Document 7M574DKdrQJmG6Jvb7q1oK0GR

REPORT OF THE AD HOC TONXITTIX TO ore v a l u a t e t h e h a z a r d l ead is pain t Praparad for tha Coniunr Produce Safety Conoiaaion National Acadaay of Seiancta November, 1973 0007-SWP--037143 :;o t ic l The project that is the subject os this nport was approved 'ay the Governing 3oarc of she National Research. Council, acting in behalf of the National Acaatay of. Scitacaa. Such approval reflects eh* Board's judgment thac she project is os natieaal lsaereanca and appropriate vich respect to both the purposes and resources os the National Research Council. The members os t:;a cjssiitee selected to unaertar.e this project end prepare this resort vere cnosen. tot recognised scholarly oocsetenee sns visn cue cor.siaararcon for ths balcr.ce cf disciplines appropriate to tho projett. Responsibility for tre detailed aspects of this report tests vitn that toaau.t-.ae. Rich report Issuing from a study conaittee of the National Research Council is rsvieued by an incependent group tf qualified individuals according to procedures established and monitored by the Report Review Cooaittei of the Natienal Academy of Sciences. Tlscribution of the report is approved, by the President of the Academy, noon satisfactory ceapietion of the reviev process. The work ca which this puolicatlon Is based as oerferaed pursuant o Contract No. TDK 72-21, Tsak Order 16 with t.-.a ?eoo and Crag Administration. 0007-SWP-037144 0007-SWP-000112840  O hoc t: hv.c ip j :? us.o ::: Dr. Mercii Zisenisud, Chalnan New University Meaical Center Or. Saauel P. Seseean University or Soucc.ten California School of Medicine Dr. Sorbert M. Bikales Rutgers University Dr. Robert A. Coyer University of North Carolina School of Mecitme Dr. Vincent F. Cuinee New York City Health Departnenc Dr. Reginald S. Uourie George Washington University School of Medicine Dr. Pearl 1. Rosser Howard University Dr. Roland S. Scott Howard University Invited Observer*: Mr. Royal A. Brown National Paint and Coatings Association, Inc. Dr. Barry C. King Saa Diego, California Dr. Del Rutnig Departoenc of Health, education, and Welfare Staff Officar: Mr. John Rednond, Ur. 0007--SWP--037145 0007-SWP-000112841 i. ::,t x o d ix c :c h On Deeeaber 31, 1972, che Sureau at Produce Safety at the food and Drug Administration (73A) became responsible tor administration of a federal rsquirsotnc that the lead concsnc of paint* cot exceed O.fZ by velghc of eh* dried, hardened film.* More recently, Che responsibili ties of che FDA In chi* area have been transferred by Cantrei* ca a aev Consumer Produce Safety Conaisslon. Among che first questions facing the Commission is wnechtr the G.5! linit should be reducea to 0.C6Z at a dace that could be as early as December 31, 1973. The 0.361 lisic originated as a recommendation in a report s' the Cosmictee on Environmental Hazards of the American Academy cf Pediatries (1972). Tht Ad Hoc Committee CO Evaluate che Hazard of lead in Paint uaa eonetituted by the national Academy of Sciences-National Research Council et the request of the Bureau of Product Safety to ascertain whether there use sufficient scientific evidence to support a reduction of che lisle from 0.5 to 0.06Z. Che Committee vas requested, if it found that sufficient scientific evidence did not exist, to reeasaend research % thee should be undertaken to obtain the required information. The basic question that the Connie tee must anever is vhnrr.ee there is a sufficient body of information to panic establishment of a limit on tht lead concanc of painct applied to surfacaa accessible to children. `throughout this report, whan the lead content of paint, drier, or other paint additive is given, the expressed percentage of lead is that in the solid dried fila. 0007-SWP-037146 0007-SWP-000112842 -2- This quescion has seen asued cany tires over ms year*, era rar.y regula tions have been proaulgated. The fine, in Carsany to 1337, prc.-.iiiteo the use of anv lead in paints applied to toys. At least 10 countries have regulated the lead content cf paints up to the presenc. except for che German law, which called for total elimination of lead :rna paints used for toys, the permissible lead concentrations have ranged from 0.5 to 22. 2. THE USE OF LEAD COMPOUHDS IN FAINT The essential components ot paints are: (a) Figments: to provide opacity, color, snd durability. (b) '.'ehicles: oils, tesins, and various polymers to bind the pigments together and to provide a continuous durable film. (c) Volatiles: organic solvent! or water (depending on type of paint) to control the consistency of the coating and to aid in its application. (d) Additives: generally m low concentrations, to aid in drying, to control conaiscency, settling, viscosity, and stability, and to ispare other special properties to che coating. In matting a white palac, or a whlte-paiet base that can be tinted to light paatel colors, it is necessary to have an opaque white pigment. The most important early opaque vhlte pigment was "white lead," the basic carbonate, whose composition approximates Z?bC03 Pb(o:3),. White lead was first produced in Holland during the sixteenth century snd was later introduced in England and the United States in the lace 1800's. Tor cany years, white lead was tne print];.-..- ,paou white 0007-SWP--037147 0007-SWP-000112843 forms reaction product* vcth oil rarer vehic.as .vegetable ails, sucn 11 linseed oil) that impart toughness md elasticity to cr.e paint, in addition to opacity. 3asic sulfate vr-ice lead '.as also used as a pain; pigment (approxisace composition, IPbSO^ - ?P0). 3asie sulfate white lead has lower hiding power (opacity) and dating strength chan basic carbonate white lead and eherefort waa not as widely used. The sulfate was sore commonly coablned with other pigments, such ss zinc oxide, and was gsmrally used in exterior paints. Whitt lead plgmancs, whan used for interior paiats, contained 10-60" lead. A representative figure for interior paints used before about 1340 would be 503. Zinc oxide was aaoufzctured tomserclally in France during the early nineteenth century and in the United States shortly thereafter. It waa followed by the manufacture and use of zinc sulfide. Uthopone. a pigment Chat contains approximately 301 tine sulfide and 702 barium sulfate, was developed by copreclpitaeing berlua sulfate and zinc sulfide from solution. Peine manufacturers now had e choice of opaque white pigments, ana ssnv paints were made with e combination of chese materials. Lithopone replaced white lead in aany interior paints, and became a very important pigment tor painc in the laac half of the nineteenth and early part of the twentieth eanturiea. Titanium dioxide, the opaque white pigment uses in aoacm paints, was being produced commercially by abouc 1920. it was introduced to the painc Industry as a titanium-barium combination pigmanc. It was shortly made available also as s titanium-calcium pigment and as the anstese grade of pure titanium dioxide. Also widely used for a while was titaoaced llthopone, containing 152 titanium dioxide. Titanium pigments had gained major acceptance by the late 1930's and largely 0007-SWP-03714B 0007-SWP-000112844 replaced lichooone, tine sulflie. m most interior punts. 3/ this ctni, mere was lizzie eeur.caic justification :ar ::.j use of unite lead in any type of interior paint. 3y 1541, me doing c; titanium dioxide was raced at 115 fo~/lb, compared with about 15 fc-/ib for the lead oigrter.ee. t: Is estimated that sore coders pignencs con taining titanium dioxide have a hiding power of about 155 fcVlb. Thus, X lb of titaniuo dioxide will provide the opacity or hiding power of about 9 lb of white lead, and for many years there haa been no necessity to use white lead pigments in interior paints. The tint uneti ail vnice lead was removes iron interior paic.ts is not known, out it nay te assuaea that relatively little white lead pigmenc was incorporated into interior paints after 1942. lead chromate yellow pigments, first sade in Europe in about 1900, have long been a valuable raw material for use in paints. Thus* pigments range froa light yellow to deep orange. Lead solybdace pigatnts range froa medium orange to deep rad, and "uhrooa greens," froa light to deep graan. .ill these contain laaa. tut in a suen less soluble fora than white lead pigatnts. These lead pigments provide excellent hiding power and color pornaner.ee, and they ari economical. They are widely used in costings for automobiles. trucks, tars satninery, uigns. traffic aarklngs. buildings, and hundreds of ocher articles. Ted lead pigatnts and lead silicochrcnace pigments are valuable fer use in anti corrosion primers for steel and iron. Tone lead pigments arc still used In exterior prlaers and paints for wood surfaces that oust with stand the effects of sunlight, ram, and weather conditions of all cypts. lead compounds sre, and will continue to be, extremely important to the paint manufacturer as essential ingredients of many types of primers, paints., and enamels far exttrier use*. 0007-SWF-037149 0007-SWP-000112845 3 . h is t o r y o f .r it iia t t t n s -.-n it ed s t a t e s ::-:i 11.0 :::t t ::t ;r ~a:::t On March 11, 1971. an crter was puilisned under Section '(p) ;1J (3) of che Federal Hazardous Substances Ac; ceciarcr.g parr.: and ct.-.er similar eurfacs-coating material containing in excess of 0.51 lead (as metal) for use in or around che household co be a hazardous substance and to be banned froa shipmanc In Interstate commerce after December 31, 1372. Separate provisions of that order banned shipment In Interstate commerce after December 31, 1973, of paint and other similar surface-coating material containing in excess of D.CSI lead Us ".seal5 for use in or around the household. The order also specifically provided, as required by Section 2(q> (1) (A) of the Act, that any toy or other article bearing such paint and other similar surface-ccating material and intended for use by children would be a banned hazardous substance efter cne c: those daces, depending on Che lead concent. On August 10, 1972, che portions of the regulation pertaining to cha 0.5: lead content were confirmed as effective. However, che portions pertaining CO the 0.06: concent were static to oe c.'.e suoiecc c a separate document to be published at a later dace. :r was fount by reviewing che cements received with regard co che March 11. 1972. order chat the two concentrations (0.SZ and 0.06S lead) and effective dates presented separate issues that required separate consideration. J.l APPLICABILITY OF THE RECITATIONS AND DEFINITION OF TERMS The provisions of che Fedenl Hazardous Substances Act are applicable to any hazardous substance in interstate commerce chat is intended or packaged in a fora suitable for use in the nouaehold or by children. 0OO7-SWP-037150 0007-SWP-000112846 The term "banned hazardous sostancs ' ::r.:i:r.a; it Section ;;; mesas iny toy or other irtic.lt intended lor use oy cr.ii.iren, which is hazaraaus substance, or unich bears or con tains a hazarcoui suastance in sucn banner as to be susceptible or access by a child to v.-.om sucn toy cr other article is entrusted end under Section 2(g) (1) (B) means any hazardous substance intended or packaged la a farm suitable for use in the household which the Secretery, by regulation classifies as a "banned hazardous substance'' on the besle of a finding chat, notwithstanding such cautionary labeling as is or may be repaired under the Act for that subscance, the degree or nature of the hazard involved in the presence or use of such subscsnce in the household is such thee the abjective of the pro tection of the public health and safecy can be adequately served only by keeping such subscance. when so intended or packaged, ouc of che channels of intcrstact eccntrct. The regulations implementing che Federal Hazardous Subatances Act--specifically, Saccion 131.1'.c) --define a "hazardous substanca Intended or packaged in a form suitable for use in the household" as any hazardous substance chat, under customary or reasonably fore seeable condition* of purchase, storage, or use, say be brought into or around a house, aparcsent. cr cc.-.er piaee where people dwell or into or around any relatad building ar shed, including but nat limited to a garage, carport, barn, or storage shed. The regulations expressly exclude industrial supplies chat might be taken into a horns by a serviceman and articles labeled and marketed solely for industrial use. The peine regulations issued under the Federal Hazardous Substances Act are applicable to paint and similar surface-coating materials con taining 0.5J lead chat are sold for consumer use. They include paint and similar coatings chat art used fot exterior end interior surfaces of d-.ullings ana related buildings, as well as surfaces or articles 0007-SWP-037151 that r* maintained in ar around households or related buildings, such as radiators, fences, furniture, and coys. The regulations ara r.oc applicable to paint and similar coatings that art labeled and marketed solely tor industrial usa, such as paints appliad at a factory to automobiles, trucks, lavn sowers, tractors, and appliances. However, painc appliad to toys and other articles intended for usa by children cannot contain more than 0.51 laid. A pacition to amend the lead-paint regulation has been received end published as a proposal. The proposed aaenenent vould exempt some paints and coatings containing in excess of Q.3Z lead from the bannedhazardous-subscance classification. Included vlchin the requested exemption are couchup coatings for autonobiles, agricultural and industrial equipment, lawn and garden equipment, outboard motors, motorized recreational vehicles, and household appliances. A proposal to exempt artists' paints from the leed-palnt regulation has bean published. Comments on che rvo proposals are currant!/ under consideration withis the Consumer Product Safety Commission. 3.2 OTHER FEDERAL LAVS DEALING WITH LEAD PAINT Congress, on January II, 1371, enacted the Lead-based Paint Poison Prevention Act of 1971. Its purpose Is to eliminate childhood poisoning by lead-based paint. Section 501(3) of the law prohibits the use of peine containing in exetas of 1.0Z lead In residantial structures built or rehabilitated by the federal government or with federal assistance. Several bills to amend this law hava been submitted to Congress during 1973, The Senate, on btoy 5, 1973, passed S507, the Lead-based 0007--SWP--037152 0007-SWP-000112848 -9- Painc poison Prevention Asenctcnts of 1573. vnii.*. -ovis aner.c Section J01(3) as follow*: (a) Prohibit the use of pair.c containing m excess zi 0.5Z Lead before Deceseer 31, 1973. (b) Prohibit the use of paint containing cn excess of O.OSI after December 31, 1973, except that, if the Secretary of the Departaent of Health, Education, and Welfare deterames chat, on the basis of studies conducted in accordance with Section 531(b), another lead content not tc exceed 0.57 Is safe, then suen ocr.er content snail becoae effective after ueceaber 31, 1973. Section 301(b) or S507 direct* the Secretary of the leoarraene of Health, education, and Welfare to concucc appropriate studies on dried paint film co deteraiae the safe lead concent on residential paint products and co report to the Congress not later than October 1, 1973. Several bills amending ere Lead-based Paint Poison Prevention Act of 1971 have been under consideration within the House of Representatives, We understand chct tne full House car-rt.-.t arc Currency Cctsiicsa has reviewed a nusoer of the bills before the House and reported favorably on the "Serrect bill," RRS920. This bill, we understand, will be sent to the floor of Che Houee to be voted cn. L'nder the provisions of this bill. Section 501(3) of the Lead-beied Paint Poison Prevention Act cf 1971 would be mended to prehibic '.he use of paint containing note than 0.5Z lead. Section 301(b) of the bill directs the Secretary of the Ceparcaenc of Health, education, and Welfare co conduct appropriate research on eulciple layers o: cried peint filas with'respect to safe lead eontenc and to report the results of such investigations co Congress rot later chan Decease- 51. l'7t. 0007-SWP-037153 0007-SWP-000112849 _ 3. 4. HISTORY OF FRC3LLM Of C3MJTJMTY 120 FCIaC.SIXG Laad poisoning* anon* young children living In deteriorating ianer-city housing emerged as an ursah problem In the Jnited States as early as ch second decade of this eentury (Williams et ai., 13521. Those* and Slacken (1914) of the Johns Hopkins Hospital in Baltimore ware the first to describe in the American literature the clinical and pathologic effects of lead-induced encephalopathy la children, Williams and his co-workers point out that aulciple eases of lead poisoning had already been reported from 19 separate communities before 1951. and it was recognised that this problem was related to pica, the habit of chewing cribs, toys, furniture, and woodwork, such as window sills, .id the eating of painted plaster and fallan paint flakes. Of the effected children, 50t were between 1 and 2 years old. and fiver than 3T of the children were over 5 years old. During the 20-year period 1931-1951 in Baltimore, 293 eases were found to have clinical lead poisoning de fined by a blood lead content greater than 50 ,,g/100 ml associated vich a clinical manifestation of lead toxicity `.anemia or central nervous system symptoms); 85 of the patients died. After the early Baltimore experience, public-health departments of other major American cities began efforts to detsrmine the extent of lesd poisoning. Generally, two steps wers taken: lead poisoning *Lead poisoning is defined as s case in which the clinical signs and sympeoms co be discussed later are present. Some investigators would include the presence of biochamical changes such as a reduction in delta-aminolevulinic acid dehydrase or an increase in free ervcirocycic protoporphyrin. For the purposes of this report such ehanges are considered to be compensatory and not pathognomonic of load poisoning. 0007-SWP--037154 0007-SWP-000112850 vis aid* * reportable disease, and separate programs for control c: lead poisoning vere established (in 1950 In rniiadelphia). a report of the results of these measures in Philadelphia froa 1955 to I960 (Ingalls ft el_., 1961) noted that about 50 cases of lead poisoning were reported each year, compared vith the average of 11 per year reported by the Baltimore City Health Oepartaenc in 1918-1951 (Williams ee. al., 1952). From 10 co 201 of diagnosed patients died in that period ia Baltimore (Williams et jii., 1952), and neurologic dis orders, including aental recardetion, persisted as sequelae m s o c k ol those who survived (?erlstein and Attala, 1966). la mere recent years, casts of severs lead poisoning seen to have been less frtqutnt. In New York. City, the health, department reports that fatal eases have been reduced to one or tvo per year, compartd vith about 20 per year two decades ago. But there is little information on the frequency of occurrence of the various stagts of lead poisoning short of death. During tr.e lost 20 years, the puolic-haairh. programs of many cities have been expended to include large-scale screening of children at risk. The reaulta of some of the most significant of cheae screening programs are suoamariiad in Tibia 1. A more complete summary of screeningprogram results is found in a report from the National Eureau of Standards (Silsinn, 19?2). The children Included In these surveys are usually between 1 and 6 years old and said to be at risk for undue absorption of lead because they reside in deteriorating, pre-World Uar II housing. The eurveys, for the most part, involve areas at risk vlthin very large metropolitan communities. Hovever, the study from Portland, Mains 0007-SWP-037155 0007-SWP-000112851 (Clark and Kallact, 1971), suggests c.nac the "risk factor'' Is not neceissrlly the tit* of the city but, richer, Che age of the housing. This notion is supported by the ttudy of children at risk In H locermediate-sixsd Illinois communities (Fin* tc_ el., 1972). there Is a definite seasonal variation In blood lead content; the incidence of lead poisoning In young children peaks during the turner sonths (Chisolm and Harrison, 1956; Ingalls, 1961; Slanksma t al_., 1969; Guinea, 1972), the larger screening programs have collected blood samples during all concha of Che year, but some smaller studies have been restricted to the sumtr months. The methods of blood lead measurement are varied, but the dithnone procedure ana atomic-absorption sptctroscopy hava basn used most oftan in recant.years. Anodic stripping voltansecry has basn introduced recendy (DHEW Publication, *3-10002, 1972), as has X-ray fluoreseanca (Knaip and Laurtr, 1972). The studies indleste that 9.1-43.52 of children surveyed have blood lead concentrations eoove 40 ug/100 ml and that up co 12.52 have concentrations above 60 ug/100 ml* The Bureau of Community Environmental Management and National Bureau of Standards (Oilsinn, 1972) report that about 232 of children et risk have high blood lead concent (above 40 ug/al) and that about 52 of theie children have clinical syspeoma. 4.1 CORRELATION OF BLOOD LEAD CONTENT WITH PATHOLOGIC EFFECTS There seems to be general agreement that blood lead content la the most informative single lade* of exposure to lead, particularly vhan eorrtlited with biochemical and clinical indices : lead intoxication. 0007--SWP--037156 0007-SWP-000112852 31ood lead concent has been uatd extensively fir '.he control zz exposure of workmen to lead, as well if the recognition of lean poisoning In young children with environmental ot accidental exposure :o lead. Nevertheless, despite ell this experience, it has been difficult to de termine a blood lead content above which a person can be regarded as having lead poisoning and a blood lead content belov which one can con fidently predict no adverse health effect. It is recognited that in creasing blood lead eoncentraciona ate associated with a continuum of probable effect], extending from the cor.centrarion at ..aich no effect is seen to chose at which manifestations of lead poisoning are highly probable. It is also recognized chat there say be an intermediate range of blood lead concencracicni at which biochemical changes of unknown pathologic or eiiniciL significance are seen. 3uch considera tions have resulted in division of tha "lead effect" into three to five categories (3r. hed. 1968; Coyer and Chisolm. 1972'. A simple scheme far correlating blood lead content with clinical manifestations of lead texicitv is pttsentso in Table i ;Cover mo Rhyne, 1971). The diagnostic criteria are divided into three phases; no effect, an adaptive or subclinical phase, and overt or clinical toxicity. Tha bounoarlcs of these categories reflect present knowledge and are subjact to modification as new information becomes available. Furthermore, the cable does not reflect individual differences in susceptibility to che effects of lead. /, compensated lead-industry worker may have a blood lead concent near 80 or even 170 cg/lQO ml without overt symptoms of lead toxicity (Amarican Academy of Pediatrics, 1961). However, children with blood lead concentrations greater than -.0 .gi.nl are usually rtrsrded as experiencing lead ir.c'.< oration because 0007--SWP-037157 of Ch* frequency of associatec ac.-erse effaces cue :o .ead (Chissln. 1971). Blood lead concentration, however, as noc In itself a neasura of pathologic effecc of lied, but reuse be correlated with ocher biochtaieal, functional, or clinical nanifestacions of lead eoxiciby for the diagnosis of lead poisoning :o be established in a particular parson. 4.2 RECOGNITION OF CLINICAL LEAD POISONING Tht Public Health Service (Steer.feid, 1571) has suggested that a child chose bleed lead content es ever SO ugrlGO oi should be considered unequivocally to ha-re lead oeisoning ind should be handled as a aadical emergency. A blood lead content over cO vj/iCC nl should be Interpreted aa evidenta of undue lead absorption. Blood lead concen tration! over 80 .g/100 si are usually associated with fivefold or greater increases in urinsry telti-aalnolevulinio acid and esprcDorphyrtn, as veil as an increase in free erythrocyte protoporphyrin {Coyer ana Chisola, 1972). each of these chiracttrtstics reflects ispaiment of heat synthesis; such changaa are usually aetcctabic at lever blood lead concentrations than those associated with ancsia. Nervous systea and renal effects of lead arc usually recognisable only during the phaaa of overt lead toxicity. In children with blood lead concentrations above 103 eg/100 nl of uhola blood, the risk of acute encephalopathy is high and the onset unpredictable. Adults with blood lead concentrations over 123 ug/100 ol are regarded as having "dangerous" exposure with possible icute syaptoaa and. long-tern sequelae. Nerve conduction, as aeasured by net"/* inpulse aaplltude, say be decreased in the adaptive phase of lead tbxieity, aa shown by Fullerton and Harrison (1989) in vorxars vicn excessive exposure to lead. 0007--SWP--037158 0007-SWP-000112854 Clinical ttul effects of lead toxicity--naneiy, rtr.al tubular dysfunction of the Fanconi syndrome type--occur only during clinics! Itad toxicity. Industrial workers with excessive laad exposure and Increased urinary excretion of laad but without sign* of clinical. Itad toxicity have only minor increases la urinary amino acid excretion (Clarkson and Kcneh, 1956; Cover _et _al., 1972). It it unlikely, there fore, chat renal tubular function la impaired to a oaaiurable dtgrtc during the adaptive phaae. Nevertheless, intranuclear inclusion bodies (lesd-procein eomplsxes) occur la renal tubular lining calls at -rata at a lower dosaje of laad than any functional signs of lead toxicity. It is suggested, therefore, that inclusion body formation Involving the binding of renal laad in a nondiffusible lead-protein complex probably occurs during chi adaptive phase of Increased exposure to lead. Overt clinical toxicity nay be subdivided into early, reversible, end Irreversible phases. "Reversibility" is more useful than "-.cure" and "chronic,'1 because the latter tarns inply tine as a factor. A child with acute lean intoxication cay have core significant irreversible central nervous syscem sequelae than one uich more prolonged but lest severe exposure to lead. And a child with neurologic stouela* cf laad toxicity may have a normal blood lead content. 4.3 RECOOUTIOH 0T S8KUXICAL LEAD POISCSIKG The closer the blood lead concent gets to 80 ug/100 ml, tha more likely are clinical manlfaeration*. The "Statement on Diagnosis and Treatnenc of Lead Poisoning in Childhood" Issued by tha American Academy of Pediatrics in 1961 recommended that "two successive determinations of 60 eg. 100 1 of whole blood or nisjher should ba obtain' . for a definite O007-SWP-Q37159 0007-SWP-000112855 -.j- diagnosis of lead poisoning," Chisolm (1565) -iter suggested that :-.e limit of "normal" blooa lead concentration should he -overec to -Z .j/iCO ml-- t reconnendttion chat his Seen endorsed by Steinfeid (1971). Although blood lead concentrations at 40-60 ug/100 ml (in the early adaptive phase) are not usually associated vlch clinical or even bio* cheaical evidence of toxicity, it is not necessarily true that there are oo harmful effects, tvo paths of investigation have been directed toward demonstrating that adverse health effects of lead may occur vlch a blood lead content as low as 40 ug/100 al; one concerns chit biochemical effects of lead on hene-synchesizm; enev--es. and the second involves detection of subclinical central nervous system effects. The most sensitive bioeneaicil indicscor of an increase in blood Iced is in vitro assay of delta-aminolevulinic acid dehydrate (ALAD) in stroma of circulating red blood cells. Hernberg and co-vorkers (1970) have recently shown chat a decrease in ALAD activity is correlated with increased blood lead concent end is a parctculariv useful indicator when the blood lead eontent is 40-10 ug/100 al (Hernberg and Hikkanen, 1972). When cr-.e blood lead concent is higher, the accivicy of the enzyme Is too lov to be useful clinically. Whether the leed-aseoelaees decrease In ALAD represents any adverse health effect is uncertain. It oust be kept in mind that this cast neasures the in vicro activity of aLaD in blood henolysace and does not necessarily reflect uny impair ment of this enzyme in the intact red blood cell in vivo. Because of the extreme sensitivity of this test, its passible clinical significance deserves full evaluation. 0007-SWP-037160 0007-SWP-000112856 Keeen: studies suggest thic tootle e;i:cts on centric nervous function, particularly intelligence and behavioral accivirv. ire present in children with blooc lead concentrations over 4; .5/ICC ai. A comprehensive study or 58 asymptomatic children with blooa lead concentrations over 53 eg/130 ai Cor over -0 ug/100 ai vich urine lead concent exceeding 5C3 vg/21 hr after chyieneeiaxineceeriacecate provocation) vat conducted by Futtcnel and eo-vorkecs in Boston (1971). A history of mild CCS syaptoas, such as cluasmesi and irritability, vas obtained in aoout cr.**third a: the 53 children. Minor r.euroiogic dysfunction iiu vantus toms 0: nocor impairment vsre detected by aore elaborate cesctr.g 1= 22-2'T or t.-.e children tasted. Chelation therapy vas adsiniscertsd, and measures vcre taken to isprove chair hose environment. eighteen nor.too later, significant increase in soiee areas c: Intellectual performance vas ooierved. Stollariv, David ana co-yorkers (19721 found higher blood and urine lead concentrations alter challenge vich a single dose at a chelating aoanc ir. rr'neractit-e cniliren cnan on ncnnvpiraotivs children, suggesting a relation ateveen increaaea lead content in theae body fluids and hyperactivity. More chan naif the hyperactive children (23 of 51) had biooa lead concentrations between 25 and 65 ug/100 ai. These workers ergue chac any blood lead .oncentrscion over 24.5 -g/100 ml is dangerous and nay product central nervous system effects. In aedilian, ca In Sure* ar.o CUoace (1972) shoved that 70 aayiaptonatic 4-yesr-old children vich increased blood lead concentrations (scan, 53 .g/100 til; range, iy-lOO -g/100 ai) or a lead content of at least 35 -g/100 ai with positive radiographic findings 0: leaa lines in long bones or metallic densities in the Intestine* had deficits in fine motor function and behavior 0007-SWF-037161 0007-SWP-000112857 ;<i contrast with previous understancir.*, a recent Ir.gi;s-. si'jsy suggescs chat anesaa it eaeson in children with bioou lead concentrations betveen 37 and 60 ig/100 *1 t3e:ts e_c i., 1973). The coma conclusion of each sc chest studies is chat blood lead csntent over 40 ug/100 ai rase be regarded as potentially haxardaus to health. 4.4 ESTL'iATE OF THE BOMBER OF U. S. CHILDREN WITH INCREASED 3LCOD LEAD . the National Sureau of Stiticaros has recently ccbiisbeo the results of ratheaacical aodel: vich tne assuaocions and data used to foraulate than fOilsitm, 1972). Estimates are given of the nuaber of children who have increased blocd lead concentrations (> 40 .g/100 ni) in 241 Standard Metropolitan Statistical Areas in the United States. Present esclaates based on chela r.odels suggest that approximately 600,000 children would show increased cloud lead ccntcnc if tested. The oodels and sssuaptions have been only partially validated. Sy using the National Eureau ef Stanccris aodel in conjunction with data froo tha oajor screening programs, it is possible to con struct Tabla 3, which gives tht estirates of the nuabers of cases cf childhood lead poisoning of various decrees chat cay occur annually in the United 5:stes (Anderson, D., J. Reed, and V. Header.. personal comunicacion 1. These estimates sr.ould be regarded as first approximations that can serve only to suggest the general magnitude of the proolea. better data susc await the results o; wall-designed epidemiologic studies conducted on a national stale. 0007-SWP-037162 0007-SWP-000112858 5. >27ac;s v? z? is a s lead poisoning is a preventable disease that ;cn be controlled lr. three way*; by eliminating the source* of lead; bv controlling che Beam by which lead enters che body; or by finding and creating cate* early, inclination of the sources of lead Is certainly c.-.e nose Important approach over the long Cera and conforms with cine- honored public-health practices directed at control of the vectors of disease. The xost significant identifiable source of lead poisoning today is leiri-containtng paint in houses to vmch young children have access. However, there are other sources of lead exposure whose epidemiologic significance is not known--for example, surface dirt and the lead chat cones from che us* of leac-contalning gasoline. A host of other lead-containing substances around households have been Identified as potential sources of lead exposure, such as the peine on pencils, avaporaced-milk cans, toothpaste tubes, porcelain,and earthenware. Their contribution to :.-.e ieed-ocisonm; problem is considered to se substantially less chan chat of lead paint on veils end woodwork of old houses, old toys, end beds, it Is unlikely that sources other chan lead paints can ba responsibla theaaelvee for che cates of Increased blood lead concern under discussion, but it is of course possible chat they could make a difference in borderline cases. Thus, control can be achieved by removing children from delapidared housing in which peeling coats of lesded paint are available to rhea or by removing ieaatd paints frea the interiors of suen buildings. It may also be possible to reduce the tendency toward pica by dealing with the underlying social and environmental factors cha- have been 0007-SWP-037163 0007-SWP-000112859 -19- jhovn to have a role in this benaviorai ar.omaiv. However, this l;=ittee has been appointed to assist in developing federal policies rha: -til prevent future lead poisoning associated with paints yet to be applied to surfacee accessible CO children with pica; hence, the Committee -.us: focus on future sources of exposure, not present or past. Recently, the Coroiceee on Environmental Hazards of the American Academy of Pediatrics (1972) recommended that the lead content of paints be reduced to less than 0.06Z. This recommendation vet based on the assumption that the risk, of lead intoxication in cnildrer. is Increased when the dally incase, from sources ocher than food, exceeds ISO _g/day. Estimates of daily Incakc from food, water, and air have also been mice by Barlcrop, who gives a total of 136 .g of lead per day. Earltrop goes on to reduce the daily permissible intake of 6C0 .g/day for an adult to 180 eg/day for a J-year-old, and further correcta this number for calorie requirements of a child, thereby ending up uich a final value o: 113 .g/day, which he suggests at a maximal permissible safe intake (3arltrop, 1971). A maximal permissible lend concent of paint t'C.CSZ of dried film) was then derived from a number of assumptions, including: (a) that gastro intestinal absorption of lead is the same from paint as from food; <b) chat a child eats 1 la.2 of paint per day; and (c) that six layers of paint have accumulated, the validity of the recommended maximal lead content is sensitive to these and ocher assumptions in the calculation. 5.1 LIMITATIONS TS THE AVAILABLE KNOWLEDGE OS WHICH A STANDARD COULD EE BASED If a limit is to be established on a rational basis, the following questions should be answerable, particularly for children in the susccptiolc age group. 0007-SVJP-037164 0007-SWP-000112860 fa) may t-arcer. ci lead ts ajacrmted wish v.--.ptccs of lead toxicity? (b) How is blood leia reiiced to bocy barren of lead and signs or symptoms of lead intoxication? (c) '-`bit daily incite of lead in paint will result in me oaxiaal permissible body burden oi lead or the maximal permissible blood lead content.' (d) How ouch surface area ii nibbled by er.iidrcn? <e) '.liat limit cn tr.e percentage of lead in pain: curd keep the blood lead content or the body burden or leae within acceptable Units? The following brie: summaries of me state of our knowledge with respect to each of these guescior.s mould serve to illustrate the serious limitations in the present state of cur knowledge. o.i a s s o c iat :::: o f b o d y a'jRor: o f u a d *:t h s y .'3To :o o f l e a d t o x ic t t y It mould be enanasicta tear leoc ceoasrtec m the skeisten is only potentially toxic, as opposed to lead in soft tissues, such as kidney, brain, and liver. Thus, the significance of a given bodv burden of lead will dtpend not only on the total amount of lead present in ch body, but on its distribution between the skeleton and the soft tissues. Barry and Mossman (1970) measured the lead concentrations in the tissues of 10 English children and 19 adults described as having bean exposed co a normal urban environment. Table 1 summarises their data. The total lead body burden of the children ranged from 6.5 Co 3.1 eg, vcm c scan of 1.: rtg. .'.ppresmctecy b-C of me Lead m the skeletons 0007--SWP-037165 0007-SWP-000112861 of the children, casoarea v;:h 951 ir. ".e adults. The scan :;:ai bcev burden of che 29 adult sales was aoouc 150 r.g, cospared with about 113 sg for che 20 adult resales. An interesting cozaenc made by che authors Is that "the relatively high proportion of lead in soft cissue, coopered to the lead levels in bone of young children, may be accounted for by che lack, of hard, dense bone at this stage of life which, when developed in lacer life, appears Co cake up and retain leed. It is suggested that this cay account, in s o bs censure, for the adverse response ir. young children to severe lead exposure." The relation o: either clinical signs of lead toxicity or changes in che early indicators of abnormal lead exposures, such as blood lead concentration, erythreeyce AiAD, and free erythrocyct protoporphyrin, to either che soft-tissue or the skeletal lead burden is poorly deflr.aa. Inasouch as lead concentrations in tissues are not usually neasurad before autopsy, chere is no basis for a correlation between signs and synpeoas snd the boiy burden, other than fer ratal eacephalocac.-.y. Chls'oin and Harrison (1956) and Eehoe e_r al. (1333) have measures the body burdens of lead in children who died o: lead intoxication. Their results indicate that tne asaociated soft-tisaue bedy burdens ringed fron 20 to 100 ag, or from about 35 eo about 200 tinea che "normal" soft-tissue burden. The skelecsl burden, as escicaced iron rib analysis, varied froa 100 to 400 zg, or 100-400 tiaas the "normal" skeletal burden. The "normal" values were deterziaed In Englano and zay not be applicable to a U. S. population. In sunnary, only a few data are available to describe e.-.e normal lead content in children's tissues, and no data are available for cases of 11--! intoxication other than fatal encepnalopathv. 0007-SWP-037166 0007-SWP-000112862 5.3 j iu t t o n o f si:oo :i.o t o b o o t 3-j z o f x c f h a d a i;d t o s y x p t o x s o f b ia s ::;t o x :c a t ic :; The blood lead concentration car. reflect either recent exposure or an equilibrium relationship to lead In the skeleton and soft tissues. To evaluate the terser, it is necessary to understand the clearance rates of lead fros blood. Using lead-110 as a tracer, it has oeen determined in the baboon chat lead clears in three exponential com ponents: approximately 735 of the blood lead 1 day after injection is resovad with a biologic half-clae of 1.1 days, HI with a biologic halftise of 10 days, and 35 with a biologic r.aif-tine cf - r.oncns lichen et_ el., 1970). So infonsacion is available frcn which estinace the reservoir of lead in the tissues of a person vno has a blood laad concentration higher than normal, but who is reaovsd froo exposure. The relation of blood lead concentration to symptoas of intoxication is not adequately definaa. If the blood lead concentration coes not exceed 40 vg/100 al of whole blood, there are ao clinically coservable effects in adults or children, although erythrocyte aLAD activiev aay be less at these concentrations than sc blood lead concentrations oelov 40 ug/100 al (Hemberg it ii., 1970). The ten "asympeonaeit increased lead absorption'1 has teen coined to designate the gray ares of blood lead concentrations chac are signifi cantly higher than the normal range, or froa 40 to 60 ug/100 ai of blood (NAS, 1972). The available information concerning blood lead.concentrations la relation co signs and syaptoos, as sumxarlzed by the NAS Connietee on Biologic affects of Ataospheric Pollutants in 1972, is given in 0007-SWP-037167 0007-SWP-000112863 Tail* i' It should he noted, however, that these data have cesr. scratr.ec, for the host part, from studies on acults. 5.4 DAILY ::~AK C? LEAS 1" PACT THAI RISVLTD I!i MAXIMAL PES.1ISSI5LE BLOOD LEAD COSIEST Concentrations of lead in the blood of unexposed children <11-36 aonchs old) have been reported to range from 15 co 40 ug/100 ml of whole blood, with a aedian of II cg/lOO al (Robinson et el., 1958). On the basis of Tapper's observations on adult intake <1971), the total intake of lead for a child would be 116-006 .c/day. The contribution of inspired air to the estimated totals for average lead intake is approxi mately 3-61. On the basis of a gastrointestinal-absorption factor of 101, approximately 95-135 -g/day should be excreted in feces. In fact, Chisolm and Harrison (1956) and Barltrop and Killala (1967) observed a daily excretion of 110-175 eg in feces, with a mean of 13d .g/aay. The percentage ct ingested lead absorbed from the gastrointestinal tract of children is one of the major uncertainties, Alexander et al. (1973) have recently reported, based en metabolic raiante studies, in S children over l 3-day period, that absorption in children aey be as 'nigh as 50T with an avarage retention value of 18Z, Lead concentrations in the blood of children of 40 wg/100 ml or higher ere considered evidence of undue absorption of lead. On cht basis of data on excretion of lead in feces Immediately after the cessation of pica and of the results of balance studies (Kehoe, 1961) Involving the experimental intake of soluble forms of lead. King (1971a) has esti mated that a daily intake of 300 ug of lead would not result in a signifi cant increase in the blood lead concentration. Doubling of this intake over u period o: 1-6 months would result in a bieod le* . etneenerntion that could exceed the defined toxicity value of 60 ug/100 0007-SWP-037168 0007-SWP-000112864 3.5 nr eac e aeea i;:33iED 5: :;-::i:~.z:; The quantity of lead ingested wits paint is related to paint-enip size, percentage af lead in the paint, and the number si layers pair.: on a particularchip. On the tana of 6.5 mg of paint par square centi meter per layer of interiorpaint and 15.0 ag of paint per square tentiaacer per layer of exteriorpalr.t, Tadic 6 lists the amounts of paint naeessary to obtain ICO ug of lead, or cvo-cnirds the dally calculated permissible intake tot different oercenteges of lead in paint and differtne numbers of layers (King, l?71b). "or 0.06,7 and six layers of interior paint, iris -ouii correspond to a chip of about 3.5 on tr 1.1 in." It should be noted that the rite of absorption of lead from paint chips is hot known and nay in fact be highly variable. The American Aoadaay of Pediatrics report assumes a chip intake o: 1 ir.r/day. This would be equivalent to about 1.5 ftv year. There ic no basis for stating whether this is a reaeonaole assumption, -no it may in practice be impossible to obtain realistic data. 5.6 LIMIT C.\' 7ICCI'.T.i51. 1 ~ LEAD "AI7T THAT A'EL'LD KEEP LEAD I'.TTAXE EEL3V DAILY PERMISSIBLE INTAKE Assuming e uaily mcake of 1 in.- of six layers of paint per cav, and 5-10Z absorption of lead, 0.06' laad in paint would keep tr.e dally lead intake below the recommended 300 eg. This was the line ot reasoning adopted by the American Academy of Pediatrics. However, -.his conclusion could be grbisly modified by varying the assumptions noted above. 6. DISCUSSION It is apparent that there is not sufficient information'on which to srcnulgate a st3hdarc baaed .;n knowledge of the essential quantitative relations that link the leas content of paint to aympcj.,.j of intoxication. 0007-SWP-037169 0007-SWP-000112865 standards have been established by ir.it-- id people vno cake judgments based on whatever fact* are available. An alternative to a Unit based cn firs scientific evidence mljht be one founded on a oere pragmatic approach. Jne night establish a liaic on the basis of the louesc lead content of painta found in dwellings in which lead poisoning has been reported, the only statement in the Literature that deals with tail question coses froa Chisels and Harrison (1956), who scaced, in relation to their own experience: ":;o case of lead intoxication has beer, found wnere the only source of lead contained less chan it of leaa ir. the creed cm: surface." .Uthougn this conclusion was published 17 years ago, it has not been refuted by any subsequent publications. The paints used before about i>10 con tained about 50S lead on the average, end it is not surprising that a fiftyfold reduction in the lead content would reduce the attack rate to tht point where cases of lead intoxication would not be observed. This sight serve ss e basis for setting a liaic. However, cne cannoc be assured chac effects or lead intcxicaticn so subtle as to escape atten tion do not occur at lead concentrations lower than it. A third approecn, and one that has been used in public-health practice, would be to require chac tht lead in interior peincs be reduced to the lowest practicable concentration. By "lowest practicable4' 1 meant Che loweat concentration chat can be achieved by existing tech nology. It it lsplied that the lowest practicable concentration will be interpreted wich restraint ond with cue recognition given to the available scientific and sealcal ir.ioraation, as well as the administrative and economic factors. A decision could be made to prohibit completely the :,sd ir. paints, but lend cun hu expected to occur in trace quantities 0007-SWP-037170 0007-SWP-000112866 -re al an industrial impurity ir. the mgrecieacs that are used to :r~uiate paint*. This require* that the pnraae "r.p iaad" he defined. 1: lead is net used in paint manufacture, some other materials mist tilt* irs place. A judgment must be made a* to whother the substitute material* involve less risk to the public health. "Inally, ic Is possible that eacn progressive reduction in the lead content of paint will involve greater cost, and commensurate benefit to the public health should be ensured. Thus, reducing ltad to the lowest praeticabla content suet inevitably involve a value judgmenc in which one belances the likelihood of health damage at a given lead concentration against the Likelihood of health daaagt fraa substitutt materials, the effect of the chang* on tha per formance of the paint, and the cost of making the cnange. The various approaches ace fundamentally different. Tha first two involve incerprecaclon cf scientific data and a decision as to the ltad conttnc of paint that will keep lead poisoning from developing in che future. The "lowest practicable" approach requires value judgments in vnieh semisuantiticivt, aiaost intuitive reasoning is used to arrive at a conclusion. A standard baaed on che first evo approaches is clearly one that can bast ba dtvalopad by scientists. However, scientists are net uniquely qualified to recommend a standard based on che "lowest practicable" concept. As has been noted, in insufficient body of Information exists to permit establishment of a standard for lead ir. paint based on scientific facts. Although lead has bean known co ba a toxic material for centuries and is a major industrial chemical, chert has baen inadequate research. Although lead in paint hat bean identified as an acialogic factor in 1-ad j.'isoning irong children v.tn pica, rhurc is a pa- .icy of epidemiologic 0007-SWP-037171 0007-SWP-000112867 with adequate case histones ay =*ar.s or vr.ich one ccuic describe the association of a given child's blood lead cancer.cration to tie condition of the painted auriace* to vnieh the child had Seen exoosed. Ihcre should he core information about ehc clinical significance of blood lead short of full-blown lead poisoning. Such information cannot be expected to cone Into being in less than a few years. Any proposal to reduce the lead content of paints, in addition to being concerned with the health aspects, should also consider the effect of such a change on manufacturing practices and on the quality and safety of the codified products. The course of action ultimately selected should protect the public with a minimum ot dele terious effects, either on the economics of the industry or an the quality of the products. Lead eeepounds ere used in paints principally far three reasons: as pigoencs, as driers, and as agents :o prevent so-called loss of drying in storage. The use of lead ir. pigaencs requires such high coneentracians in the painc formulation tear current regulations setting a maximua of C.5X lead have for all practical purposes already eliminated lead pigments in household paints. Driers (cecal salts or factv acids) help to speed the oxidative hardening of the paint film when the vehicle concains unsacuratea components, such as vegetable oils or aikyd resins (Stewart, 1969; Bikales, 1964, 1956, 1970). Lead driers (typically lead 2-echylhexoece, lead naphehenate, or lead callate used in lead concentrations of 0.2-0.4* based on weitht of dried paint film) ate particularly-valued, because they effect relatively rapid drying throughout the mass of the film. Other triers--such as various fatty acid salts of calcium, cobalt. 0007--SWP-037172 0007-SWP-000112868 manganese, tine, sad tircor.ri3--re sssscniy i3S3 in. with lead driers in empirical formulations designed :c give the cesired race and thoroughness of drying at widely varying temperature and tumidity (Stewart, 1969). A further use oi lead compounds is as additives to retard so-called loss of drying, i.e., the deterioration in drying properties of paints that can occur in storage. For this use, proprietary lead complexes are apparently preferred and are added in concentrations about equal to or somewhat lower than those of the lead driers (based on lead content). Selaciveiy little indorsation is available on the types of compounds used or or. the mechanisa of their action (Stewart, 1969). A reduction in the permissible concentration of lead in paints to 0.061 would in effect prohibit any intentional addition of lead compounds to pigments, driers, or ocher paint additives. Faints based on oleoresinous substances would require reformulation to eliminate lead driers and all otner lead compounds. Analytic procedures would be necessary to ensure that no accidental oar.pasinacion py lead cospounds had taken place during manufacture, .iconic-absorption spectrophocomecry is particularly suitable for tnis purpose, end e simple colorimetric method has been devised to indicate whether the proposed maximal concentration of 0.061 has been exceeded (ASTM, 1971). It can be expected that reforaulacion to the 0.061 lead content and the associ ated testing would require at least a year. The burden would be heaviest on the many stall paint manufacturers chat lack the necessary technical scaff and resources. 0007-SWP-037173 household paints are generally classified as intended for interior or exterior use. Interior paints are likely co represent the greacer potential harard because of their greater accessibility and because children, at their cost susceptible age, are note often left unattended uhen indoors. Ac present, most interior paint is based on aqueous emulsions; this type of paint dots not usually depend on auto-oxidation of uneaturated conpounds to harden and therefore does not require any netai salts as driers. Although emulsion-based paints noraally produce surfaces vich little gloss, new types that can give a stmiglossy finish are now on the carkte. These are expecced to make inroads into the last major use of oltoresinous paints in the interior of households -- surfaces vith glossy finishes, decause interior paints usually dry under more controlled conditions inti are noc subjected to as severe weathering conditions as exterior paincs, adequate paints of both the eoulsion and tha oleoreslnoua types can be formulated for interior use without any intentional addition of lead compounds. Paints designed for application co exterior surfaces require a useful race of drying and adequate durability under wide veriacions of clisatie conditions. The combination of low caaperacure and high humidity (e.g., 50Fand 7OX RH) is particularly stringent. The use of eaulsion-besed exterior psincs, which require little or no drier, is increasing rapidly, but oltoresinous paincs still account for a large part of tha market. Lead driers play an important pare in the formulation of Che latter type. Lead-containing primers are also useful on heavily chalked surfaces and to prevent staining by the water-soluble extractives present in tome types of wood. 0007-SWP-037.174 -jo in the formulation of paint*, tit* lead, after* cannot usually oe eliainated by mere substitution or an equal mount of another metal *alt of a tatty acid. A combination of ocher metal drier* must be fitted to each particular recipe, and there is *oae question es to whether paints so reformulated are equivalent in quality to chose containing lead driers. The substitution of other driers for the lead salts also raises the important question of the safety of the substitute materials. Under current regulations, the food and Drug Administration permits the use of some driers for costings that come into contact with food-- neatly, sons fatty add salts of clusir.ua, calcium, cerium, cobalt. Iron, lichlua, magnesian, manganese, zinc, and circonlum (Code of Federal Regulations, Federal Food, Drug, and Cosmetic Act). As already pointed out, several of these aettl stirs are normally added to paint in con junction vith the lead coapounds. It is likely that paint manufacturers vill use combination* of chest same driers if the lead content must be reduced to a maximum of 0.Q6Z. Zirconium-cased driers appear to be the most useful single substitute. The cost of the substitute driers, being higher than that of the lead salts, would raise the raw-material cost of the reformulated paint by several ctncs a gallon. The Committee has been apprised of che fact that Chicago, Illinois, a.ready has a local ordinance calling for a maximal lead concent in painc of 0.06Z of dry-weight solids. This regulation was effective on the l*t of July, 1972, and is applicable only to interior surface* of dwellings 0r dwelling units (domiciles). It specifically exempts varnishes, oil stsins, floor punts, and coatings in aerosol cans. Convcr-ation; utth Chiecgo city officials have indicac* '.hat comoliance 0007-SWP-037175 0007-SWP-000112871 -31vieti the ordinance has been successt.il perr.aos 50 . c: the crt-f.eshelf" paints tested, Furthermore, the test of paint ptsdueed is the Chicago area was reported to be no higher than the national average. In terms of paint already existing on wall surfaces, the Chicago ordinance calls for a liait of no sore than 1 ag of lead per square centiaeter of surface. Ac the present ciae, there have not been enough epidemiological data collected to determine whether the 0.0621 regulation has resulted in a change in the number of cases of increased blood lead in children screened within the City of Chicsgo. 1: is hoped thee, in tine, the experience of the City of Chicago in adsiniscerlng this ordinance will provide Che C?SC with additional useful information relative to many of cha points raised in this report. 7. CONCLUSION'S AND RECOSMEJDAIIOSS (a) Although it would be desirable to establish a limit on the lead concent of paints sold to consumers by a quantitative raclonale chac cakes into consideration cha quantity ot paint apt to ba ingested by children with pica, the rat* ci absorption of lead from the gastrointescinal trace, and the amount of absorbed lead that will produce intoxication, the Committee concludes chac there is at present insufficient information to permit arriving at a recommendation on that bails. A broad program of research is required to understand better the mechanisms involvad in lead intoxication and nechods by which the disease can be controlled. National and local health education programs to alert parents to the health harard to children era recommended. (b) A more pragmatic approach would ba to ascertain, through epidemiologic methods, the lowest concentration of lead in paint chat -is nc-t-n associated with lead intoxication oncr.g childr', with pica. The only statement in the literature chat deals with this --- 0007--SWP--03717 6 0007-SWP-000112872 -12- vas published II years ago and static that r.u cast a: lead ;r.:s*ie*t;cn had bean found -here the oniy source ci lead contained lees than 11 of lead in the dried paint surface. Alchougn thi* coneiusion has r.ot since been refuted, the Comictee is unable to conclude that subtle but nevertheless significant forms of lead mtoxicatiou that nay have escaped clinical detection have not occurred from exposure to paint films with lead con* cencrations lover than If. (c) The Coenittee has iearnad free reprasentacivas of the paint manufacturing industry that the present requirement that the lead con tent of paints be limited to 0.51 alreaay precludes tr.a use of lead compounds as pigments. Kovever. lead driers are widely used at con centrations of 0.2-0.11 (based on lead ccntant of the dried paint film), to help speed the oxidative hardening o: the paint film when the vehicle contains unsscuratcd components, such as vegetable oils or alkyd resins. In particular, lead driers (typically lead 2-echylhexoace. lead naphthertate, or lead callute) used in lead concentrations e: 0.2-0.11 are especially valued because they effete relatively rapid drying throughout the mass of the fiir.. Other lead conpounds retard che so-called loss of drying on storage. A reduction in the permissiele concentration of lead in paints to 0.061 would prohibit the intentional us* of lead compounds as driers or as additives to retard tht so-called loss of drying. (d) If the leed concent of paints is limited to C.062, it would be necesaary to reformulate lead driers fer paints based on oieoresinous substances. This would probably require substitution of metals other than lead. Althougn the Committee has no reason to believe that the :tc metals veuid introduce new coxicolo.'.ic problr should he considered before any steps are taken chat will this possiuilitv 0007-SWP--037177 0007-SWP-000112873 -33- (e) A program o: reformulation of criers to ceer a 0.36* lead requirement would take ac leeat a ytar co implement. (f) Evidence made available co the Commtree sakas it dear that the intentional incorporation of lead into pigments and drier* can be eliminated for conjumer paints applied co interior*, toy*, and furniture and that It may be po**ible to eliminate the deliberate u*e of lead in paint* for outdoor use. However, some lead nay nevertheless be present in these products, owing to its adventitious presence in process material*. <g) Vncil more scientific information can be accumulated from t.-.e research programs recommended in this report, the Committee suggest* that it might be wise for the Consumer Product Safety Commission to institute an interim program o: controls based on the concept that the lead in paint sold Co consumers be reduced to the lowest practicable concentration. Che administration of this concept should be Implemented with due recognition of the need tor balancing cost* against benefits. It should also be recognized that the weighing of societal costs against societal benefits may not always involve easily quantifiable considerations; it may be necessary to define the lowest practicable lead content on the basis of the judgments of informed people rscher than scientific *n*ly*i*. Tests recently undertaken by Che American Society for Testing ^**t*ials have shown chat "lead-free" paints contained a* much as 0.03T lead. This may be due to impurities in the materials used for paint manufacture and to the occasional carryover of lead from one industrial proc**s to the other or co uncertainties in the analytic procedures. There is no assurance at present that the lead content of lead-free painc* could not exceed Q.06X owing co these factors. Thus, any regulation t*!t - 'ern' tec -snximal lead content of paint product- -.use ho based on O007-SWP-O37178 0007-SWP-000112874 -34- considcracion or the practtcaot-ity or ccncrolli..? -me lead ---at er..ers -he process adventitiously and of the availability of reliable analytic procedures (h) The Consumer Produce Safety Commission Jhoultl develop a national paint surveillance system to ensure that established standard* are being met. As part of the development of chip surveillance network. It will be aeeessary to sponsor the development of better analytic aetheds for measurement of trace quantities of lead in off-the-shelf painc samples. (i) Any standard issued to limit Che lead ddnter.c of paint should be reviewed biannually in the ii;hc of whatever additional information becomes available, the limits nsy be raised or lowered, depending on circumstances. However, ample time must be permitted for orderly reformulation of paints and driers, and no changes should be made without adequate consideration of the effects on the public health, of the cost, and of the effects on paint quality, the overriding considerations muse of course be related to protection of the public health. Cl) the Consumer Product Safety Commission should sponsor research to identify the sources of adventitious lead in paints and driers, the unusual opportunities for absorption of lead by children with pics has caused the Committee to recoeesend chat use of lead in paints be reduced to the greatest practicable extent. However, the Committee emphasises that there may be other usea of lead, now and in the future, that could bring significant benefits to the consumer. In accordance with good public-health practice, more oust be learned about the mecha nisms of lead intoxication, so that, as future applications for lead ate cuvfeJcsed, they may be incorporated into consumer products without unaue 0007--SWP-037179 0007-SWP-000112875 -55- rik. The Cosaittee has identified several research objectives as having particular importance. 3. RESEARCH REQUXREhEHXS (a) Ihe "normal" body burden of lead in people of various ages should be better established for a variety of aodts of habitation and socioeconomic classes. (b) The absorption of lead froa the gastrointestinal tract should be aeasured in experimental anneals and children having a normal dietary intake of lead. The studies of children can be sccboplished using ent lsad content of che norsal diet. (c) Comparative studies of the absorption of lead froa the gastro intestinal tract of suitable experiaencal animals should be undertaken with regard to lead in the noraal diet and various paints and driers. (d) The clinical significance of increased blood lead content should be studied in children, with particular emphasis on the adaptive or subclinical phases. (e) Epidemiologic studies snsuid be extended to include che sequelae of overt lead intoxication in children who survive acute toxic manifestations. (f) Better analytic methods should be developed to aessure lead la off-the-shelf pelnt samples and body tissues, especially blood. (g) Htalth departments snd hospitals of major urban centers should be encouraged to adopt mutually compatible protocols for mass screening of children snd for identification o: the sign* and symptoms of lead poisoning. Standard procedure* should also be adopted'for documenting che lead content of paint to which Che chiidrtn were exposed. 0007-SWP-037180 0007-SWP-000112876 (h) The Consunet Prroucc 5a:e:v Cccmc.sscon J.nouid serve as a national registry fcr data accumulated ir. the screening program and should issue consolidated annual reports of the findings cf such studies and the incidence of community lead poisoning in the United States. 0007--SWP--037181 0007-SWP-000112877 TABLE rmf ro l uV c <i V ( O8 w* n mS c -- t6-9 99 ttet*. s *2 --cVc *nuuo# oe i? -i .2 3 0007-SWP-037182 0007-SWP-000112878 -38TkZLZ 2 Relations of Various Measurements of Lead Toxicity to Category of lead Efface (Modified from Coyer and Rhyne, 1973) 1 Blood Lead cp/100 ml FEP I Ho effect a <40 -g/100 ml Ha Adaptive, 40-60 pg/100 ad **b Subclinlcsl, 60-60 jg/100 nl nocrzil slight increase Ill Clinical Toxicity, '80 ug/100 ml large increase Urinary ALA . Urinary C? Anemia Nervous systeio effects Renal effects normal none none none clight increase retieulecytosis decreased nerve conduction? none (inclusion bodies?) > J fold usunlly ataxia, coca convulsions Fanconi syndroeie chronic nephropathy A1A * Oelca-Ajnlnolevuiinic Acid. CP * roproporphyr in PEP * free erythrocyte protoporphyrin 0007-SWP-037183 0007-SWP-000112879 -39- IA2LE 3 National Data on Incidence and Medical Significance OF COMMUNITY CHILDHOOD LEAD POISONING Children in Susceptible AgeCroup................................................................. 20,000,000 (under 5 year* old) Children at Risk.................................................................................................... 2,500,000 (under 5 yeera'sld, live in aeccopolitan areas, {sallies in poverty classification) Children vlth Increased Blood Lead Content............................................. (blood lead content above 10 ug/100 ml) 00,000 Children vith Symptomatic Lead Poisoning per Year............................. 30,000 Children vith Asymptomatic Lead Poisoning per Year........................... (all should be treated) 30,000 Children vith Neurologic Handicaps, Including Mental Retardation.................................... ...................................................................... 6,000 Children Requiring LifetimeInstitutional Cere...................................... 150 Deaths per Year........................................................................................................ (Includes acute and long-carm consequences of lead poisoning) 200 The children in susceptible age group and children at risk are based on Bureau of Cantus data which have bean rounded off. Children at risk are under 6 years old living in dilapidated housing containing hazardous concentrations of lead. Of those at risk, 24Z are estimated to have blood lead concentrations of at least 40 ug/100 el of vhole blood. The percentage is the median values of surveys in Illinois and Nev York City. If other cities ere used, the percentage is higher. There is, hovever, little information from chewett and from small cities. 0007-SWP-037184 0007-SWP-000112880 Z.'S.t 3 - continued -io- From current screening programs--sucn as tr.rse m Saw :cra . Philadelphia. and Chicago--it appears that about 31 or the children vlth blood lead concentrations over 40 .g/100 nl have clinical signs or symptoms---convulsions, anemia, cramps, etc. The estimate of asymptomatic children with blood leed concen trations about 60 ug/100 ml of whole blood Is 3.2! of the population at risk. This estimate is based on the results of Illinois and Hew York City screening projects. Children with neurologic hendlcaps, including mental retardation, are estimated at 2C! of the cases of symptomatic lead poisoning, on the basis of follow-up studies in Chicago, 1 0007-SWP--037185 0007-SWP-000112881  o ? 22-e5 JwS A t S i&i01 6 e w* i w3 wuH 2 e* < 0007-SWP-037186 0007-SWP- 000112882 -42- TABLE 5 LVI and Typri of Effoeu of Inarpmc U:d idi r.ri-Hid is Eilimno ef Varioua Until of Abjorplion-Ricrrl an*i Rf-nntt Type of Cffeet* Lrmllt So Otmoxw^ m nrO fclfttt Uni It; Minimal Subeumeit Metahohr Ufcrt t.svotlll: Comren-ouif* Uieioftc Vsviannrm Invoked LmtIV: Acute Lead Foilsnut; MM Seme Mtiibei.c (4:cw:n Chjn-in; UiiiiK ii# \eir ALAIF* tfjft ef h:me Slight otin uimiry ALA OUT N preaent ALA. VL*r. a l a ucr. rrp Otngf*m*etr iftetcwed tnertaud J to )00fe4d rores>n;i ilerutopuK-u* None Widow oeM iu Ov Ij i funcuu*) Nirne Son# known None known $hwrie*ed rwd iilt lifepn. fvKoiinvy* li*VN <1 I (revmiHw) ' Shortened rcd<etf hfe-apin 4i># Kticaloeytetit %\tn ef niigvi antma (revetitWe) Amino* ) artconi aciduria. irKtyeetuno d*om* lUte- tirrtto *emUl itto) Lent V: Latelffecta ef Chrome et Reeve* tent Acute Ltid foitonmf Ineteawd vf eiem't raooiuro rrrent. but may not t* : eimed if itmim Upeaute rtmott Anemia U) (rsurwbk) Chrome nepAtepatny* tpetnuAcnti Cestui f.e*oui i*i:c3i njr< . So-ic SOM Ckiwsl e'l-cu N*0 !nCr\ of :\;t ef tewflt Of cm tent iW *:0'.ien: SJoadMoU. nttonjor klivli N--a UifX . -J irMi'cr <*o - Vono known Nuno know* None known % Non.fs'nfic r-t.d ymj* h.vMtf.tar H tu? :rt part in c-tmmlily ti^aMl) Mild injury (?? re*efMbiei Aare Colic. im> lability. omttmi Sewremjory StT injury* tpeimo* (permanent) ntiu) Aire Impaired eonduetten Knit. foot drop tvjHy imps'* iJuuty. Put mr be permanent) A-.3M1. HU* Mental Psficirfity pet. coma. (may be profound). cojtrvmon* ieuu:e eneidet. renal jnui:'f*cie0` ({out) (oerma- nent) 40-40 <10 SM30* <1 JO >to ><0 With enema. mtcrcvocM dimatf: 5C-IOO* >U0 >oo l.'Uy be hat in tcvete illnets) May Pc normal Sponuneoot eterciioft mop *e normal Sc p HOC <.- h'-CUi'-e.i>m*if siia*-n* U*fli of ALSIV c .i unluoiiv ftvpArup.ifiiv i\ prtmvc; miv or n iy nut be iiu;i>* in permanent ecnlut Mnont lyutm injury. .Vatier.il cadcny of Sciences (1972) . 0007-SWP-037187 0007-SWP-000112883 l.caJ Content o f P o in t* c4 w cc C JC u 9 w a. w wu UV J1 . -* y t: o* * 3 ./} i- -1 C -*> <** n^ SM m UQ *w C3 * 0 3 900 2 w. t> n w to s~s o c -- c*> i's-~ U N *: *4 V PI -- 0 , * fc. V5 H 9 i 0 -- M Pe-- u o s ^ u </) <o ue o er Vi v. V "! w ve C* v; i3 n /i T! ^ <e ? P-4 ** * -J n *m- fmf> rr** < > o o o o < * c* /i O / O iA n o -- (N rtOiAO--- O u-v o N c w* f^. r* *3 '<G C W VV\ 4 v p*y ir**n * 1 r ioo o o o o o ** O * ** *i ** ** C*n mO rC> 'rpi v? n c> ^ O - n n 'j Nmn^eo^ (S \5 -NNON/>C" 9 n&c. e a9 e ** cou C9* -u3 0 o V w n y u VJ -- -- 0 --* uw 9 9 w2 -4 /. <t * rp s-- H U c o 0 3 *5 0 " oM- o\ O*/% C' *<""* *C >n onN*-m* n n u& r *rv o 0O 6w* 0 0- 'o^ ^O QC -- o o o --w. 3*. > * o * e* 3 N O S C ej o# cs r-\ -- o< 6 ** f O c fi. oCl o >or\ oa o voS Ifton -4000000 h* u * 007-SWp_037l8s 0007-SWP-000112884 4*6" Alexander, F. W., H. P. Selvaa, and a. . Clayton. 7tit uptake and eiatretlon by children of lead end ocher contaminants, pp. 319-331. In Proceeding* of International Sysposium on Eavironaantal Health Aspect* o Lead. EUR 300* d-e-C, Luxembour g: Coseaisaion of Che European Communities, 1970. AsMrican Academy of Pediatric*, Subcommittee on Accidental Poisoning. Statement on diagnosis and treatccnc of lead poisoning in childhood. Pediatrics 27:676-680, 1961. American Academy of Pediatrics, Csmictee on Environmental Hatards. Lead content of paint applied to surfaces accessible to young children. Pediatrics 49:918-921, 1972. Amarlean Society for Testing and Materials, Report of Cosnlttee D01, 2103. Philadelphia, 1973. (Unpublished notarial) Barltrop, D., and S. J. P. Killala. Fecal excretion of lead by children. Lancet 2:1017-1019, 1967. Barltrop, D. Sources and significance of environmental lead for children, pp. 675-681. In Proceedings of International Syoposiun on Environmental Health Aspects of Lead. EUR 5004 d-e-f. Luxembourg: Concussion of the Europten Coaminitlea, 1973. *rTT P* S. I., and D. B. Mossman. Lead concentration* in human tissue*. Brit. J. Induat. Med. 27:339-351, 1970. Beet*, p. R,, R, Aatlay, and D. N. Rain*. Lead intoxication in children in Birmingham. Brit. Med. J. 1:402-406, 1973. ** *"* H., Ed. Encyclopedia of Polymer Science end Technology. vl. l, pp, 705-727 (1964); Vol. 5, pp. 126-139, 216-234 (1966); "Ol . 13, pp. 186-533 (1970). Sew 'fork: Interscienee Publisher*. 0007-SWP-037189 0007-SWP-000112885 -45- Blsnksaa, U. A., H. K. Sachs, t. F. Murray, and M. J. O'Connell- Incidence of high blood lead level* In Chicago children. Pediatrics 14:661-667, 1969. British Hadleal Journal (Editorial). Diagnosis of inorganic lead poisoning: A statement. Brie. Med. J. 4:601, 1968. Chisels, J. J., Jr., and H. E. Harrison. The es^osure of children to lead. Pediatries 18:943-958, 1956. Chisoln, J. J., Jr. Chronic lead Intoxication in children. Develop. Med. Child Neurol. 7:529-536. 1965. Chisoln, J. J., Jr. Screening techniques for undue lead exposure in children: Biological and practical considerations. J. Pediatrics 79:719-725, 1971. Clark, A. J., and C. U. Halleet. lead poisoning survey - Portland, Maine, July-August, 1970. J. Maine Med. Aasoe. 62:6-7, 1971. Clarkson, T. W., and J. E. Ranch. Urinary excretion of asino acids by sen absorbing heavy neeals. Blochea. J. 62:361-372. 1956. Cohen, N., M. Elsenbud, and M. E. tfrenn. The Retention and Distribution of Laad-210 in the Adult Baboon. Radioactivity Studies Progress Report iff0-3086-10, Vol. 1, 1970. Devid. 0., J. Clark, and R. Voeller. Lead and hyperactivity. Lancet 2:900-903, 1972. de la Burde, B., and M. S. Choate, Jr. Doe* asymptomatic lead exposure In children have latent sequelae? J. Pediatrics 81:1088-1091, 1972. federal Food, Drug, and Cosaecie Act. Regulations, Part 121, Chapter 1, Title 21. Code of Federel Regulation*, Subpart F, Paragraph 121.2514. * C. V. Thomas, R. H. Suha, R. E. Cohnberg, and B. A. Flaahnar. fedlatrie blood lead levels. A study In 14 Illinois cities of intermediate population. JAMA 221:1475-1479, 1972. 0007--SWP-037190 0007-SWP-000112886 -46' Fullerton, ? M*, and M. J. C. Harriton. Subelinical lead neuropathy in ana. Elaetroencephelog. Clin. Seuropbytiol. 27 (7):?18-719, 1969. Clltinn, J. f. Eatiaate* of th* Nature and Extant of Lead Paint Poiaoning in th* United State*. (NBS Technical Kota 746) Vathington, B.C.: National Bureau of Standard*, 1972. 131 pp. Goy*r, R. A., and J. J. Chisolm, Jr. Lead (Chapter 3, pp. 57-95). In D. H. K. Laa, Ed. Metallic ConcaBinant* and Human Health. Haw York: Academic Pt *, 1972. Goyar, R. A., and 1. C. Rhyne. Pathological effect* of lead. Internat. lav. Exp. Path. 12:1-77, 1973. Goyar, R. A., K. Ttuchiya, D. L. Leonard, and H. Kahyo. Aminoaciduria in Japan*** worker* in lead and cadmium iaduatria*. Amor. J. Clin. Path. 57:635-642, 1972. Guinea, V. F. Lead poiaoning. Amar. J. Mad. 52:263-268, 1972. Hernberg, S., and J. Nlkkanan. Effect of lead on 4-amiaolaevullnle acid dehydrate**. A *el*ctive review. Praeov, Lak. 24:77-83, 1972. Harnbarg, S., J. Nikkanen, C. Mallln, and H. Lillua. i-aminolevulinic acid dehydrate a* a maaaura of lead expoaur*. Arch. Environ. Health 21:140-145, 1970. Ingalls, T. H., E. A. Tibonl, and H. Uerria. Lead poiaoning in Philadelphia, 1955-1960. Arch, Environ. Health 3:375-579, 1961. Xahoa, i. a . the normal metabolism of lead, (rrom The Karban Lecture*, i960: The Metabolism of Lead in Han in Health tad Disease) J. Roy. laat. Pub. Health 24:81-97, 1961. Kehoe, A. a. Th* me tabslien of lead under abnormal condition*. (Fro* Th* H*rben Ucturaa) J. Roy. In*t. Pub. Health 24:101-120; 129-143, 1961. Kehoa, R. a , Pretent hygienic problem* relating to the absorption of lead. (Fro# The Harben lectures) J. Roy. ln*t. Pub. Health *4:177-203, 1961. 0007-SWP-037191 0007-SWP-000112887 -47K*hot, R. A., F. Thomson, snd J. Choltk. On th normal absorption and tierstion of lud. IV. '.ud absorption and excretion In infenc* snd children. J. Induct. Hyg. 15:301-305, 1933. Klnt> B. G> Maximum dally intake of lead without excessive body lead-burden in children. Anar. J. Ola. Child. 122:337-340, 1971-a. Kins, 8. C. Memorandum: Criteria for Evaluating Lead Raised of Related Surfaces. Bur. of Community Environmental Management, May 197i-b. Kaaip, I. J., and C. X. Usurer. Isotope excited x-ray fluorescence. Analytical Chen. 44:57A-67A. 1972. Lin-Fu, J. S. Undue absorption of lead among children. A new look sc an old problea. hew En|. J. Med. 286:702-710, 1972. National Academy of Sciences, Committee on Biologic Effects of Air Pollutants. Lead - Airborne Lead in Perspective. Washington, D.C.: National Academy of Sciences, 1972. 330 pp. Perlatein, M. A., end X. Attala. Neurologic sequelae of plunblsa in children. Clin. Pediat. 5:292-298, 1966. Putsch* 1, S. H., L. Koptto, and S. Schwachman. Children with n Increased lead burdan. A screening snd follow-up study. JAMA 222:462-468, 1972. Robinson, M. J., C. E. Karpinskl. snd H. Brisgtr. The concentration of load in plasma, whole blood and erythrocytes of infanta and children. Pediattic# 21:793-797,' 195B. Srelate Id, J. L. Medical aspects of childhood lead poisoning. Pediatrics 48:464-468, 1971. Stewere, V. j. Paint Drier. and Additives. Unit Eleven in Federetion Series on Coating. Technology. Philadelphia: Federation of Soclacla. for Paint technology, 1969. 64 pp. Tapper, L. b . Statement before the Dally Permissible Intake ed hoc Committee meeting, Cineinneti, Ohio, 1971. 0007-SWP--037192 0007-SWP-000112888 -4Thonea, H. K., and K. D. Blackfan. Recurrent senlngitis dut to lead la a child of five yeara. Anar. J. Die. Child. 8:377-3B0, 1914. United Statea Deparcoant of Health, Education, and Welfare, Public Health Service. Childhood Lead Poieonlng. A Sunaary Report of e Survey for Undue Lead Abaorption and Lead-Baaed Paint Hacard In Z7 Cltlea. OHEW Publication Ho. (HSM) 73-10002, 1972. Wllllaaa, H., E. Kaplan, C. Couchaan, and fc. R. Sayera. Lead polaoniag la young children. Pub. Health Rep. 67:230-236, 1932. 0007-SWP-037193 0007-SWP-000112889