Document x1XnKjngNdpbmp9Bo81D8ZO81

LEAD INDUSTRIES ASSOCIATION 0 IAIT 41ttl STftCCT NCW YOWK 17, H.T. Auguat 6, 1957 ' . l e ad h re re?. tod ! sxrn r k o p m Bo> 1?* To the kcaber* of the Lead Induetrie* Aoclatloni : i r ev in or cffiTia h eal t h pr o s u o b as s o c iat ed vrrs l eas Dr* tdllla E. Georga, Chief ttedlcal Officer of the Consolidated 1j m Proprietary, Ltd., Syfoey, Australia, delivered at the maul Mating of our Aiaoclatioa lut April an ddr*t on *Probleu in Plushles* ao intareating to hla bearer* that many raquaata for copiee bar* been received* Dr* Oaorge haring apoken frcai harxhrrittsn notes, d o distribution of hi* ad> dr*s M poisibl* at.til it had been developed Into nanuacrlpt, and tha facta that tha author loft our ahoraa aoon altar tha Mating and haa baaa traveling almost cotinwouely la tha intervening months hara delayed tha reproduction until now* Under tha revised tltla aat forth at tha haad of thla bulletin, a oopjr of 0 Dr, Oaorsa'a addraaa la herewith. In it, seemingly inport act aapacta of tha orarall problea of pluablom which hara hitharto had relatively littla attention in thia country art aat before us. Of tao American lnduatrial phyaiciana to whom tha nam> ! acript waa auie.it ted, on* haa cemented that tha problea of tha affect of load on tha kldr.ey ia one which ahould ba brought vigorously into tha open, and tha aacood haa nsda tha obaarration thet, tha author haring been on tha road* while preparing tha manuscript, tha extant to afr.lch, with few axe aptlone, ha baa bean abla to both raiaa and answer a aariaa of questIona ia truly remarkable* Tha account of tha 1956 episode on tha fourth pafe ia the flrrt publication of a caaa in which tha reaulta of Verseoe dalnlstration hara bean uaad to aufport a claim that lead poisoning waa tha cauaa of chronic kldbey damage* A Halted supply of additional Coplea of Dr. Oeorga'a paper ia available fear distribution to our aeafcers on request* Director of Health and Safety LIA10967 ! * /'* LEAD INDUSTRIES ASSOCIATION 0 BAST 4tx STAItT i MCW YO*K 17, H. Y. ! A KEYICT OK CEftTADt HEALTH PMSt-Ott kStOCUTTV TTTH ILkV Dr. mil lea K. Oeorgs Chief Medical Offloer Consolidated Zinc Proprietary, Ltd* Aoong probleea lnplurbisa which ere of special wedical interest et the present tic* ere the followingi- 1* The use of Vers ana la relation to industrial lead exposure vhen It la eAalalatereds (a) Curst!rely (b) pierncgtlcelly - i.e. the production of a high urinary lead excretion la markers with an In dia trial lead exposure who 1. hare aerer shown clinical eridence of pluebls*, or 11 hart suffared fron episodes of acute lead poisoning aaay years previously, or Hi* are suffering free chronic degenerative disease which could possibly be considered to be caused, aggravated, or accelerated la onset by exposure to 1 alniaal quantities of lead insufficient to produce clinical tanifestaticns of lead poisoning* (c) Prophylactically 1* to prerent the onset of disabling pluablsa la lead workers with raised urinary lead excretion but with no signs of clinical plucfclsa, 11* to prerent the possible later derelopeent of chronlo degenerative dlscaso in lead workers, both with and without raised urinary lead excretion, but with no signs of clinical plvrblaa, J 111* to all lead workers, to dlalnlsh bona end soft tissue storage of lead* 2* The ralue of oral adslnlstration of Versene as coopered with lte edaln letration by lntrerenoua infusion* A presentation at the 29th Annual Heating, Lead Industries Association, Chicago, HI,, April 2U-Z$t 19^7, with rerlatona by tha author. wm swwrvi"'-- ,vaWf fiirifcr in N 353.01 vy'jl- 'AWWWW!'kjWjcwff- LIA10968 w# Dr. Willita E. Ooorga `' -? A Review of Certain Health Problems Associated With lead 3* Po*jible ahort-ranga and long-rau^a harmful affects of Verseae edxlnletretion, lt The aaount of urinary load excretion produood by Tenant In penons with no indue trial load exposure* $* The relationehip of oerdiov*#culer-renel dieeaet to - (a) Antecedent attack* of acute lead poisoning. (b) Erpoeure during a working life to quantities of lead insufficient to produce clinical symptoms of lead poisoning but know to be hither than thoce to which the general coonunity le exposed* Thie aay be reveeled byi 1* high urinary lead concentration** 11. high urinary laad excretion* following Varaena aifalnlatration* ill. high bona laad concentration disoorered during life or at autopey, Reference* (In thia regard, the work of Dr* D. A. Henderson, in Australia, appear* to have eetabliahed that excessive laad expeeur* In childhood la frequently followed by the developcant of a progressive renal lceion which ultisately leada to early death free renal failure*) D* k* Heodereoai A follow-up of Case* of Pluablea in Children* Australasian Annals of Medicine (1951) til* 3* 219 D. A. Benderaoni Chronic Nephritis In ^leonsland* Australasian Annals of Medicine (1955) IT* 3* 163 D A* Benderaoni "The Renal Content of Bono In Chronlo Bright's Disease* Australasian Annals of Medicine (1957) (To appear shortly) (In a fourth paper* Henderson will describe the renal pathology resulting from excessive lead absorption daring childhood*) (o) The intermittent release froa storage in the tissues of increased Mounts of load as a result of infection* starvation* diet variation* ato* 3 6* The use of the Beacurotent of bone load concentration to ssoartaln the relatlonahlp of s o bs casta of chronic cardiovascularrenal disease to sxcosaiv* load absorption* slthor in childhood or in industry. f bi qjupj"ring 'V* yv if ni m lilirtl a a tto to iM ii I <III II -** *- ... LIA10969 ` Or. William I. Georgs -> A Review of Certain Health Problems Associated With Lead 7 The importance of rmt as a vehicle for tha excretion of sbsorbed lead and the effect# gsnsraXly of temperature oo lead ebecrptlon and excretion. References D, 0* Shlalsi "Tbs Elimination ol Load in Sweat11 Jluatralaalan Annals of Medicine (19fl) ITT, 3, ?2$ D, 0, Sblelsi trial Lead Poisoning In Gelation to Climate* Australasian Annals of Usdtcins (175$) Angus* 6. The affects of diet on lead absorption and excretion., including the possibility of tbs existence of metabolic chelating agents. It is impossible to refer to all the above aspects in the tine available. but reference will be cade to sons of tbsn, especially to those to which aost attectioo has been paid by Australian investigators As far as industrial lead poisoning is ooocemed, many years ago, in what ware apparently vary tad wonting conditions, scute lead poisoning frequently occurred st Broken Hill, where oxidised carbonate ore was then being mined and smelted, end at QIbrt Plrla, *.tre lead smelting and refining ware conducted, Commissions of Enquiry ware held in 1920 at Broken Hill and in 1525 at Ibrt Plrie, and in the reports of both, the incidence of lead poisoning was counted upon, 1 following these enquiries, working conditions in both industries were greatly improved, compensation was provided for incapacity as a result of lead poisoning, sod medical boards wars established to examine and certify, Thera has been very little evidence of clinical lead poisoning in either place for many years. At Broken Rill, sines 19li0, only five eases of lead poisonlx^ have bean cert illad. four of these cases quickly recovered with treatment end re turned to work - three of thas had bate working in a limited retreetmsnt process of an old dump consisting of highly oxidised material. At Port Plrie, only ona caas of plumb In has basn certified in the last six years. In both places, notlflcstlon by medical practitioners of suspected cases of lead poisoning is required under the Act, Recant interviews with general practitioners in both localities confirm that they are seeing no evidence of absorption of harmful quantities of lead. Several hundred cases of lead poisoning occurred in the early nineteenthirties in lead nines situated in the north of Queensland. At that time, carbonate ora was being mined and smelted. Medical supervision of workers wsa instituted, working conditions ware improved end the incidence of leed poisoning speedily decreated. Today, with the mining of sulphide ore, esses of lead poisoning occur only among men alloyed in the smelter section of the operations. Two or three Such olio* leal e;cs occur per year, though quite a number cf ten show laboratory avidono# of xceeslv* lead absorption, Uen so affected ere given work sway from a lead ha sard. I' muj s h 0*iW|j !,j.i 5* * }*%&' - .4>i> j a 109 70 i t \: t Dr, William Z, Ooorg# At~ A F.rrlev of Certain Health i 0II Problems Associated 91th Lead i i it I i Becondary industry contribute* few cwii of lead poleonlng per year In ill states - s.g, aaong bridge painter* employed removing old lead paint from bridges, end trcr.g ten er.ctgod In the handling of acrap bstterlas. Such men are nodie ally cm'.r.l regularly aid It la unusual for clinical lead poisoning to develop, Mao showing ralaod urinary lead excretion ere (Iren work away from thle taiard. In l9$6t the Veresnate test'* for lead poisoning wee raised at Broken Bill In claim for compensation for lead poisoning, A nicer there tec as* disabled as t result of chronic nephritis, Ha was twice exasined by the Statutory asdical board and a certificate that hie disablement was due to lead poisoning was refused. He had worked et Broken Kill, 1a eulphlde ore only, *lx>ce 1921, He had newer suffered from ywptocs of acute or execute lead poisoning and his urinary lead an:retion was 0.02 tgi per litre. He was eer.t to Sydney, where he was given an Infusion of a Vereenate. this resulted in the urinary excretion of 0.6 oga of lead per litre. Si his report following his examination of the wan, his physician stated that this result indica ted! (a) that the worker had an abnormal quantity of lead stored in his body, fb) that he had been exposed to exceedre quantities of load at his work, and - (o) that the result of Versene adbdnletrstion confined Ms opinion that the chronic nephritis fPos which the worker was suffering was due to lead poisoning. Ba quoted the d opinions of cany industrial physicians that lead could cauas renal dosage. 1 It Is thought that this Is the first occasion on which ths results of lead excretion in the urine following Vtrsens edsinletration have been used to stpport a clala that chronic nephritis was due to lead poisoning. 7e feel that, probably. If Tereene is given to any worker exposed to an industrial lead ha tard, a high urinary lead excretion will follow, compared with that produced in persons with no industrial exposure. In the present stats of our knowledge, w* do not know that ws could satis fy a court that an abnormally high amount of lead, art in ths bones as calcium lead phosphate or lying in the soft tissues, doe# not shorten the life of a workar or pre judicially effect his health, W# fsel that we have insufficient Information of the quantities of lead which could be produced, by the adeinlstretlon of Versene, In the urine of industrial lead workers with no sysptocs of illness and with no signs of di sease. If this is greater In amount than that which can be produced In nonoxposed workers in similar ag# groups, is it of any clinical significance? Some Interesting work on the excretion of lead In the sweet ha# b# re ported by Shlels. Shi els has pointed out that, at Mount Isa in the tropical north of Australia where lead wining and eaeltlng ere carried out, *11 person* excreting 0,30 mgB# or more of lasd per lltrs of urine have some evidence of clinical lead Jl poisoning, whereas in Melbourne, in the temperate south of Australis, only 62 pay & cent of workers excreting 0,30 rga* per litre or nor* show clinical evidence of lsed poisoning. He shows that, at Mount Isa, the dally excretion of fluid Is of ths order of one litre of urine and 2,$ litre* of sweat per day, whereas in Melbourne, ths twiaiWssa - u*uWSi  . .' LIA10971 ' /. . i Dr. WIIHm %, Oeorgs i $ A P.srrlow of Certain Health Problems Associated Kith Lead , dally excretion of fluid la about 0.5 litres of rmt and 1,5 litres of urine, Thus, i , with 0,30 rg-sa of l*.d p*r litre of urine aril a Ilia one antra tie n In the w*t In | each piece, the total hilly lent excretion In fluids at Urunt Isa wculd be acre than l ; or.s tpa [r <t--y, whereas In Melbourne, the dally lead excretion In fields aould sexr-nt to about C.W r c =.s cr.ly. At itouat lea the blood, organa and tissues of the i body would te in contact uith acre than one ga of lead per day. At Melbourne, with ] the urine showing the sane lead concentration, toe tlaauea would be In contact with ; only 0,6 cgn of lead. There would thua be a treater c haoce of findint case* of lead pelaonlng aaong persona excreting 0.30 aga par litre of urine at Mount Zaa than eaoog those axcretlrg 0.30 aga In Melbourne. On tha other hand, aiming a constant aoount of lead absorption dally, there would be a greater excretion of lead In tha hotter Booths than In the colder Booths, so that there would be pres usably leas tierue lead storage. There would be leas chance of lead pclaoning developing In the starter than In the winter, provided con ditions of exposure were the same. Shlels Concludes that increased sllaination of lead in tha sweat way have an lxportant bearing on variations in tha evidence of lead absorption as shows by tha aeount of urinary load. Keferrirg to noninduatrial lead poleonlrg, soas very interesting work has been reported recently frca Queensland. This stats has always been very lead oooscious* because of a foraer lead hasard to children. For Bore than 50 years, clini E cians in Queensland have been convinced that one of the sequelae of lead poisoning in childhood there has been the devclcpBect of chronic renal disease at a coopera tively early ace. In 1929, Hyw concluded that children in Queensland were exposed to , s lead haxerd whilst playing, during the wet season, on tha lead painted wooden reran* daha so cmn there. They licked rain drop* off the verandah railing*. 8a shewed that there was an abnormally high incidence of lead poisoning aarng Queensland Chil dren, e.g., fro= 1917 to 1926, 1,25 children were treated for lead poisoning in tha rr Brisbane Children's Respite?, whilst during tha asae period, only four children were treated for lead poisoning in Sydney, three in Melbourne and one in Adelaida. Along with this high Incidence of lead poisoning in children, study of tha death rate froa chronic nephritis showed that the death rata frca this disease In Queensland in the 104,0 age group was Bore than three tines as great as that In other state#. ' As s result of this and of nany other reports, legislation was introduced In Queers lend about 1930 which forbade the use of lead-containing paint on the interior of houses st heights which children could reach. Within the last year, in Queensland, L- the loglaletlon has bewt further aocr.de1 and now the tele or stanufacture of lead car ' bonate as paint substance has been completely forbidden. Wo building nay be paloe ted, either interiorly or exteriorly, with a lead paint of any description, except thst, on certain decors live boards high up in tha buildings, such ss fascia boards, a lead paint of up to 5 per orait My be used. Bed lead Bay still be used on structural steel. ' It is now claimed that, In recent yeare, an lnproveonnt in tha statistics of death froa chronic nephritis in younger sgt groups Is evident. Dr. D. A. H<ndoraon, as a result of work st the Qur.sland Institute of Medi cal Research, has recently reported seas extreaely Interesting conclusions on the S - n-afWHrrr jipjKiijj iffWfA1 1 JjJWP J^ w 1 *1 LIA10972 i 5 4 < Dr* Wllllao Osorgt 1 -6- A Review of Certain Health Prc-hi*a# Associated Tilth Lsad 4 I i i relationship between soul* lesd poisoning In childhood and the development of chronic renal Ccttu, It would appear that he has convtnclng erldene* that this connection does. In fact, exist* His work has appeared In the 'Australasian Annals of Welle Ins* at Intervals since 195b* References to these paper* hare been ilreo above* ] In his first paper, H<md#r*on describes how he studied the after histories | of children who had been treated for lead poisoning in ths Hospital for Sick Chll- j drer., Brisbane, between 1915 and 1935* There ware 131 children In the group, with I" ages ranging free 2 to 12 /wars and coeprlalng 159 Bales and 2)2 focal as, The fol low-up was aade by enquiries In the Departacnt of the Registrar Osoeral, at also-- toral offices, and by examination of carriage records, death registers, etc* Soot* Information was obtained of 35? of the LtOl children* Of these 35? children, death i certificates were seen for 101 fwalee sad 6ii Bales. These Included five war deaths* 1 ill of these deaths occurred between the ages of 1 and LO ysars* Ths Bortality rate ] for the whole series of children was lO.liOii per 100,000, whereas the average aerte* llty rets free all causes la ths general population of Queensland for persona agsd 1 to W ysars la 263 par 100,000* Of the 165 deaths, no fewer than 9li wars certified es being due to chronia nephritis) an additional lit deaths were certified . s being due to other possible re nal causae, s.g. cerebral heBorrhage, giving a total aortality rate, froa renal causes, in this group of 26,93? per 100,000. The avrags aortality rate freas all rwnal eausee in the general population of Queensland in ths 15-laO sgs group Is 36 per 100,000. 1 The duration of Ilfs before death froa renal causes, after S<hU.ssloo to hos pital with ths diagnosis of load poisoning, varied froa 6 years to 31* years* Even after the subtraction of all renal and vasoular deaths, an excess of aortality froa other causes was noted, hany of the other causes of death certified could represent the sequelae to lead poisoning, e.{. such certified causes of death as "decent!*, "encephalitis," "convulsions," "acute nephritis of pregnancy," etc* There was also s high death rate in the group froa Infective causes which could pos sibly be related to chronic 111-health associated with decreased resistance* Of the 167 seekers of the series still alive, Information about 101 was ob tained. Of these, 17 have hypertension and albuminuria, 3 hare hypertectlon, 5 are nentally defective, 3 have psychoses and 2 are blind as s result of optic atrophy* In his second paper, "Chronic Nephritis In Queensland," published In 1955, Henderson concludes that, fine* 18?0, Queensland has had s higher aortality fro chronic nephritis than the reoalnder of Australia. This higher nortallty was ob served to affect first ths younger age group* and than older age group* in succession, until the oldest age group to be affected, 50-59 years, was Involved about 1930* This higher aortality has now begun to decline, first In the younger age groups and. If ths present trend continues as appear* llicely, the aortality In the 50-59 years ag* group should drop to that of the other states of Australis about 1990* W.n the Increased aortality was at Its naxinua, chronic nephritis was cna of the ccenonly certified eauee* of death for person* under the age of 1*0 years* Ap proximately 160 persona between the age* of 10 and 60 ysars died **ch year In Queens land In excess of tha r.unbar who would have died had ths death rat* froa this die**** been the sane 4* that In other states* LIA10973 vi Dr. William t, Oeorg* 3 7- A Review of Certain Health Protlecj Associated With lead Henderson points out that this excess nortelIt y is beet explained by the aoI tton of sore nephrotoxic agent on the children of Queensland which would here oc- menced act1 r.j shout 1670 and gradually diminished after about 1920. This agent lnl* < tiated changes In the kidney which lead to death free chronic nephritis in free 10 to L- years. In this second paper, Henderson leaves it at that, but in his third paper, entitled *The Lead Content of Pone in Chronic Bright's Disease,* he conclude# that this nephrotoxic agent was excessive lead absorption in childhood. In this paper, be reports the results of the analysis of the lead content of tone from the ealvarltai and from portion of a rib from 669 autopsies in Brisbane (possible lead exposure 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 cf bone froa subjoct* aged 20 to L9 years, born and dying in Queensland froa chronio Bright's dlseato, is significantly higher than that of subject* net suffering froa this disease. In 3& ralea and 31 females, aged 20 to U9 years, bore and dying in Queensland froa chronic nephritis, the toan bone lead content was 7.J1 *ga per ICO gn* of no 1st bone In sales and 7.97 in fcsalet, whilst for persons in th# sasa age group and not suffering froa chronic Bright's disease, the wean was 3.91 (gti per 100 grass In male* and 3.3b egos in females (calvarium bone)# Henderson found that, as a result of autopsies on patients dying outside Queensland, aost cases of. chronic renal disoaae among then could be allotted by cllnioopatholcgical examination to one of three defined and generally aocepted etio logical groupei (a) chronic gloaerulonephritis, (b) chronic pyelonephritis, and (c) those associated with hypertension as tho primary condition. When, however, an atteept was cade to allocate to one of the above group* the 59 casea of death froa chronic nephritis in Queensland in the 20 to L9 age group, it was found that only 12 of these could be #o classified - fiv# to chronic glomerulo nephritis, three to pyelonephritis, four to hypertension, forty-#erm were regarded as bslng of undertarnined cause. The** cases could only be labeled *hypertan*ioa with renal failure. They had no history of acute nephritis, of long-#tending urinary infection, or of oedema, prior to that associated with terminal cardiac failure. Their urinary findings gave no indication of the etiology of this renal con dition and tha general histological picture was one of marked disappearance of renal tissue without indication of causa. Th# bone lead content of the 12 subjects with chronio Bright's disease of known cause was found to be of the same order as that of poreore not suffering from this dll****. for th# 25 females and 2? tales In th* group for which no rtlnlcglcal diag nosis ms made, th* mean lead value* in tha calvarium were 6,US t&u P*r 10 P" la aales and 6.66 in females. gyf'jWB ign "" lywig.jiwM. .p1' Dr. William X. Oeorge A Review of Certain Health Problem* Associated With Laad Henderson then proceed* to disco* a tha possibls origin of thla high bona lead and enumerates throe possible cause*! (a) As all had chronic renal disease, retention of nonsally aba' rbod load by failing kidney* nay bare bean reaponaible. (b) There My hara been aooo dirturban:a of metabolic* whereby a large proportion of normal lead intake M absorbed. (c) There say hare bean excessive abeorptlon of lead due to excessive exposure. Each of these possibilities la discussed. Be finally concludes that there had bean in these cases excessive absorption due to excessive exposure. In those with a high bone lead, in only one tale was there a history of In dustrial lead poisoning. Pour tales had a history of lead poisoning in childhood and a sibling of soother had Buffered fron childhood lead poisoning. There has been no Industrial exposure to lead of females in Queensland, and no other lead hatard to adult festales is known to exist. Six of tha fecaloa with chronic Bright* a disosaa and a high bone lead content had histories of lead poisoning in childhood. Sawaarlxlrg his conclusions. Henderson points out that it if known that there vss in Queensland for nany year* a aarioua and widespread lead haiard to chil dren and that it has been shown that, where a lead hasard exiats. inveatlgationf of iblirgs and associates of children with plteblss will reveal nscy additional In stances of grossly excessive lead absorption, with few. If any. acute clinical mo Ifestations. The above facts rake it asst probable that the excessive lead in the bones of nearly all these young individuals with chronic Bright's disease was soquire! during their childhood. He goes on to say that his Investigations provide a link between the chronic nephritis in Queensland and excessive lead absorption in childhood. He further suggests that the estimation of the lead content of bonee in caeca of chronic Bright'# disease nay well have e wider application. Ha points out that pluhblan, both industrial and nonindustrial, clinical and subclinlctl, occur in nest drill ted consunities and that, despite suase doubt, particularly In America, there is e great deal of evidence that lead absorption can produce chronic renal di-- sease. Ha suggests that cases of chronlo Bright's disease occurring outside Queensland nay also be due Vo plmMao and that tha routine determination of bone load at autopsy, in cases of chronic renal disease without obvious cause. My eluci date their etiology, Thle is supported by the fact thst, in the group bom outeldB Queensland, thereby avoiding tha special ha card in childhood, a nvarber of cases of chronlo Bright's diets** had high bone lead, Jt so happens that ell these were male* in the older age groupie, suggesting an industrial exposure. Henderson eephasltes that the bone lead content is of etiological signifi cance only Wn*n considered in conjunction with clinical and histological date. ajdOJW* .'UR^Iw^^iifwyway LIA10975 4 \ | Hr. Willlea . Oeorge | -9 A Review of Certain Health Problcne Aeeoclated Tilth Lead ] Ri(l*rioa finally conclude* that eooe ceaoe of chronic Bright** <&* In J Quoeneland In the 20-L9 age group can be escribed by clinlcopathologlcal etudle* to ) Jovowrj cauaas, but the larger propcrti.cn, 63 per cent In the present aerie*, oernot be eo allotted, the bone lead content of these cases of known etiology 1* the aaa* i as that of peracrj dying without chronic Bright's disease, the bone lead content of the group cf unknown etiology la algr.Lficar.tly higher, Tele high bone lead content is due, with few exceptions, to excessive absorption during childhood. Bona lead content can be used, In case* of chronic Bright'* dlaeeae, at a valid Io dic at Lon of exceaelvo lead absorption, and Its eetlaatlon Bay provide a clue to the etiology of tone of thee. In a fourth paper, Bendereon Intends to dlecuea the pathology of the kidney aa soo latod with the preeeace of high bone lead content. hiiit4 k n ii il nnjfci iii^ii^AHh^MMfcifciiM^ik^i^M^i 5