Document wqq5Bg1152eedd3BajY39pNoQ

' - .n v^KuS*-*? Vt* ^ %*/ ^ - -.- '*`t j LEAD INDUSTRIES ASSOCIATION. INC. It* MAOIION AVfHUI HCW YORK. N. V. 10017 nunWM - *A(A CAM .' i ".` S f /obruwy 8, 1966 Tot AU HnUn of tho UA-U2JG L**4 Bo*lth ud Safety Ccoolttoo Attache! 1* A copy of popor written At our rt*J**t by Dr. Haloy m*J d**loo4 to bo pubU*bo4 in tho AMI Arrhlw of terlrorarotal s**lta. X vouM bo scot lster*to4 to fcorloe jrwf iwactlcoo, eoBtnU, ao 4 ertttelM of tho wort. Too vlU rtsnbtr U*t o-rorsl people At our recent Ccoaltteo noetic* tijmirS lot*root la 4 thl paper. Tory truly your*. rerttw Attocfaaoot s3u_ Coo 0. Fowler IIOHM tSKJHWeWwftffJ* Iljp ijhji,een t uw w ew r; R. fei,. I r-. i ;5 * Ui>oxtcr7 of JTuelw Hr-llclo* od button Moloy D*p*rt**ot of Mos*>ylc ul ucU*r M>411m Qblvr*lty of CollforuU School of MrticLa*, loo Aa*lM TM trtloU vi *ypporV4 by Cctr*ct At{0^-1) 0121*12 & *"* * iM AVuolo br(/ Cc m>L**1o o u i) U>* IktwiU/ of Coltfcroli* **5*fc N 384.01 I '-ijf ! -1 1 i i PTOPPUCTiai Bscsotly , gsoebenlst bu suggested that tba people of tha Ifclted States art being subjected to chroolc load Insult frc** Industrial source* with tha result that thara ara functional ahtfta In blghsr narroua activity. (l) Sa alao atatad that tha laad levels In tha lltaratura should ba sat aside. This does not sake sansa to tha tcnieolcglwt so It is necoeesry to nsnnhnta tha past and currant usa of Isad in tha Uhltad States) tha sources of tha lead entering tha biaan body) tha nataholtsa of lead Including lead balance of tha body) tha nanoer In vhlch bona seekers (such as lead, streetlim, ate.) ara discriminated against by physiological escbaat set sad last, but by no aaana least, tha overall toxicology of lead. C5Z3 Of mo Examination of tha total uses of lead for tha periods of 1925 to 1929# 1952 to 1956 and tha year* i960 to 196b lneiualve rereals only a alight Increase In cocsiatptloo of lead In tha Obi ted States (rig. 1). Such applica tions ss aaraml tloo, bearing netsIs, solder, casting Betels, weights and ballast and ao forth hare aaan slight fluctuation and, la sees cases, actual decrease la total yearly usage of lead, figure 1 shows tha actual decrease la tha usa of lead plgmtita and building naterials, l.e., lead pipe. These changes bare bean brought about by tha development of substitutes such as tltaolim pigments and copper or galnutted m well as plastic pipes, by far the greatest Increases la the usee of lead here occurred la etoraga batteries and lead alkyl gasoline actl-kcock esepounda. Thus, although large amounts of lead continue to ba used, those applications, l.e., paints and plimbing, tdtlcb were lsroleed la Inadvertent toxicity In the past have been almost elIslested st the present tine. Decreases In the uae of leadcentsIn lag Insecticide* hare also occurred as a result of the Introduction of the chlorinated hydrocarbons and phosphate Insecticides, lead Insecticides utilised la 1933 were 6000 short tone, la 19<th were 25.957 short tons and la 1959 so low that definite figures were not given (2). arn-moqt wo Auarta Xa view of the increase la usage of lead alkyls sad their indictment aa a general causa of chroolc lead Insult to ths general population (1) It la aow necessary to sxmmloe the overall picture In acre detail, figure 1 show* the Increase In lead alkyl usage for the years 1925 to Y/J* Inclusive sod this reflects the Increase In application of the automobile as ths principal mans of traosportatlcn in ths Uilled Stats*. Tbs prims qua11 cn Is not tha Increased burctng of Isad alkyls by the Internal e embus t too engine with tha subsequent release of lead compounds Into ths elr but ths type of c&stpounda released, the area of release, the particle site and solubility of these ewpcuMe and thIr overall availability to the public. )Ur seller at *1 (3) have Shown that tetraethyl lead dscoetpoee# Into f> Cl-Br, (TiCI^CWfbCl'kr, fHRthCl'JbCl'Vr, fJOt^Cl'ThCWr, fo.'JOt, IbO'PbCl'Hr* A and In the presence of phosphate additives JTb.trO^K'IVJl'Hr. However, tfm distribution of the various compounds depeadd an both the sutomoblls and Its nethod of operation. 1 -arswuVV LIA11734,;' ,/ * r * _' "* - ' " -2 - A nirtur* composed of the smcolua-laad-halide complexes ppe*n predominantly under city driving condition*) whereas ft>-Cl-Br appears et full-throttle acceleration*. Moreover, the forcer caaplsxss ere most often formed la duel* exheuet systesa* which operate et lower temperatures. Comparison of eleea versus dirty exheuet eyeteae indicate* that the forcer emits 20 per cent of the lead burned wfcll* the letter emit* up to 60 per cent. Sever* aerrlce tend* to clean the exheuet *y*tea. The range of particle all** emitted rang* frae 0.01 micron to several millimeter* In diameter with thorn* eaaller then 1 micron, although more numerous, accounting for cnly 5 per cent of the emitted lead. City-type driving reeulte in the cmladen of 27 per cent of the lead ae partlclee 5 mlcruc* and larger while acceleration lncreaeea this emleeloo to 39 per cent. The particle site distribution and composition are Independent of the amount of lead alkyl In the gasoline. The Inorganic compound* under disease loo are relatively Insoluble and the aasonlis-lead-halld* so unstable that tven the water In the exhaust pMi can cause It to decompose to more of the Inorganic lead coepounde. It Is well known that the larger particles, above 5 ale rocs, have a tendency to settle rapidly and those that are Inhaled are trapped In the external naree. Particle# la the lower ell* ranges are removed by two mechanisms: entrapment In the brcocheolar mucous eecrrtloo as a result of centrifugal action produced when the air stream reaches the various brcocheolar bifurcations and direct precipitation on the s u c o t i* secretions. In both cases ciliary action removes the particles fro* the lungs and allows them to be expectorated or (wallowed and excreted via the gastro-lntestInal tract. The particles below 1 mlcroo can reach the depths of the alveoli and be absorbed directly or phagocytlred by the tissue tmerophages. In either 0 event the total amount absorbed via the lung* 1* only a email proportion of the dally lead Intake compared to that sisorbed from food and water. ?:ss =1 FOOT LEAD OCWTTTfT In discussing sutomchtl* exhaust. It beccme* quite apparent that the lead compound* released are rather Insoluble and thus can only be small contributors to the lead content of the body. Only 0.03 eg of the dally lead Intake comes vie air-born* tmterlalj whereas food and llqald Intake contribute 0.3 ( to the total lead Intake of 0.33 mg (<). Kafcce (5) bee shown that almost every food stuff and beverage eootalns ten* lead ae a natural constituent of Its total mineral composition. This le not surprising because most soils In this country contain between 15 and 20 ppm of lead which Is taken up by plants and transferred to animals eventually ending up In the biaao food chain. Similar conditions apply to the water supply tAore yeatherlrg and leaching of rocks add lead to the water supply. Lead ae lb** le constantly released from the earth's crust a* a result of decay of the uranium series of nuclides. Mayneord et al (6) have shown that this alpha emitter 1* takeo up by grasee* and other plant* Which are eaten as forage by animal* which In turn become part of the human food chain. Kill (7) ha* shewn that the lead-210 which escapes Into the atmosphere 1* returned to earth with rain and aide to the natural radio activity In the fond chain, hurt cm and Otewart (9) found that the mesa residence tin of lead-210 In the atocephare 1* about k week*, sufficiently long enough for mixing to eocur but short compared to this nuclide's haLf-llfs of 21.k year*. Water supplies also contain lead-210 as * result of rein nr frees leaching of the earth's cruet by river water (9). The total amount of l#ed-21Q 1* snail compared to Stable lead but the** Buell4* aeasuremsnt* again point to the dally food and liquid sun*.septic* s* the most Important sources of lead Intake by the biamn. Kate* ()) baa pointed cut that, although n^PP-i *3- lead coctaaloetlco of food tod drink ctn oceur during harvesting tad processing, It It reaarkable that tuck contaalnatloo It of such t low order tt to contribute very llttlt to th overall lead Intake. Lead excretloo follows t definite pttttra vlth fsces containing 0.3 ng per &y tad urlnt containing 0.03 * per day. Thus the average Individual It la lttd balance tad not accuxulatlng excess lttd to add to bit total bod/ burden. Changing tnvlrocaestal ooadltloat can cbanga both tbt lctakt tod excretion pattern but the bod/ adjusts to ttintaln Its noratl lttd btltact. Distribution of lead In tbt bod/ rereals t 1t*t order of concentration of tbe aleaent In tbt soft t Issue i other than the liver vlth 0.0b to 0.25 a*/ 100 G* and tbe kidney vlth 0.01} to 0.l Mg/ 100 0a. Tbe largest lead depot In tbe bod/ la In tbt akeleton where tbe aaount varies with different types of booe, being 0.21 to 1.11 ag/ 100 pa In flat bona acd 0.67 to 3-59 &/ 100 gje In long boot (3). Recent etuilee of 150 caeea by Tipton and Cook (10) pointed out that there vaa a vide variation In the lead content of all body tissues but tbe values obtained vers in agreement vlth those Keboe et al (11) reported 23 years earlier. Slalltr results have been obtained by guebata et al (12) for bone easplea obtained In tbe Lee Angelas area. They found no correlation between lead concentration and tlaa of residence la tbe are* and no correlation between conceetratloa and age In tbe 173 cases analysed. Coetparlsco of their results and those obtained by others la given In Table 1. It can be seen that there baa been little change la booe lead concentration over a period of J1 years tfcen the use of lead alkyle baa shown such a large increase (see figure 1). Thus, again tbe unavailability of the lead confounds in autccctlre exhaust la apparent. furthenacre, BoItrasa (l-l8) baa abeam that lead-210 fron tbe food-chain also appears In tbe hvsntn ; skeleton as veil as tbe soft tissues. 1 LEAD TRAJt5P0RT A/D KHAbOLISM After absorption Mostly via tbe gaetro-Intestinal tract, lead Is carried to various tissues by tbe blood. Tbe distribution of lead In tbe blood stress has been shown by Keboe (3) to bet plaeaa, 0.001} ag/100 gaj erythrocytes, 0.02k ag/ 100 pa or a total of 0.027 ag/100 gts for whole blood. Recently tbe Oh1 ted states Public Health Service conducted a survey of blood and urinary lead aaccg group# of Individuals In Cincinnati, Los Aegele* and fbllsdelpbU. (1?) Heart blood levels were! Cincinnati, 0.02) to 0.02} ag/lOCps) toe Angelee, 0.019 to 0.C21 ng/lOOps and R> 1 lade 1 pita, 0.01) to 0.CC6 a*/100 pi. Urinary lead value* vervt 0.026 to 0.028 ag/Lj O.O^k to 0.021 ag/L and O.C20 to 0.033 Mg/t respectively. These data aerved to confine those obtained earlier by Kehoe (}) ExperWwntal Ingestion of lead at a cooetant level of 0.) ag per day produced no detectable elerallco of blood lead In k20 day*. After k year* of lrg.elloo of 1 Mg of lead dally tbe blood lead reached 0.0*6 ag/100 ps. When tbe dally doee vae raised to 2 ag for.2 years tbe blood value vae 0.06} ag/100 pt and when lrgseted lead Mia increased to ) ag dally for k moths tbe blood level reached 0.0} ag/lOO pa. Kxjerisental ln.'.alat loo of air ccnlatnlrg 0.1} sg of lead/M^ for 37*3 hours per week for ICO weeks Increased the blood level to O.kJ ag/100 pt. Ctovloualy both experimental lngsstlon and Inhalation Increase blood lead levels but there was also a cooccmlttaot Increase In urinary lead amounting to 0.0)k to 0.11 ag/L after lngsstlon to 0.71* ag/L after lnhalatloo. Here agata the body was adjusting to Increased lead Intake by Increasing lead acretlco via the kidney (20). There 1# also Increased lead la the feces, the principal route of excretion, and thl* partially explains why even vlth a controlled experlneot It la rary difficult to Increase the body burdaa of lead. . - ' Another aechanlsa exists for decreasing the aaouat of load la transit, neatly, deposition la bone. MacDonald at al (20) hava shown that both lead aad atroetiua ara bound to ben# by adsorption or Ionic exchange at the surfaces of boo# salt crystals or combined vlth the sulfata la the organic astrlx. Boo# as*ling slaasnts such as lead aad strooti\a ara also dlscrla* lasted against by the kidney. McDonald at al (21) hava shown that td*n both calc iua aad atroetiua art available for skeletal retention, the kidney preferenttally excretes the latter* UXD TSTOXICATICW In the previous dlscuasloe the various s mo i whereby lead asters aad exits fros the body have been covered. In so Instance baa frank lead Intoxication been discovered la the thousands of case* discussed. This la probably, as has been shown, due to lead balance la which excretion has kept up vlth Ingestion. When this balance breaks dews, three ferae of lead Intoxication caa result! prlaary lntoxlcatloo, characterised by Intestinal tract dysfunction, loss of appetite, constipation, colic and general ealalse aad weaknessj secondary Intoxication, characterised by weakness and ease atrophy or even paralysis of the foreara extensor auacletj finally, the lead encephalopathy frequently seen la Infant* and children. In all three instances changes la beantcpolesl* vlth basophilic stippling of the erythrocytes and reticulocytes are seen. The aala causes of lead poisoning la the population are Industrial exposure, burning of battery cate#, sating of leal bated paint. Ingestion of lead Insecticides, etc. Dangerous exposure to lead give blood lead values ranging frea 0.C7 to 0.2 ag/100 gn and urinary value* ranging fron 0.06 to O.h atg/L. flenlng (23) has pointed out that the application of good Industrial hygiene practices has prevented any cases of lead Intoxication la the nanufacturlng of lead alkyls in the last 30 years. Stellar exemplary records have been compiled for the other se&aeots of the lead Industry, tree cases of Inadvertent poisoning by lead have been reduced to very lew figures, but no one caa guarantee absolute prevention of scute lead Intoxication la the population. Bcwever, the development of chelation therapy hee prevented lethality and decreased the possible danaglng effects of lead. Chronic lead Intoxication fros Inhalation of the breakdown products of lead alkyls has not been deaocstrated In the 2)00 Individuals covered In the trl*cltlss survey caodse-ted by the tkilted Stats* Public Health Service durlrg the period June V/j X through May X'/S (19). Thus, again It beccasa apparent that td cause either acute or chronlo lntoxlcatloo the toxlo agent oust be Id a fora that can be readily absorbed and transported to lta target organs. This has nod been demonstrated for ths decotgosltlon products of lead alkyls, PtWAHT It has been shown that the population of the United States Is la lead balance and the old causes of acute and chronlo lead Intoxication have bees reduced Vo very low levels by change* la technology. There is no such entity "-aapiw!LM.ewi esr- ..-utawii- * u r*tuml l**d bod/ burd*nj b+c*u* th population hu baan xpo*#4 to ApproxinAtaly th* ib m BOut ot l*Ad In tha solid and liquid conpooeota ot the diet since very early la tine. The earth's cruet contains the lead vhleb eventually enters the body vie the food chain end It bee been shown. that, although people have been exposed to Increased concentrations of lead, canpounds, these are not eveliable end the body burden has not Increased over the last 30 years. TAB1I 1 *d l e a d ooicnrmncsi w b o b* Klcrocraae per One of Ash Tear flat boos Lana Bone Calvarlist Mb Reference 1933 1954 50*55 eeeea - 55 ?6-5*> -- -- 13 -- 25-65 IK 195T -- 74 X 65 7 39 X 33 r 15 l?6l 32 69 m-- 5 19 7* X 63 r 75 X 60 P 12 i M mi* 1 P - Pmele I .;j aw^-iWHBR^'^es^jwspiasjaysjBesse!^ !^.kS WI? W&mtiWQgig&f *~awMwa8MMi f >- riah-ffaltiwh iUf'laWi mi* ymggreES 1. ritUnod) C. C,, Coot**lotted tad Dtturtl l**d *nrircrawtrt* of mb . Arch. Environ. H**lth U, 3W-360 (1965). 2. Callsv*y,H. V., L*td| A aattritla rurvey, Infcraattco Circular 8o83 Bureau of Min**, 0. 8. D*pt. of th* Interior, 1962, pp. 119-129. 3. Blrachltr, D. A., Gilbert, L. 7., I*b, 7. V. tod BUbylakl, L. K., Particulate load coopousda la autonotlr* exhaust |Mf lad. Eh*. Cha. *2, 1131-11U2 (1957). 1, Xehoe, R. A., Bernal aettbollaa of ld, Arch. Environ 8**lth, 8, 232-235, (19&). 5. fcthoe, R. A., The netabollta of lead la nta la b+tlth a&d dlt*t*. J. Regr. Inst. Pub. Health By*. 2k, 81-97 (lS6l). 6. Htyotord, V. T.t turur, R. C. tod Mltj, J. M.# Aljfct Ktlrlty of certain botanical saterial*, Betur* 107. 206-211 (1960), 7. BUI, C. R., Load-210 tod Polocii-210 la pl, Bttur* 107, 2U-212, (I960). 8. Burtoo, V. M. tod Btevtrt, I. 0., U*e of Icr-g-lived natural radio activity tt to tttot^trle tracer, Batur* l6o, 58^*59 (i960). 9. ftssn, H.K. tod Ooldbert, l. 0., Lead-210 la Dtlurtl vatera, 0ei*oe* 1, 96-99 (l?6l). 10. Tiptoe, I. B. tad Cook. M. J., Trace *laa*ote la huana tlsau*. Part IX Adult aubjecta frot the United statea, Bealth fhyalca, , 103-lkJ (1963). 11. Kbo, R. A., Choltk, J. tod Story, R. 7., A epectroefaealeal ttudy of tb oonatl ranges of concentration of certain trtc* natal* la biologic*! aturltlt, J. Sutr. 12, 579-592 (l9*o). 12. Ruabaua, R. B., Butt, B. N., Ollnour, T. C. tad DlDlo, 8. L, Relation of tlr pollutlco to trtc* tattl* la be*. Arch, Environ. B**lth 10, 227-232 (1965). 13. Keho*, R. A., Theataa, 7. tnd Choltk, J., Lead absorption end excretion la relation to diagnosis of lead poisoning. J. Xndustr. Bn.'-15. 320-3)9 (1933). Ik. Twtp**tt, 0. L. Leteraloatlon tad dlttrlbutlcn of 1**4 la hutto tleeuee tod excreta, Th* Analyst CU, 330-339 (1956). 15. B*nd*rce, D. A. tad Ingllt, J. A.. load content of boo* la obrenta Bright' disease, Autt. Aon. Md. 6, l*.5-13k (I957), .UJMWMJ'" *># ^ 111 '..'jwrw- j t g.'-wiiw j k 'i -Sit #JL. 16. Holtman. R. B., Heacuroaent of th* natural content of RaD (lb2*1) and Rtf (Po21) In hioan boo* -- Ectlnabe* of vbol*-body burden*. Baalth TbyUs* , 305-l*OO (1963). IT* Boltmen, R. B., lb* aourca of un*upport*d Pa^^RaP) la tt**u*. B*alth Phytic* 10, 763-76!* (196b). 18. Holtman, R. B., 210rb (RaD) la Inhabitant# of * Caribbean Ialaod, Bealth fbyalc* n, 1*77-100 (X9&5). 19. Survey of Lead la tb Atao*phr* of Ihr** Urban Ccanunltl**, RI3 Publ. Vo. 999 AP-12, J*o. 1965 , 9** p. 20. Echo*, R. A., Metabolic* of lead m4*r abnornal condition*, Arch, Environ. Health 0, 235-2*3 (IS***)- 21. MtcDcoald, V. 8., Vu*b*\a, R. X., Eralrllan, T., Barbara, R. C.# Spain, P. and touoda, 0. I.. Hecbanlaa* In tkelrtal accunulatloa at loo*. Arch. Btoctet*. Blojfay. 2, 110-126 (1993)* 22. MacDonald, V. 8., Voya*, P. and Doric*, P. C., Dl*crl*ln*tloo of calcium and itrootlua by tha kidney. Aacr. J. Rgrtiol. 186, 131*136 (1997). 23. Pleninc, A. J., Inductrial hygiene and scdlcal control procedure*. Arch ftsriron. E**ltfc, 6, 266-270 (196A). i. aita .. y% Jkw*4suij^tiyii*sgja^f^^