne t al. , 1980 ; Gran t e t al. , 1980 ; Overman ne t al. , 1981 ; Winnek e e t al. , 1977 ; 1982b ; Schlipkote r and Winneke , 1980 ; Fo xe t al. , 1977 , 1982 ; McCaule ye t al. , 1982) .P. 6

D-3 8 Pregnan t wome nwh o live di nhome s wit hexcessiv e drinkin g wate r lea dconcentration s (>80 0 ppm ) bor e a significantl yhighe r proportio no f retarde dinfant s (Beatti e e t al. , 1975) . Childre no f wome nwh o ha dworke d andlive dnea r a smelte r durin g pregnanc yhadlowe r birthweight s anda n increase dfrequenc yo f singl e andmultipl e malformation s althoug hth e caus e i s unclea r give nth e possibl e exposure s bot ho f th e mother s and presumably , th e fathers , t o hig hconcentration s o f arsenic , mercury , cadmium , sulfu r dioxide , a s wel l a s lea d(Nordstro me t al. , 1978 ; 1979a,b) . Anincrease dincidenc e i nth e overal l numbe r o f mino r congenita l anomalies , suc ha s benig ntumor s andcyst s andmino r ski ndefects , wa s reporte d i nnewbor nchildre nwit hmildl yelevate dumbilica l cor dlea dlevel s ( > 6. 3 ug/dl ) afte r controllin g fo r othe r covariates , althoug hn o singl e anatomi c defec t wa s individuall yassociate dwit hlea d(Needlema ne t al. , 1984) . Thi s suggeste dt o th e author s tha t lea dma yinterac t wit hothe r teratogeni c ris k factor s t o enhanc e th e possibilit yo f anabnorma l outcome . No associatio nwa s foun dbetwee ncor dPb B level s andincrease s i nmajo r congenita l anomalies . Furthe r investigatio no f lead' s possibl e interaction s wit hothe r teratogen s a t lo wlevel s i s neede dbefor e definitiv e conclusion s ca nb e made . Mor e subtl e effect s o nth e fetu s andnewborn , suc ha s inhibite dhem e synthesis , ma yals o b e importan t consequence s o f materna l lea dexposur e belo w3 0 ug/d l andtransplacenta l transfe r (Hubermon t e t al. , 1976 ; Hayash i , 1983a,b ; Gerbe r andMaes , 1978) . Severa l mechanism s ca nexplai nlead' s teratogeni c activity : a ) disturbanc e o f DN Asynthesi s andcel l proliferation ; (Choi e andRichter , 1974a ; Sirove r andLoeb , 1976) ; b ) chromosoma l aberrations ; (CD , Tabl e 12-20) ; c ) interferenc e wit hembryoni c nutritio nthroug hcompetitio nwit hcalcium , iron , andzin c (Mahaffe yandMichaelson , 1980) ; andd ) interferenc e wit hembryoni c energ yP. 7

D-3 9 suppl yb

ydepressin g mitochondria l functio nandcytochrom e synthesi s (Holtzma nandShe nHsu , 1976) . Lea dals o affect s th e mal e gamete . Industria l exposur e o f me nresultin g i nPb B level s possibl ya s lo wa s 40-5 0 ug/d l resulte di nabnorma l sper m numbe r andvigo r (Lancraja ne t al. , 1975 ; Wi1d t e t al. , 1983) . Sper m abnormalities , reduce dfertility , andaltere dtesticula r functio nhav e als o bee nobserve damon g mal e mic e expose dt o lo wdose s o f lea d(Hilderbran d e t al. , 1973 ; Make r e t al. , 1975 ; Wryobec k andBruce , 1978 ; Donova ne t al. , 1980) . Suc hchange s ma yb e relate dt o observation s o f compromise d viabilit yo f progenyt o mic e expose dt o lea dbefor e conceptio n(Stow e and Goyer , 1971) . Althoug hth e dat a bas e i s limited , th e availabl e studie s sugges t tha t lo wleve l exposur e o f mother s andfather s t o lea dmigh t induc e post-nata l developmenta l delay s andincreas e th e ris k o f reproductiv e abnormalities . OSHAreviewe dth e availabl e literatur e i n197 8 andconclude dtha t me nand wome nplannin g t o hav e childre nshoul dmaintai nPb B level s a t o r belo w3 0 ug/d l (OSHA , 1978) . Definin g a Pb B a t whic heffect s o nothe r aspect s o f reproductiv e functio n(e.g. , los s o f vigor , erectil e dysfunction ) woul d begi nt o b e o f concer nmus t awai t furthe r research . 6 . Possibl e Genotoxicity/Carcinogenicit y A t hig hconcentration s (>50 0 ppm) , dietar ylea dacetat e induce d rena l tumor s i nexperimenta l animal s (Aza r e t al. , 1973 ; se e CD , Figur e 12.5) . Adietar ylea dacetat e leve l o f 50 0 ppmproduce da Pb B o f 8 0 ug/d l i ndog s withi n2 years ; definin g a correspondin g exposur e leve l b e i n human s i s difficul t t o determine , however . Sinc e lea di s capabl e o f transformin g cell s directl yi ncultur e (Dipaol o e t al. , 1978 ; Cast o e t al. , 1979 ) andaffectin g DNA-to-DNAand DNA-to-RNAtranscriptio n(Sirove r andLoeb , 1976 ; Robinso ne t al. , 1984) ,P. 8

D-4 0 lea dma yserv e a s aninitiato r o f carcinogeni c activity . Lead' s abilit yt o induc e chromosoma l aberration s (CD , Tabl e 12-20 ) i s als o indicativ e o f it s abilit yt o initiat e carcinogeni c activity . I naddition , lea dma yb e a promote r o f carcinogenesis , a s indicate db yit s abilit yt o increas e DNA , RNA , andprotei nsynthesi s (Choi e andRichter , 197 4 a,b ) andt o enhanc e th e developmen t o f rena l tumor s i nrat s previousl ytreate dwit ha knowncarcinogeni c initiato r (Hias u e t al. , 1983) . Lead' s sequestratio n i nth e for mo f "inclusio nbodies " i nkidne ycel l nucle i ma yb e linke dt o it s carcinogeni c effect s (CD , p . 12-225) . Epidemiologica l studie s o f lead-expose dworker s and.childre nsugges t tha t lea dma yinduc e chromosoma l aberration s tha t ma yb e associate d wit hcertai nform s o f cance r (Grandjea ne t al. , 1983 ; Dalpr a e t al. , 1983) . Littl e ca nb e reliabl yconclude dfro mth e conflictin g occupationa l finding s o nkidne ytumo r incidenc e andexces s cance r mortalit y(Coope r andGaffey , 1975 ; Kan g e t al. , 1980 ; Bake r e t al. , 1980 ; Lilis , 1981 ; Coope r 1981 ; McMichae l andJohnson , 1982 ; Seleva ne t al. , 1984) , althoug h th e significan t elevation s i nrespirator yanddigestiv e trac t cance r i n worker s expose dt o lea dandothe r agent s warran t concer n(CD , p . 12-225) . Thes e latte r finding s shoul dno t b e over-interprete d give ndifference s i nag e distribution s amon g th e population s studie dandinadequat e control s fo r factor s suc ha s smoking , diet , ethnicity , andgeographica l location . Furthermore , thes e studie s provid e n o specifi c informatio no n th e long-ter mlea dexposur e level s o r th e lea dcompound s t o whic hworker s wer e exposed . Lea demission s fro mothe r smelter s andrefinerie s includ e lea dsulfat e andoxide s o f lea dwhil e windblow ndus t fro mstore dor e concentrat e andcontaminate dsoi l i s predominantl ylea dsulfid e (Jennet t e t al. , 1977) . Exposur e t o eve nrelativel yinsolubl e lea dcompound s (e.g . lea dsulfide ) however , coul daccoun t fo r th e observe dgastrointestina lP. 9

D-4 1

and respirator ycancer s (CD , p . 12-206) . Th e criteri a documen t conclude s that : "Sinc e lea dacetat e ca nproduc e rena l tumor s i nsom e experimenta l animals , i t seem s reasonabl e t o conclud e tha t a t leas t tha t particula r lea dcompoun dshoul d b e regarde d andtreate d a s a huma ncarcinoge n(a s pe r recommendation s o f th e Internationa l Agenc yfo r Researc ho nCarcinogenicity) . However , thi s statemen t i s qualifie db

ynotin g tha t lea dha s bee nsee nt o increas e tumori

genesi s rate s i nanimal s onl ya t relativel yhig hconcentrations , andtherefor e doe s no t see ma poten t carcinogen . I nvitr o studie s furthe r suppor t th e genotoxi c and carcinogeni c rol e o f lead , bu t als o indicat e tha t lea d i s no t poten t i nthes e systems " (CD , p . 12-268) . I t i s importan t t o not e tha t th e IAR C recommendation s wer e publishe d i n198 0 andd o no t reflec t finding s fro msevera l recen t experimenta l and occupationa l studie s cite di nth e criteri a documen t tha t sugges t tha t othe r inorgani c lea d compound s beside s lea dacetate ma yb e carcinogenic . I t appears , therefore , tha t ther e i s som e nee dfo r cautio nand furthe r researc ho nth e carcinogenicit yo f lea d compounds,othe r tha nlea dacetate , tha t ar e presen t i nth e atmospher e andothe r exposur e media . 7 . Effect s o nth e Immun e Syste m Lea d interfere s wit hhos t immun e defens e mechanism s a s indicate d b y increase dsusceptibilit yt o infectiou s agent s (CD , Tabl e 12-22) , endotoxin s (Coo k e t al. , 1974) , andincrease dincidenc e o f tumor s (CD , Sectio n12.8.2.2) , i nlead-expose danimals . Ther e i s suggestiv e evidenc e tha t huma nresistanc e t o infectio nma yb e lowere d b yelevate dlea d exposur e (Sachs , 1978 ; Ewer s e t al. , 1982) , althoug hn o dose-respons e informatio ni s available . Lead
induce dimmunosuppression , possibl ythroug hdirec t interferenc e wit hmacrophag e functio n(Lawrence , 1981 ) occur s a t low-leve l exposure s i nanimal s (PbB level s o f 20-4 0 ug/dl ) (CD . p . 12-268) . Althoug hthes e effect s d o no t induc e over t toxicity , they , nevertheless , ma yb e detrimenta l t o healt handlead' s immunosuppressiv e capabilt y"shoul db e carefull yconsidered " (CD , p . 12-241) .P.1 0

D-4 2 8 . Effect s o nth e Hepati c Syste m Th e metaboli c breakdow nb yth e live r o f som e pharmacologicall yactiv e substance s (e.g. , drugs , hormones , environmenta l toxins ) depend s o nth e availabilityo f th e hemoprotein , cytochrom e p-45 0 an dconsequently , th e synthesi s o f hem e (Remme r e t al. , 1966) . Lea dexposur e impair s th e detoxificatio n capabilitie s o f experimenta l animals , whil e dru g metabolis mandlive r functio n i nchildre nappea r t o b e affecte da t fairl yhig hexposure s (>4 0 ug/dl ) (Alvare s e t al. , 1975 ; Saenge r e t al. , 1984) . A s discusse di nAppendi xD.l(b) , i nth e absenc e o f conclusiv e dat a i t mus t b e assume dtha t anyindicatio no f significantl yaltere dhem e biosynthesi s (e.g. , elevate dEP ) ma yals o indicat e a possibl e inhibitio no f live r detoxificatio nfunction . 9 . Effect s o nth e Gastrointestina l Syste m Typica l gastrointestina l sign s andsymptom s cause db ylea dintoxicatio n includ e constipatio no r diarrhea , abdomina l pain , nausea , indigestion , and anorexia . Mil dsymptom s hav e bee nassociate dwit hPb B level s i nth e 5 0 t o 7 0 ug/d l range , anda s lo wa s 3 0 ug/d l (Haennine ne t al. , 1979 ; Fischbei ne t al. , 1980) . Ther e i s insufficien t information , however , t o establis ha clea r dos e effec t relationshi p fo r th e genera l populatio na t ambien t exposur e level s (CD , p . 12-247) . 10 . Effect s o nth e Endocrin e Syste m Relativel yhig hleve l lea dexposure s affec t variou s endocrin e processe s (e.g. , impaire dthyroi dfunction ) (Sandstea dandGalloway , 1967 ; Sandstea d e t al. , 1969 , 1970) . Apar t fro mth e previousl ydiscusse dalteration s i n vitami nD hormon e metabolis mtha t i s secondar yt o interferenc e wit hhem e synthesis , endocrin e processe s d o no t appea r t o b e impaire db ylea da t Pb B level s belo w3 0 ug/dl .P.1 1

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lands : Elsevier/North-Hollan dBiomedica l Press ; pp . 225-277 . Fowler , B.A. ; Kimmel , C.A. ; Woods , J.S. ; McConnell , E.E. ; Grant , L.D . (1980 ) Chroni c low-leve l lea dtoxicit yi nth e rat : III . anintegrate d assessmen t o f long-ter mtoxicit ywit hspecia l referenc e t o th e kidney . Toxicol . Appl . Pharmacol . 56 : 59-77 . Fowler , B.A. ; Squibb , K.S. ; Oskarsson , A . (1981b ) Mitochondria l membran e potentia l andenergy-linke d membran e transformation : inhibitio nb y P bbindin g i nvitro . J . Cel l Biol . 91 : 287a .P.2 5 1 3 Dubas , T.C ; Stevenson , A. ; Singhal , R.L. ; Hrdina , P.D . (1978 ) Regiona l alteration s o f brai nbiogeni c amine s i nyoun g rat s followin g chroni c lea dexposure . Toxicolog y9 : 185-190 . Duce , R.A. ; Hoffman , G.L. ; Zoller , W.H . (1975 ) Atmospheri c trac e metal s a t remot e norther nandsouther nhemispher e sites : pollutio no r natural ? Scienc e (Washington , D.C. ) 187 : 59-61 . Duggan , M.J . (1983 ) Th e uptak e andexcretio no f lea db yyoun g children . Arch . Env . Healt h38 : 246-247 . Duggan , M.J. ; Williams , S . (1977 ) Lead-in-dus t i ncit ystreets . Sci . Tota l Environ . 7 : 91-97 . Dzubay , T.G. ; Stevens , R.K . (1973 ) Application s o f X-rayfluorescenc e t o particulat e meaaurements . In : Secon djoin t conferenc e o nsensin g o f environmenta l pollutants ; December ; Washington , D.C . Pittsburgh , PA : Instrumen t Societ yo f America ; pp . 211-216 . Edelstein , S. ; Fullmer , C.S. ; Wasserman , R.H . (1984 ) Gastrointestina l absorptio no f lea di nchicks : involvemen t o f th e cholecalcifero l endocrin e system . Inpress . Edwards , H.W. ; Rosenvold , R.J. ; Wheat , H.G . (1975 ) Sorptio no f organi c lea dvapo r o natmospheri c dus t particles . In : Trac e substance s i nenvironmenta l health--IX ; proceedings o f Universit yo f Missouri' s 9t hannua l conferenc e o ntrac e substance s i nenvironmenta l healt h (D.D . Hemphill , ed) ; June ; Columbia , MO . Universit yo f Missouri

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1 7 Grandjean , P . (1978 ) Regiona l distributio no f lea d i nhuma nbrains . Toxicol . Lett . 2 : 65-69 . Grandjean , P. ; Lintrup , J . (1978 ) Erythrocyte-Zn-protoporphyri na s an indicato r o f lea dexposure . Scand . J . Clin . Lab . Invest . 38 : 669-675 . Grandjean , P. ; Wulf , H.C ; Niebuhr , E . (1983 ) Siste r chromati dexchang e i nrespons e t o variation s i noccupationa l lea d exposure . Environ . Res . 32 : 199-204 . Granick , J.L. ; Sassa , S. ; Granick , S. ; Levere , R.D. ; Kappas , A . (1973 ) Studie s i nlea dpoisoning : II . correlatio nbetwee nth e rati o o f activate dt o inactivate dd-aminolevulini c aci d dehydratas e o f whol e bloo dandth e bloo dlea d level . Biochem . Med . 8 : 149-159 . Granick , J.L. ; Sassa , S. ; Kappas , A . (1978 ) Som e biochemica l and clinica l aspect s o f lea dintoxication . Adv . Clin . Chem . 20 : 288-339 . Grant , L.D. ; Kimmel , C.A. ; West , G.L. ; Martinez-Vargas , CM. ; Howard , J.L . (1980 ) Chroni c low-leve l lea d toxicit yi nth e rat : II . effect s o n postnata l physica l and behaviora l development . Toxicol . App . Pharmacol . 56 : 42-58 . Griffin , T.B. ; Coulston , F. ; Wills , H. ; Russell , J.C ; Knelson , J.H . (1975 ) Clinica l studie s o nme ncontinuousl yexpose d t o airborn e particulat e lead . In : Griffin , T.B. ; Knelson , J.H. , eds . Lead . Ne wYork , NY : Academi c Press ; pp . 221-240 . (Coulston , F. ; Korte , F. , eds . Environmenta l qualit y and safety : supplemen t v . 2) . Gross , S.B . (1981 ) Huma nora l andinhalatio nexposure s t o lead : summar yo f Keho e balanc e experiments . J . Toxicol . Environ . Healt h8 : 333-337 . Gross , S.B. ; Pfitzer , E.A . (1974 ) Influenc e o f pathologica l chang e o nlea d i nhuma ntissues . In : Hemphill , D.D. , ed . Trac e substance s i n environmenta l healt h- VIII : [proceeding s o f Universit yo f Missouri' s 8t hannua l conferenc e o ntrac e substance s i nenvironmenta l health] : June ; Columbia , MO : Universit yo f Missouri-Columbia ; pp . 335-340 . Gross , S.B. ; Pfitzer , E.A. ; Yeager , D.W. ; Kehoe , R.A . (1975 ) Lea d i nhuma n tissues . Toxicol . Appl . Pharmacol . 32 : 638-651 . Gross-Selbeck , E. ; Gross-Selbeck , M . (1981 ) Change s i noperan t behavio r o f rat s expose d t o lea d a t th e accepte d no-effec t level . Clin . Toxicol . 18 : 1247-1256 . Habermann , E. ; Crowell , K. ; Janicki , P . (1983 ) Lea dand othe r metal s ca n substitut e fo r Ca + 2 i ncalmodulin . Arch . Toxicol . 54 : 61-70 . Habibi , K. ; Jacobs , E.S. ; Kunz , W.G. , Jr. ; Pastell , D.L . (1970 ) Characterizatio nand contro l o f gaseou s and particulat e exhaus t emission s fro m

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### 1 8 Haenninen , H. ; Mantere , P. ; Hernberg , S. ; Seppalainen , A.M. ; Kock , B . (1979 ) Subjectiv e symptom s i nlow-leve l exposur e t o lead . Neuro toxicolog y1 : 333-347 . Halpern , M . (1978 ) Indoor/outdoo r ai r pollutio ncontinuit yrelationships . J . Ai r Pollut . Contro l Assoc . 28 : 689-691 . Hambidge , R.M . (1977 ) Th e rol e o f zin c andothe r trac e metal s i npediatri c nutritio nan dhealth . Pediatr . Clin . Nort hAm . 24 : 95-106 . Hammond , P.B. ; Bornschein , R.L. ; Succop , P . (1984 ) Dose-effec t anddose
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### 19 Harvey , P.G. ; Hamlin , M.W. ; Kumar , R. ; Delves , H.T
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