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I * J 1 | LEAD INDUSTRIES ASSOCIATION *0 IAIT 4Sh * TMtCT NBW YWW 17, H.T. I Auguat 6, 1957 Lno h inrys and SJSIZJ bi'LLHVI So. l?li To the ksober* of the Lead Industries laeoclattoni k Bnnar or c b iu j x h zu x h mmac as s o c iat ed vrrs uu> Dr. Rlllla K. Oeorg*, Chief Medical Officer of tha Con*olid*tod tins Proprietary, Ltd., Sy^ay, Australia, delivered at tin annual meeting of our Aj o o c lo tion lut April an addresa 00 "Problem* in Plusblaa* oo interesting to his bearer* that many requests for copies bara ben received* Dr. Oeorge having apolean free* handwritten notes, d o distribution of bla ad* draaa was possible until it had been developed into Exnuaorlpt, and tha facta that tha author laft our ahoraa toon after tha meeting and haa been traveling almost co tlououaly la tha intervening months have delayad tha reproduction until now* Under tha revised title aat forth at tha head of thia bulletin, a oopjr of Dr, Oeorge'a addraaa la barawith. In it, seemingly inport ant aapacta of tha cverall problaa of pluablow which have hitherto had relatival/ little attenttoo In thia country are eat btfera at. Of two American industrial physician# to whoa tha nanu! ecript was submitted, one haa cemented that the problem of tha affect of lead on tha kidney is one which should be brought vigorously into tha open, and the aacood has aide tha observation thet, tha author haring been "on tha road* while preparing tha aar.uacri.pt, tha extant to which, with few exceptlone, he haa been able to both raise and enswer a aeries of questions la truly remerkable. Tha account of tha 1956 episode on tha fourth page is tha first publication of a case in which the results of Tenene administration have been used to support a elsla that lead poisoning was tha causa of chronic kidney damage* A limited supply of additional copies of Dr. Oeorga'a paper is available for distribution to our meafeera on request* Director of Health and Safety m*A-,yiw. n1 V1 LIA10967 ! /'* LEAD INDUSTRIES ASSOCIATION 0 *ABT 41 STMICT i HW YOWK IT, H. V. ! A KEYICT OK CEftTADt HEALTH PifflSLOq kStOCUTTV TTTH ILkV Dr. nilUa K. Oeorgs Chief Medical Offloer Consolidated Zinc Proprietary, Ltd, Anong probleea lnplurbtsa t.hlch ara of special Medical icrterert at tha present tine are tha followings- 1* The use of Versene In relation to Industrial lead exposure vhen it is adalniateredi (a) Curetlrely (b) piarncBtically - l.e. the production of a high urinary lead excretion in markers with an in dustrial lead exposure who i. have never eboen clinical evidence of plucblsw, or ii have suffered fron episodes of scuta load poisoning aany years previously, or ill. are suffering free chronic degenerative disease which could possibly be considered to be caused, aegravatod, or accelerated In onset by exposure to 1 alnisal quantities of lead insufficient to produce clinical tanifestaticns of lead poisoning* (c) Prophylsctically 1. to prevent the onset of disabling pluablaa in laad workers with raised urinary lead excretion but with no signs of clinical plucfclsn, 11* to prevent the possible later developsent of chronlo degenerative dlscaso in lead workers, both with and without raised urinary lead excretion, but with no signs of clinical plvrbiaa, J ill* to all lead workers, to dialnish bone end soft tissue storage of lead, Z* The value of oral administration of Versene as coopered with its edalnietretlon by lntrevenoue infusion* A presentation at tha Z9th Annual Heating, Lead Industries Association, Chicago, HI,, April 2lt-ZSt 19"J7, with revlalons by tha author. ^ ' in N 353.01 LIA10968 ............. .... ........------------------------------------------------------------------------ - ' Dr. Willita E. George A Review of Cart tin Health frobleas Associated With lead 3. Possible thort-rangs tad long-rsu^s baneful effacts of Tsrssa* adulnlstretion. It. Ths anount of urinary lead excretion produoad by Tersene In persons with no industrial lead exposure, 5, The relationship of cardiovascular-renal disease to (*) Anteoedeot attacks of tout* lead poisoning, (b) trpoeurs during working lift to quantities of load insufficient to prodocs clinical syuptoas of load poisoning but know to b higher than those to which tho general cooBunity la exposed, Thl* uy bo revesled byi 1* high urinary load concentrations, ii. high urinary load axeretIona following Torotoo sdcinls tration. lii. high bona load concentration diooorered during lift or at autopay. Saferone a (In thii regard, the writ of Dr. D. A. Hondoroon, in Australis, appeara to have established that excessive load exposure In childhood la frequently followed by tho derelcpcor.t of a progressiva rsnal lesion which ultimately loads to oarly death froa renal failure.) D* A. Haodorsoni D. A. Bondcrooni A follow-up of Casas of Pluablsa in Children* Australasian Annals of Uedlclne (195ii) HZ. 3. 219 Chronic Nephritis in Queensland* Australasian Annals of Medic ins (195$) IT. 3. 163 D. A. Handareont "Iks Renal Content of Bone in Chronlo Bright's Disease" Australasian Annals of Kodlclns (1?57) (To appoar shortly) (Ins fourth paper. Henderson will describe the rsnal pathology resulting froa excessive lead absorption daring childhood.) (o) The internment release froa storage in the tissues of increased Mounts of load as a result of infection, starvation, diet variation, etc, 6. The use of the ucasuratont of bone load concentration to ascertain the relationship of sons casts of chronlo cardlovasoular- renal dlseass to excessive lead absorption, either in childhood or in indietry. 1 w;*wj.r m n .gn 'Mk| in-PMT" ' ^Wj-f qa ?wtiijAipj i:vyr ?r-" LIA10969 Dr. William I. George -> A Review of Certain Health problea* Associated VIth Load ? The importance of mt as a vehicle for the excretion of abaorbed lead and the effect# generally of tenpereture ec lead absorption and excretion. Reference* D. 0* Shielsi *fba Hidnation 1 Load in Sweat* Auatralaalan Annals of Mediclna (1951) ITT, 3, 72$ D. 0. Bblelai Indiatrial Lead Poisoning In Relation to Cllx*to* Auatralaalan Annala of Medicine (1?SS) Acpat 6. Tba affeeta of dlt on lead absorption and excretion. Including tha peulblllty of tba existence of metebolle chelating agents. It la Impossible to rafar to all tha above aspects in tba ties available, but reference will be &ada to sooe of then, especially to thoaa to which west attectioo baa been paid by Auatrallan Invaatigatore. Aa far aa industrial lead poisoning la ooneemed, many year* ago. In what were apparently vary tad working condition*, acuta laad polaoning frequently occurred at Broken Hill, whera cxldleed carbonate ora waa than being mined and awaited, and at QJbrt Plrla, Acre laad auditing and refining ware conducted. Coaalaalona of Enquiry ware held In 1920 at Brokaa Hill and In 1925 at Jbrt Plrla, and In the reporta of both, tha Incidence of laad polaoning waa comanted upon. following these enquiries, working condition* In both industries ware greatly Improved, coapenaatlon waa provided for Incapacity aa a result of lead poisoning, and aedlcal board* ware established to examine and certify. There has been very little evidence of clinical lead poisoning in either place for many year*. At Broken Rill, since 19li0, only five eases of laad poleonlr^ have bean certified, four of these cases quickly recovered with treatment and re turned to work - three of than had been working In a licited retraataent process of an old dusp consisting of highly oxidised materiel. At Jbrt Plrla, only one case of plush lea has bean certified In the last six years. In both places, notification by aedlcal practitioners of suspected cases of lead polaoning la required under the Act. Recent interviews with general practitioners In both localities confirm that they are aeelng no evidence of ebsorptlon of baraful quantities of lead. Several hundred oases of laad polaoning occurred in tha early nineteenthirties In lead dree situated In the north of Queeneland. At that tlae, carbonate ore waa being dried and sselted. Medical supenrlfion of workers was Instituted, working conditions ware Improved and tha Incidence of laad poleonlng epeedily de er** ted, Today, with the mining of sulphide oro, case* of lead poleonlng occur only among en employed In tha shelter aeotlon of tha operation*. Two or three such clin ical east* occur per year, though quite a nusher cf ten show lsboratory evidence of excessive lead ebaorptlon. Man ao affected ere given work away from e lead ha sard. -saiirtfrlSWiaafci, ai Dr. Willi** t, Qeorge A Review of Certain Health Problems Associated With lead <eondary industry contribute# few c u h of 1**4 polaonlng p*r j mt la all flat** - e.g. Macng bridge painter* employed reoovinf ol4 leed paint fro* brldgee, and cncr.f men er.ce.god In the handling of acrap batteries. 8uoh men *r* nodie ally cxar.ir.ed re p ilarly end It la unusual for clinical 1**4 polecning to develop, Kao hewing rslsod urinary l*ad excretion arc (Ivan work away fro* thla haterd. In 1956. th* nereeaat* tut1 tor l*ad poieoning waa relsed at Broken Bill la a clai* for ccapensstlon for laad poisoning. A nlner thr* became disabled aa * result of chronic nephritis, Ha was t*lca examined by the atatutory medical board and * certificate that hla disablement was due to lead polaonlng ni refused, He had aorked at Broken Kill, la aulphlde or* only, ainea 192U. He had never *uff#r*d fro* aywptosf of acute or execute lead polaonlng aad hla urinary lead excretion re* 0.02 *g* per litre. He m aer.t to Sydney, where ha wee given an infusion of a Taraenate. thla reaulted la the urinary axeration of 0.6 eg* of lead per litre. la hla report following hla examination of the nan. hla phyalclaa atated that thla remit ladlefe teds (a) that th* worker had aa abnormal quantity of leed stored la hla body. Cb) that he had been exposed to exceed** quantities of lead at hla work, and (e) that the result of Yertea* administration confined his opinion that the chronic nephritis fros which the worker wea a offering waa due to leed polaonlng. Be quoted the opinion* of cany industrial phyalclaa* that leed could cauaa renal dexaga. It la thought that thla la the flrat occasion oe which the result* of lead excretion la the urine following Tersene Kfcin1stration hare been used to support a del* that chronic nephritis waa due to lead polaonlng. 7* feel that, probably. If Varsane la given to any aorkar exposed to aa Industrial leed he terd. a high urinary lead axcretlon will follow, cosperri with that produced la persona with no industrial exposure. In the present state of our knowledge, we do not know that w* could satis fy a court that an abnormally high amount of leed. set la th* bones a* celclua lead phosphate or lying la the soft tissues, does not shorten the life of a workar or pre judicially affect hla health, he feel thst we have Insufficient Information of the quentltlts of leed which could b# produced, by th* administration of Teraena, la th* urine of Industrial lead workers with no aysptoaa of Illness and with no alga* of disees *. If thl* la greater la amount then that which can be produced la oonexposed workers la similar eg* group#, la It of any clinical significance! Son* interacting work on th# excretion of leed la th# sweet has b# re ported by Shlela, SMels he# pointed out that, at Mount lea la th# tropical north of Auetrail* where lesd ainlng and smelting ere carried out, ell pereon* excreting 0.30 mgns or nor* of leed per litre of urine have aon* evldonce of clinical leed poisoning, whereat in Melbourne, In the teeperata aouth of Australia, only 62 per & cent of worker# excreting 0.30 egaa per litre or t*>r* stow clinical evidence f lead polaonlng. H* shows that, at Mount las, the dally axcretlon of fluid is of the order of one litre of urine and 2.5 litres of sweet per day, whereas la Melbourne, th* -tHfari^eer;  j w h j ih .w i mm mimui .p w nmw t o .< LIA10971 ./ i Dr* WIIIIm %, Osorgs ii $ A P.srrlew of Certain Keelth Problems Associated nth Lea4 dally excretion of fluid la about 0.5 litres of m*t and 1.5 litres of urine, Tins, with 0,30 rg-sa of le'.d p*r litre of urine arid a like concentration In the v*st in i each piece, the total daily lend excretion in fluids at Ifount Isa weald be acre than or.e epa [r ct.-.y, whereas In Melbourne, the daily lead excretion in fluids would count to about C.6D r c m cr.Iy. At Uxunt lea the blood, organa and tie rues of the body wrald be in contact trlth acre than one aga of lead par day. At Melbourne, with the urine showing the taaa lead concentration, toe tiaauea would be In contact with only 0.6 cgn of lead. There would thus be a greeter chance of finding cases of lead poisoning easng persona excreting 0.30 wga per litre of urine at Mount Zaa than anoog those axe reting 0.30 wga In Melbourne. i On the other hand, aa raxing a constant aaount of lead absorption dally, there would be a greater excretion of lead In the hotter wor.tha than in the colder Booths, so that there would be presumably lees tiirue lead storage. There would be leee chance of lead poisoning developing la the ouster than In the winter, provided con ditions of exporure were the a an*. 3Mela concludes that Increased aUrination of lead In the sweat way have an important bearing on variations In the evidence of lead absorption as shows by the aoount of urinary lead. Referring to nnntndugt rial lead poiaonlrg, aoae very interesting work has been reported recently irca Queensland, inis state has always been very "lead eoo- scious* beceuae of a fomer lead haaard to children. For Bore than 50 years, clinl-- 5 clans In Queensland have been convinced that one of the eequelae of lead poisoning in childhood there has baen the development of chronic renal disease at a compara tively early ace. In 1929, Hy concluded that children in Qaee&sland were exposed to s lead haxard whilst playing, during the wet season, on the lead painted wooden versa- daha ao coenon there. They licked rain drupe off the verandah railings. 8s showed * ; that there was an abnormally high Incidence of lead poisoning earng Quoanland Chll-- <irn, e.g., fros 1 rl7 to 1926, ii25 children were treated for lead poisoning In the Brisbane Children** Respite?, whilst during the ase>* period, only four children sere treated for lead poisoning in Sydney, three In Melbourne and ooa la Adelaida* Along with this high incidence of lead poisoning In children, study of the death rate froa chronic nephritis showed that the death rats frca this disease la Queensland la the 10li0 age group was sore than three tines as great as that In otbar rtatea. A* a result of this and of many other reports, legislation was introduced la Queensland about 1930 which forbade the use of lead-containing paint on the Interior of house* at height* which children could reach, irlthin the last year, in Queensland, the legislation ha* be.m further anended and now the sale or sianufseture of lead car ' bonate as a paint substance ha* been completely forbidden, Ro building cay be palo* ted, either Interiorly or exteriorly, with a lead paint of any description, except that, on certain decorative beards high up in the buildings, such a* fascia beards, a lead paint of up to 5 per orait My be used. Red lead m/ still be used on structural steel. r It Is now claimed that, in recent year*, an lBprov<*wsnt In the statistics of death froa chronic nephritis in youngor sg# groups is evident. Dr. D. A, H<ndir*on, as s result of work at the Qua <r.s land Institute of Medi cal Reeearch, has recently reported soma extremely interesting conclusions on the ! driver WiKie SBH LIA10972 i 4 < Dr. tmiM J. Oeorg# 1 --6-- A Review of Certain Health Prohi*as Associated Tilth Lead i I i i relationship between aoute lead poisoning In childhood end the development of chronio renal Cmn, It would appear that he has convincing evidence thet this connection doea, In feet, exist* Hie work ha# appeared In the ^Australasian Annals of Medicine* et intervals einoe 195h* Reference* to the** peper* heve been (Iren above. In hie first paper* ft<nd*ron doecribe* how he studied the after histories of children who had been treeted for lead poisoning in the Ho* pitel for Sick Chil dren, Brisbane, between 1915 axvd 1915. There were U31 children In the group, with ace* rengine free* 2 to 12 years end comprising 169 Bale* end 2)2 ftaales* The fol low-up we* ned* by enquiries in the Department of the Registrar Oeneral, et *1*0- torel office*, and by examination of Marriage records, deeth register*, etc* Sow* lnforwstlon wa* obtained of 152 of the LtOl children* Of thee* 152 children, death certificates were eeen for 101 f<rale* end 61i Bala*. Thee* Included five war deaths. IlTcTf the?# death* occurred between the egea of 1 end LO years* The Mortality reto for the whole aerie* of children was hO.bOii per 100,000, whereas tha everec* Morta lity ret* froa all causes in tha general population of Queensland for persona aged 1 to W year* la 26) per 100,000, Of the 165 deaths, no fewer then 5li were certified ae b#ln< due to chronic nephritis) an additional lit daaths were certified . s being due to other possible rwnal cause*, e.c. cerebral henorrhage, giving a total nortality rate, froa renal caua**, in this croup of 26,9)2 per 100,000. The *vr*c* Mortality rate froa all re nal causae In the general population of Qu*n*land In the 15-1*0 age group Is )6 per 100,000. i The duration of lift before deeth froa renal causes, after adkaiesion to hos pital with tha diagnosis of lead poisoning, varied froa 6 years to 31* years* Even after the subtraction of all renal and vascular deaths, an excess of Mortality froa other cause* wa* noted. Many of the other causes of deeth Certified could rpr*snt the sequela* to lead poisoning, e.g. such certified cause* of death as deoentls," encephalitis,* conrulslcns, acute nephritis of pregnancy,* etc* There wae also s high death ret* in the group fron infective causes which could pos sibly be related to chronic 111-health associated with decreased resistance. Of the I67 weaker* of the aeries still slive, Information ebout 101 was ob tained. Of these, 17 have hypertension end albuK.lr.uris, 3 hare hyperteetlon, 5 are Mentally defective, 3 have psychoses end 2 ere blind as a result of optic atrophy. In hi# second paper, Chronic Hephritis In Queensland, published In 1955# Henderson conclude* thet, since 18?0, Queeneland he* had a higher Mortality frow chronic nephrltle than the remainder of Australia. This higher Mortality was ob served to effect first the younger eg* group* end then older *g* group# in succession, until the oldest age group to be affected, 50-59 years, was involved about 1930* Thla higher Mortality has now begun to decline, first in the yourger age groups and, if the present trend continues ss appears likely, the Mortality in the 50-59 years age group should drop to that of tha other etttes of Australia about 1990* *.n the increased scrtellty was at its MaxisuM, chronic nephritis wa# cos of the coseonly certified cause* of death for person* under the eg# of 10 years* Approxlnstely 160 person# between the sget of 10 and 60 year* died eech year in Queens land in excess of the nuabsr who would have died had tha death rat# fro this diseas* been the sue 4* thet in other stetea. jyii gjiajpgm^egapwiggwiP!gHwpp^ap^ W!Wppp|iipiiWS|i| Or. William t, Oeorg* -7- k Review of Certain Health Problena Associated kith I<ead Henderson point# out thit this excess mortality 1# beet explained by the eotlon of sore nephrotoxic agent on the children of Queensland which would here oos menced acting sheet 1670 and gradually nlsinlahed alter about 1920, This agent Ini tiated changes In Uvo kidney which lead to death froe chronic nephritis In free 10 to Ln years. In this second paper, Henderson leaves It st that, but In his third paper, entitled *The Lead Content of Pons in Chronic Bright's Disease, hs concludes that this nephrotoxic agent eras excesslvs lead absorption In childhood. In this paper, b* reports the results of the analysis of the lead content of tons from the ealvariiss and from portion of a rib froa 669 autopsies in Brisbane (possible lead exposura in childiood) and 197 in Sydney (no childhood exposure). He found that the bone lead content of persons without chronic Bright's disease and who resided In Queensland is of the sue order as those who had lived outside that state. He also shows that the lead content of bone froa subjocta aged 20 to L9 years, born and dying la Queensland froa chronio Bright's dlseato, is significantly higher than that of rub)acts not suffering froa this disease. In 3& tales and 31 fscales, aged 20 to U9 years, bom end dying In Queensland froa chronic nephritis, the toan bone lead content was 7J1 aga per ICO gna of zsolst tone in calcs and 7,97 in females, whilst for persons la ths sass ags group and not suffering froa chronic Bright's disease, tbs Man was 3,91 (gsi per 100 grsaa In males and 3,3^ cgts la female* (calvariua boos), Henderson found that, as a result of autopsies on patient* dying outside Queensland, cost esses of. chronic renal disease coong th.ee could b allotted by clinicopathological examination to one of three defined and generally aocepted etio logical groupai (a) chronic glomerulonephritis, (b) chronic pyelonephritis, and (c) those associated with hypertension as tho prlsary condition, When, bouever, an atteept was cade to allocate to one of the sbove group* the 59 esse* of death froa chronic nephritis in Queensland in the 20 to L9 age group. It was found that only 12 of these could be so classified - five to chronic gloeerulonephritls, three to pyelonephritis, four to hypertension. Forty-seven were regarded as being of underterclned cause. These esses could only be labeled hypertension ith renal failure,* They had no history of acuta nephritis, of long-standing urinary infection, or of oedema, prior to that associated with terminal cardiac failure. Their urinary findings gave no lndloatlon of the etiology of this renal con dition and ths general histological picture was one of marked disappearance of renal tissue without Indication of cause* The bone lead content of the 12 subject* with chronic Bright's dies**# of known cause was found to be of the same order as that of persor* not suffering from this disease. For ths 25 females and 2? males In ths group for which no etiological diag nosis stas nsds, tha mean lead values In the calvarium were 6,US ngms per 100 gw* in male! and 6,66 in females. -.gwgwgf.'jwi Iff"/" T LIA109 74 Dr. Wllli.ua t, Oeorge A Review of Certain Health Frobl*** Associated With Laad Henderson than proceed* to discues tha possible origin of thla high bona lead and enumerates three possible cauieai s i (a) As all had chronic renal disease, retention of nomslly abso rbed load by falling kidney* nay have boon retpoo- albla. (b) tv.era may Kara been sooe disturbance of aetebollaa whereby a large proportion of norxal load Intake m absorbed. (c) Thera nay hero boon excessive absorption of load daw to excessive exposure. Each of these pcsslbllltlee la discussed. Be finally concludes that thara had boon In these cases excessive absorption due to ezcasslTo exposure. In those with a high bona lead, in only one Bale was thara a history of In dustrial lead poisoning* Four Bales had a history of lead poisoning in childhood and a sibling of another had suffered fron childhood load poisoning. There has boon no industrial exposure to load of fecialaa in Queensland, and no other load hatard to adult females is known to exist. Six of the fscales with chronic Bright* a disease and a high bone lead content had histories of lead poisoning in childhood. ; Sunaarixirg his conclusions. Henderson points out that it is known that r.E there was in Queensland for cany years a sarlous and widespread load hatard to chil dren and that it has been shown that, where a lead hatard exists, investigations of siblings end associates of children with plisbiss will reveal cany additional in r stances of grossly excessive lead absorption, with few, if any, acuta clinical maaXfestations. The above facts cake it asst probable that tha excessive lead in the bones of nearly all these young individuals with chronic Bright's disease was ao- quired during their childhood. Ha goes on to say that his investigations provide a link between tha chronic nephritis In Queensland and excessive lead absorption In childhood. He further suggests that the estimation of the lead content of bones in cases of chronic Bright's disease cay well have a wider application. Ha points out that plunblsa, both industrial and nonlndustrial, clinical and subcllnlctl, occurs in Best drill red c-orcunities and that, despite *u*j doubt, particularly in Aaerlee, there is a groat deal of evidence that load absorption can produce chronic renal di sease, Ho suggests that cases of chronio Bright's disease occurring outside Queensland coy also be due to pltssblso and that the routine determination of bone lued at autopsy. In esses of chronic renal disease without obvious cause, nay eluci date their etiology. This is supported by the fact thet, in the group bom outslds Queensland, thereby avoiding the special hatard in childhood, a number of cases of chronio Bright's disease had high tone lead, Jt so happen* that all theaa were Balae ' in the older age groupie, suggesting an industrial exposure. i Henderson estphasite* that tha bon* load content is of etiological signifi es^* only twn considered in conjunction with clinical and histological data. rj ajSOwW* ly-r fsinws jimgAgs'ss-b..i* * km.' '.u w .'UR^Iw^^iifwyway LIA10975 4 \ | Hr. Willlaa . Oeorg# | -9 A Rrrlev of Certain Health Problcn* Aaaoclated Tilth Lead ] Ri(l*rioa finally conclude* that aooe caeca of chronic Bright** diaeta* In J Quoer.aland In th* 20-L9 age group can be escribed by clinlcopathologlcal atudle* to ) Jovowrj cauats, but the larger propcrtlsn, 63 per cent In the prceent aerie*, cannot be eo allotted, the bone lead content of those case* of known etiology 1* the aaae i as th*t of peracrj dying without chrcr.lc Bright'* <ii***a*, the bone lead content of the group cf unknown etiology la algr.Lficertly higher, Ttia high bone lead content Is due, with term exception*, to crceaalra absorption during childhood. Bona lead content can be uaed. In caeca of chronlo Bright** diaaaae, a* a walld Io dic t Lon of excessive lead absorption, and It* Mtlnatlon Bay provide a clue to the etiology of toe* of thee. In a fourth paper, Benderaon Intend* to dlecua* the pathology of th* kidney associated with th* presence of high bone lead content. hiiit4 k n ii il nnjfci iii^ii^AHh^MMfcifciiM^ik^i^M^i 5