Document OEQr8e2zwOzbOX7ZjpDrQo1jK

LIA17434 Lead Industries Association, Inc. 792 Madaon kww M> Yo.9, N T. 10012 Tttaphcna: (M2J *7V*M* March 5, 1974 !I I i i j RHJKTi LEAD IW RAIXT 0 TO THE OrrXCZAL KEJfflERS or THE LEAD INDUSTRIES ASSOCIATION, WC. Tha attached aatarial may bn of intaraat to Kaaom within your organixatioo Sincnraly, JTStla Attachxamt Sac ratary 4 Ganaral Manamar i o ^pippwi!^^|iiiMfMPHPWiwpw^ 0 LI A 17435 *m*nw mmw v Lead Industries Association, Inc. 2UIMWiw k Nr. Itrx K V. 10017 - Trtrphonrc tflt) SMWJ Environmental Health Department February 8, 197* _Jj j _ All Heebars of the LLA Environmental Bee 1 th Coemittea froo: Jerome F,, Cola Sob 1act: u*i in felat Caotle Enclosed Is a "Eeport of the Ad Hoc Coastttaa to Evaluate the Retard of Lead la Paint" prepared for the Consumer Froduct Safety Gconlssloe by the Rational Academy of Sciences. This report presents considerable Interesting Information on lead and, of course, attribute! Inner city elevated blood lead concentration! la children to old lead paint. We call your attention to a aectlon on page 18 of the report noting that "It le unlikely that eourcea other than lead paints can be responsible thens el vs! for the cases of Increased blood lead content under discussion, but It Is of course possible that they could stake a difference la borderlisa cases." Sincerely, Director, bvlroosental Health Enclosure s N 3414.01 WjWiiliBWWM^MPWWUUyHWiW L I M.7 A 3 6 REPORT 0? THE AD HOC COMMITTEE TO e v a l u a t e t h e h a z ar d or l ea d is ?a is ? h*rrtl for th Cooauasr Product Sfty Com!uloa r ; >2\ i ** $ Katloaol Acdnjr of SclcncM Soroobor, 1973 N 3414.02 il^|EWjl^||)lg|jglBPf^^ "' IjilffPiW11 -lijMW.'-W'-'l |l.lll.i W-WfMl'W UIP-WW-PW-WWlWfP1 L I /s 17 437 ~< .'.-n'k.nii-' I * *j w .M .A-.'fca<Atoii. n o t ic i The project that i the subject of this report w* approved by the Governing Board of the National Research Council, acting in behalf of the National Acadeay of Sciences. Such spprovsl reflects the Board's judgasat that the project is of national icportance and appropriate with respect to both the purposes and resources of the National Research Council. The (cabers of the coaslttee selected to undertake this project and prepare this report were chosen for recognlied scholarly competence and with due consideration for the balance of disciplines appropriate Co the project. Responsibility for the derailed aspects of this report rests -with that cowittee. Each report Issuing Iron a study cocslttee of the National Research Council is reviewed by an independent gvnttn of -frvMw-Mn*l$ according to procedures eetabliehed and Donltored by the Report Review Condtcee of the National Acadeay of Sciences. Distribution of the report Is approved, by the President of the Acadeay, upon satisfactory eoepletion of the review process. The work on which this publication is based was perforsed pursuant to Contract No. FDA 70-22, Task Order 16 with the Food and Drug Ad sdnlat ration. .--- ^ . i'^T*-- J *-*`: -- 9 >BS3|pHiP^ > I WPWPPf MMWSWWPM I'JWiiiyWI Wl!|giPltfW>|gW"MPtg^ LIA17A38 -u PH%--IW1 AD HOC COMMITTEE TO EVALUATE THE HAZARD Of LEAP IS PAINT Dr. Kerril Eisanbud, Chalrtin Hew York University Medical Center Dr. Sasuel P. Beeeaan University of Southern Califoral* School of Medicine Dr. Norbart M. Bikales Burgers University Dr. Sobert A. Coyer University of Sorth Caroline School of. Medicine Dr. Vincent 7. Culnee Km York City Health Department Dr. Eaglnald S. Louris Ceorge Washington University School of Medicine Dr. Pearl L. Xoeaar Howard University Dr. koland . Scott Howard University 1 (Invited Observers! Mr. Boyal A. Brown Xatlonal Faint and Coatings Association, Inc. Dr. Barry C. King San Diego, California Dr. Dal Buthig * Department of Health, Education, and Valfars Staff Officer! Mr. John Xedaond, Jr. UlLU!lJMaWttipWWW MIW JHWMMWBiy TglBPWppppWjWpWWI^W. LIA17A39 *sis.* \ REPORT or THE AD HOC COMMITTEE TO EVALUATE THE HAZARD OF LEAD IS PAINT 1. imODUCTICW , On December 31, 1972, the Bureau of Product Safety of the Pood and Drug Administration (EDA) Vacua responsible for administration of fadaral requirement that the load contant of paints not exceed 0.3X by weight of tha drlad, hardanad film.* Mora recently, tha responslblli- tlas of tha EDA In this araa have Vaan transfarrad by Congresa to a now Cooauaar Product Safety Commission. Among tha first question* ' facias tha Commission la vhathar tha 0.5X Halt should ba raducad to 0.06X at a data that could ba as early as Dec cuber 31, 1973. Tha 0.06X Halt originated as a reconendatlon In a report of Che Committee on Environmental Hazards of the American Acadeay of Pediatrics (1972). Tha Ad loc Coaazlttaa to Evaluate the Hazard of Lead In Paint was constituted by tha National Acadeay of Sclcncas-Katlonal Research Council at tha request of the Bureau of Product Safety to ascertain vhathar there vas sufficient scientific evidence to support a reduction of tha Unit fron O.S to 0.06X. Tha Cosxzlttee vas requested. If it found that sufficient scientific evidence did not exist, to recoooend research that should be undertaken to obtain the required Information. Tha basic question that tha Cctnaittee Bust answer la whether there Is a sufficient body of Information to permit establishment of a limit on the lead content of paints applied to surfaces accessible to children. `Throughout this report, when the lead content of paint, drier, or other paint additive la given, tha expressed percentage of lead la that la tha solid dried film. k'^sUJ `V . *t ,, .%$ .' jiii.jin.iiLii.iii!.ii i.. :"~i--f---------------- " ------- .. /1 ............. ..................................... ................................. ........ LIA17^0 .1 i 2- - This question ha* keen ssked many tla** over tha y**r, and many regula tions hava been promulgated. Tha first, In Germany In 1887, prohibited the uaa of any load In paints applied to toy*. At leaat 10 countries hava tabulated the laad content of paints up to th* present. Except for th* Carmen law, which called for total allalnatlon of laad fro* paints used for toys, tba permissible laad concentrations have ranged fros 0.3 to IX. 2. THE USE Of LEAD COMPOUNDS IN PAINT The essential components of paints arsi (a) Plptnti; to provide opacity, color, and durability. (b) Vehicles: oils, resins, and various polymers to bind tha pigments together and to provide a continuous durable film. (c) Volatiles: organic solvents or water (depending oa type of paint) to control the consistency of the coating and to aid in its application. (d) Additives: generally in low concentrations, to aid in drying, to control consistency, settling, viscosity, and stability, and to lnpart other special properties to the coating. In asking e white paint, or a whlte-palnt base that can be tinted to light pastel colors, it Is necessary to have an opaque white plgnent. The noSt Important early opaque white pigment waa "white lead," the basic carbonate, whose composition approxlaetee 2PbC0j * Fb(0H)j. White lead was first produced In Holland during the sixteenth century .and vaa liter introduced in England and the United States In the lste 1800's. For many years, whits lesd was the prlnclpsl opaque white pigment used In both Interior end exterior paints. Whits lead pigment LIAIT^Z SPSS - .. -Li-*- -2- This question hss been aiVed sen/ times over the years, end many regula tions have been promulgated. The first. In Cermany In 1S37, prohibited the use of any lead la paints applied to toys. At least 10 countries have regulated the lead content of paints up to the present. Except for the Carman law, which called for total elimination of lead from palnta used for toys, the permissible lead concentrations have ranged from 0.5 to 22. 2.THE OSE Or LEAD C0K?0UX3S EAIWT The eesentlal components of palate are: (a) Elgnente: to provide opacity, color, and durability. (b) Vehicles: oils, resins, and various polysers to bind the plgnente together and to provide a continuous durable film. (c) Volatiles: organic solventa or water (depending om type of paint) to control the consistency of the coating and to aid la ita application. (d) Additives: generally in low concentrations, to aid in drying, to control consistency, settling, viscosity, * fc end stability, and to impart other special properties & to the coating. In making white paint, or a vhlte-palnt base that can be tinted to light pastel colors. It le necessary to have an opaqua white pigment. The most Important early opaque white pigment was "white lead," the basic carbonate, whose composition approximates EPbCOj * ?b(OH)j. '* Whits load waa first produced 1m Holland during the sixteenth century .and was later introduced la England and the United States la tha late 1800's, for many years, white lead was the principal opaqua white h pigment used In both Interior and axterlor palnta. White lead pigment uiwi'ij" mvwmat-'fw iwD>mt.'i!iii.-i--)w^,.i)iiiji ii iiwgjaw^pwwiwa^ LIA17443 * > form* rctloo product* with oil paint vhlcl (vegttabla oil*, auch as llnesed oil) that impart toughness and elasticity to th* paint, la addition to opacity. Sasic sulfat* whit* lead was also used aa a paint pigment (approximate compoaltlon, 2PbS0g PbO). Basle sulfate white lead has lovsr hiding power (opacity) and tinting strength than basic carbonate vhita lead and therefore va* not as widely used. The sulfate was more commonly combined with other pigments, such aa sine oxide, and was generally used in exterior palnte. White lead plgaanta, vhen used for interior palnte, contained 40-601 lead. A representative figure for interior paints used before about 1940 would he 501. Zinc oxide was manufactured cocmercially in Franca during the early nineteenth century and in the United States shortly thereafter. It was followed by the manufacture and use of tine sulfide. Litho-- pone, e pigment that contains approximately 30X tine sulfide end 70X barium sulfate, was developed by coprecipitating barium sulfate aad sine eulflde from solution. Faint manufacturers now had a choice of opaque white pigmente, end many paints vere made with a combination of these materiale. lltbopone replaced white lead in many interior paints, i and became e very Important pigment for paint in tha last half of the nineteenth end early part of the twentieth centuries. Titanium dioxide, tbs opaque white pigment used in modern paints, wee being produced commercially by about 1920. It was Introduced to the paint industry aa a titanium-barium combination pigment. It was shortly made available also aa a titanium-calcium pigment end as tha anatase grade of pure titanium dioxide. Also widely used for a while was tltanated llthopone, containing 15Z titanium dioxide. Titanium pigments had gained major acceptance by the late 1930's and largaly : lum 'wii'jwgnwwgFiw.'- .."ir Ill III 1111111 iniff .......... ................ ...... III ,1" ' Via Suit- mm....."".........r*..................................................................... Mill III I ............. ..... L ...... ........................................ o u ; replaced llthopone, sloe sulfide, tc., In neat Interior point*. By thll time, Char* wes lied* economic justification for tb* u of whit* lead In any type of Interior paint. By 1941, the hiding powar of tltanlua dioxide wa* rated at 115 ft^/lb, compared with about 15 ft*/lb for tba lead pigment*. It 1* estimated that wore modern pigments con taining tltanlua dioxide have a biding power of about 155 ftfylb. Thus, 1 lb of tltanlua dioxide will provide the opacity or biding power of bout 9 lb of white lead, and for aany years there ha* been no necessity to ue* whit* lead pigment* In Interior paint*. The tine when all wblto load wa* removed froa Interior paint* 1* not known, but It may be attuned that relatively little vhlte lead pigment wa* Incorporated Into Interior paint* after 1942. Lead chromate yellow pigments, first made la Europe la about 1800, have long been a valuable raw material for use in paint*. Then* plgsent* range froa light yellow to deep orange. Lead aolybdate plgsent* rang* froa aedlua orange to deep red, and "chrome greens," froa light to deep green. All these contain lead, but In a much less soluble fora than vhlte lead plgaents. These lead plgsent* provide excellent hiding power end color permanence, and they are economical. They are widely used in coating* for *utoaoblle*, trucks, farm machinery, signs. ' traffic markings, buildings, and hundred* of other article*, led lead plgaents and lead *lllcochromate pigments are valuable for use la anti corrosion primers for steel and Iron. Some lead pigment* nr* *tUl used In exterior primer* and paints for wood surfaces that au*t with stand the affect* of sunlight, rain, and weather conditions of all type*. Lead compounds are, and will continue to be, extreaely Important to the paint manufacturer a* essential Ingredients of many types of primer*, paint*, and enamel* for exterior use*. |^!I <]-.^Ig^gCTWWpg .-*->3w LI A 17444 k.**? .>:V<*si'. 3 i im '.yyp" wM.^.yi'w.^ ;w' ff.-iim* W 11 iw m fWfp.i>w M ` 0 ft * * rsplsesd llthopone, line sulflds, etc., In nose Interior paints. By tilla time, there vas lied* economic justification for the us* of white lead In any type of Interior paint. By 1941, the hiding power of titanium dioxide waa rated at 115 ft*/lb, compared with about 15 ft*/lb for the lead pigments. It la estimated that more modern pigments coo* talninj titanium dioxide have a hiding power of about 135 ft^/lb. Thus, 1 lb of tltanlua dioxide will provide the opacity or hiding power of about 9 lb of vhlte lead, and for oany years there has bean no necessity Co use vhlte lead pigments la Interior paints. The ties, when all white lead was removed froa Interior paints is not known, but It may be assumed that relatively little white lead pigment was Incorporated Into Interior paints after 1942. Lead chromate yellow pigments, first made in Europe In about 1800, have long been a valuable raw material for uaa in palnta. Theaa plgsMnts range froa light yellow to deep orange. Lead molybdate pigments range froa medium orange to deep red, and "chrome greens," froa light to deep green. All these contain lead, but In e much less soluble form than white lead pigments. These lead pigments provide excellent hiding power and color permanence, end they are economical. They ere widely used In coat Inga for automobiles, trucks, farm machinery, signs, traffic markings, buildlegs, and hundreds of other articles. led lead pigments and lead slllcochromate pigments ara valuable for use In anti corrosion primers for steel end iron. Some lead pigments are still weed In exterior primers end paints for wood surfaces that must with stand the effects of sunlight, rsln, and weather conditions of all types. Lead compounds ars, and will continue to be, extremely Important to the paint manufacturer as sasentlal Ingredients of many types of primers, paints, and enamels for exterior uses. i111.^1i;^ .jI i jwuu,.;jyjj myrgy s^BpgBIWiilWilBIWliWlB^UI^WpWWWWW^^ LIA17445 lywgMft-rwiiwF -5- 3. BISTORT Or PECULATIONS LIMITING THE LEAD CONTENT OF PAINT IN THE UNITED STATES On Kerch 11, 1972, an order vaa published under Section 2(q) (1) (8) r of the Fadaral Batardoua Substances Act declaring paint and other similar surface-coating materiel containing In exceaa of O.SS lead (as natal) for 0 use In or around the household to be a hazardous aubstance and to be banned free shipment in Interstate cocemerce after December 31, 1972. Separate provisions of that order banned shipment In Interstate commerce after Deccaber 31, 1973, of paint and other similar surfece-costlag tseterlei containing In exceaa of 0.061 load (aa metal) for use la or around the household. The order also specifically provided, as required by Section 2(q) (1) (A) of the Act, that any toy or ether article bearing such paint end other almller aurface-coating material and intended for use by children would he e banned hazardoua substance after one of those s ueLee, d'tpvwulug vs Llw ImmI wuslsuit Oo August 10, 1972, the portions of the regulation pertaining to the 0.5Z leed content vers confirmed as effective. Bovevar, the portions pertaining to the 0.06T content were stated to be the subject of a saperate document to he published at a later date. It vee found by reviewing the consents received with regerd to the Kerch 11, 1972, order that the two concentrations (0.3Z end 0.06Z leed) end effective detee presented asperate Issues that required separate consideration. 3.1 APPLICABILITY Or THE REGULATIONS AND DEFINITION OF TERMS The provisions of the Federal Hazardous Substances Act are applicable to any hazardous substance In Interstate cosnerce that la Intended or packaged In a fora sultabla for usa In the household or by children. i^JPMiWwa > ** mi<m^ hj ;"jigy*,'ijjwiJiP.ijiRpuw'jnpwnwiiiim 'MLIA17446 - o The tern "banned hazardous substance" contained 1b Ssetion 2(q) (1) (a.) any toy or other article intended for use by children, which la a hazardous aubatance, or which bears or con tains a hazardous substance In such Banner aa to be susceptible of access by a child to whoa Such toy or othar article la entrusted and under Section 2(q) (1) (1) aeeng eny hazardous substance Intended or packaged In a font aulcsblo for uae In the household which the Secretary, by regulation class If lee as e "banned hazardous substance" cu the basis of a finding that, notwithstanding such cautionary labeling as Is or Bay be requlrtd under the Act for that substance, the degree or nature of the hazard Involved in the presence or use of such aubetanco la the household is such that the objective of the pro tection of the public health and safety can be adequately served only by keeping such substance, when so Intended or packaged, out of the channels of Interstate coooerce. The regulations lnpleaentlng the Federal Hazardous Substances Act--specifically, Ssctlon 191.1(c)--define a "hazardous substance Intended or packaged In a fora suitable for use la the household" as any hazardous substance that, under customary or reasonably fore seeable conditions of purchase, storage, or use, cay be brought Into or around a bouse, apartment, or other place where people dwell or into or around eny related building or shed. Including but not Halted to e garage, carport, barn, or storage abed. The regulations expressly exclude Industrial supplies that Bight be taken Into a boss by c serviceman and articles labeled and nsrkated solely for Industrial uae. The paint regulations Issued under the Federal Hazardous Substances Act are applicable to paint and alallar surface-coating naterlals con taining 0.3X lead that are sold for conauser uae. They Include paint end elnllar coatings that are used for exterior and Interior surfaces of dwellings and related buildings, as well at surfaces of articles 3Sb LI A 17447 that are maintained In or around households or ralatad building*, such aa radlatora, lance*, furniture, and toya. The regulation* are not applicable to palat and alaliar coatInga that ara labeled and aarVated solely for lnduatrlal uae, such aa palata applied at a factory to autonoblla*, truck*, lawn nowere, tractor*, sad appliance*. However, palat applied to toys aad other article# Intended for nee by children cannot contain nore than 0.3X lead. A petition to aeertd the lead-paint regulation baa been racalvad and publlehed as a proposal. Tba proposed aaandneat would except toe* pelnte and coatings containing la cxcasa of 0.3X lead froa the bacnedhsxardoue-eubstanca claaalf lcatloa. Included vlthla the requested exceptloo are toucbup coatInge for aotonobllea, agricultural ead Industrial equipment, leva aad garden equlpaent, outboard notors, notorlsed recreetlonel vehicles, and household appliances. A proposal to except artiste' palate fro** the laed-palnt regulation baa been published. Consents on the two proposals are currently under consideratloa within the Coaeuaer Product Safety Coilielw. 3.2 OTHEX PEDEXAL UVS DEALING WITH LEAD 7AI*T Congress, on January 13, 1971, enacted the Lead-based Palat Poison Prevantloo Act of 1971. Its purpoaa la to sllalnate childhood poisoning by laad-baaad paint. Sactlon 501(3) of the lew prohibits the nee of paint containing la excass of 1.0X laad la residential structures built or rehabilitated by the federal govarnoant or with federal assistance. Several bills to aaead this law have been subaltted to Congress during 1973. The Senate, on Kay 3, 1973, passed S607, the Laad-baaad O ..ijeuei iii ilipjjatfpgp^lW IIUL, j|if i jiiipirTiini]jr I~n"~l-- ~"l T"" "" ' " LI A 17 448 PalnC Polion Prevention Amendments of 1973, which would amend Section 501(3) aa follow*t (a) Prohibit the us* of paint containing In excess of 0.5Z lead before December 31, 1973. (b) Prohibit tha u** of paint containing In excess of 0.04X after December 31, 1973, except that. If the Secretary of the Department of Health, Education, and Welfare determine* that, on the has la of todlea conducted in accordance with Section 301(b), another lead content not to exceed O.SZ 1* safe, then such other content shall become effective after December 31, 1973. Section 301(b) of S607 direct* the Secretary of the Department of Health, Education, and Welfare to conduct appropriate etudle* on dried paint films to determine the safe lead content in residential paint products and to report to the Congress not leter than October 1, 1973. Several bills amending the Lead-based Pslnt Poison Prevention Act of 1971 have been under consideration within the Rouse of Representatives. We understand that the full Bouse Ranking and Currency Cosnlttee baa reviewed a number of the bills before the Bouse and reported favorably on the "Barrett hill," HR892C. This bill, we understand, will be sent to the floor of the House to be voted on. Coder the provisions of this bill. Section 501(3) of tbe Lead-based Paint Poison Prevention Act of 1971 would be amended to prohibit the use of paint containing mors than 0.5T lead. Section 301(b) of the bill directs the Secretary of the Department of Health, Education, and Welfare to conduct appropriate research on multiple layers of dried paint films with respect to aafs lead content and to report the results of such invaatigstIons to Congrsss not later than December 31, 1974. . .* . jliliiliPillihillll ' *".. ^ .. ' ^ - j i uijiiinmnnipipifiwn mm nun i .11111. irrrrr:.T"--' ........ ....... ... ' .......... "" *'' w--im L. I A 17449 -9- 4. HISTORY OF PROBLEM OF COMMUNITY LEAD POISONING Lead poisoning* among young children ll/ing la deteriorating inner-city homing emerged > an urban problem In the United Stataa aa early aa the second dec ada of thia century (Williams t il,, 1932). Thomas and Blaekfan (1914) of the Johsa Hopkins Hospital la laltlaor* -vara the first to describe in the American literature the clinical and pathologic affects of lead-induced encephalopathy la children. VIIHaas and hie co-vorhare point out that nultlple cases of lead poisoning had already been reported from 19 separata eonsunltlea before 1951, and It wee recognized that this problem was related to pica, the habit of chewing cribs, toys, furniture, and woodwork, such as window sills, and the eating of painted plaster and fallen paint flakes. Of the affected children, 60Z were between 1 and 2 years old, and fever thaw 3X of the children were over 3 years old. During the 20-year period 1931-1951 in Baltimore, 293 cases vers found to have clinical lead poisoning de fined by a blood lead content greater than 50 ug/100 ml associated with a clinical manifestation of lead toxicity (aneala or central nervous aystea symptoms): SS of the patients died. After the early Baltlaore experience, public-health departments of other major American cities bagan efforts to dstermine the extent of lead poisoning. Generally, two ataps were taken: lead poisoning *Lesd poisoning is defined aa a case in which the clinical signs and symptoms to be discussed later ate present. Some investigators would include the presence of biochemical changes such as a reduction in delta-amlnolevullnlc acid dehydrate or an Increase in free erythro cytic protoporphyrin. For the purposes of this report such changes are < considered to be compensatory and not pathognomonic of lead poisoning. 3 l t! WJWPW ipiu-wiwwfpj LIA17450 -10- w>s udi a reportebl* disease, and separata progress for control of load poisoning vert established (In 1950 In Philadelphia). A report of the results of these aeasures In Philadelphia froa 1955 to 1960 (Ingalls <(t al_., 1961) noted that about 50 cases of lead poisoning vers reported each year, cospared with the average of 41 per year reported by the Baltimore City Health Department In 1966-1951 (Wllllana at el., 1952). froa 10 to 20Z of diagnosed patients died la that period In Baltimore (Ullllsas j^t a_l., 1952), end neurologic dle- orders, including mental retardation, persisted ea sequelae In eoaa of those who survived (Perlsceln and Attala, 1966). In aore recent years, cases of severe lead poisoning seem to have been less frequent. In New Tork City, the health department reports that fatal cases have been reduced to one or two per year, Cuapwauu wail* *uuvi 2C yni /mi two uSC&dts -a-* t-1 there is little Information on the frequency of occurrence of the various stages of , lead poisoning short of death. During the last 20 years, the public-health programs of many cities have been expended to Include large-scale screening of children at risk. The results of some of the most significant of these screening programs are summarized In Table 1. A more complete summery of screening- program results Is found'In a report from the Rational Bureau of Standards (Cllslnn, 1972). The children Included In these survey* ere usually between 1 end 6 years old end said to be at risk for undue absorption of ld because they reside In deteriorating, pre-World War II housing. The surveys, for the aost port, Involve areas at risk within very 6 large metropolitan communitlee. However, the study froa Portland, Main* imh ^'iw w w w iw wffjpippifiiwwpwiiagcwp Wj^ipujiii'!!- ,wi*www!wppw^j^`fiWii.ffg.^jHl^ iw u mbiw w w im LIA17451 (dark and Rallstt, 1971), tugs*at* chat the "risk factor** la act necessarily tha alia of th city but, rathar, tha aga of tha boualng. Thla notion la supports! by tha study of children at risk in 14 intermediate-slzsd Illinois communities (Tina st_*l_., 1972). Tbara la a daflnlta seasonal variation In blood lead content; tha Incidence of lead poisoning in young children peaks during tha susBtar nonths (Chlsola and Earrison, 1956; Ingalls, .1961; Blanksma at el., 1969; Cuinee, 1972). The larger screening pragmas hava collected blood saoples during all Booths of the year, but sons eaaller studies have been restricted to tha lunar eonthe. Tha aethods of blood lead measurement are varied, but tha dithiserne procedure and atrale-absorption spectroscopy hava been used Boat often In recent years. Anodic stripping voltametry has been Introduced recently (DEEM Publication. 73-10002, 1972), as 1mm X-ray fluorescence (Knalp and Laurer, 1972). The atudles Indicate that 9.1-45.5Z of children surveyed hava blood lead concentrations above 40 ug/100 nl and that up to 12.5X have concentrations above 60 ug/100 nl. The Bureau of Community Environmental Hanageaent and Rational Bureau of Standards (Cllslnn, 1972) report that about 23Z of children at risk have high blood lead content (above 40 vg/al) -and that about 5Z of these children >hava clinical ayaptons. 4.1 CORRELATION OF BLOOD LEAD CURIERI WITH PATHOLOGIC EFFECTS There seems to be general agteeoent that blood lead content la the moat informative slngls Index of exposure to lead, particularly when correlated with biochemical and clinical Indices of lead intoxication. O gNjUMJaggp? ! 1 LI A17452 t -12- (t F Blood lead content ha* beta used extensively for the control of Industrial exposure of vorknen to load, a* well a* the recognition of lead poisoning In young children with environmental or accidental exposure Co lead. Kevartheless, despite all this experience. It hae been difficult to da-- i t ternlne a blood lead content above vhlch a person can be regarded as having lead poisoning and a blood lead content below vhlch one can con f. fidently predict no adverse health effect. It la recognised that ln- ereaeing blood lead concentrations are associated with a continuum of probable effects, extending from the concentration at which no effect la seen to those at vhlch aanlfe*tations of lead poisoning are highly probable. It la also recognized that there nay be an Internedlata range of blood lead concentrations at which biochemical changea of unknown pathologic or clinical algnlflcanca are seen. Such conaidera- i tlons have resulted In division of the "lead sffect" Into three to five . categories (Br. Med. J.. 1968; Coyer end Chisola, 1972). , i A staple scheme for correlsting blood lead content with clinical ! manifestations of lead toxicity la presented in Table 2 (Coyer end Rhyne, 1973). The diagnostic criteria are divided into three phssest no effect, an adaptive or subclinlcal phase, and overt or clinical toxicity. The boundaries of these categories reflect present knowledge and era subject to aodlfication as new Information becomes available. Furthermore, the table does not reflect Individual differences la susceptibility to the effects of lead. A compensated lead-industry worker may have a blood lasd content near 80 or even 100 wg/100 ml without overt symptoms of lead toxicity (American Academy of Pediatrics, # 1961). However, children vlth blood lead concentrations greater than 80 pg/al are usually regarded as experiencing lead Intoxication because m u m it m i HHi'Jkriit'llftieAiiiiMlli Ml 5 t. AJ jf 'are mmmw ,L T1 AAV17'V4 ^5 .3............ ' spsi % -13- of the frequency of associated advert* effect* due to lead (Chitola, 1971). Blood lead concentration, however, la not In ltaelf a auaitr* of pathologic efface of lead, But oust be correlated with ocher bio chemical, functional, or clinical manlfestatlona of lead toxicity for tb* diagnosis of lead poisoning to b* established In a particular pareon. 4.2 BXCOQtlTIOH or CLINICAL LEAD POISOSUIC Tb* Public Health Service (Stelnfeld, 1971) baa suggested that child vhott blood lead content la over SO vg/100 al ahould bo conaidered unequivocally to have lead poisoning and ahould be handled *- ea e medical emergency. A blood lead content over 40 ug/100 ml should be Interpreted aa evidence of undue lead absorption. Blood laad concen tretlone over 80 i>g/100 ml ara usually associated with fivefold or greater Increases In urinary dalta-aainolsvullnic acid and coproporphyria, as well aa aa increase In free erythrocyte protoporphyrin (Coyer and i Chisolm, 1972). Each of these characteristics reflects Impairment of heme synthesis; such changes are usually detectable at lower blood laad concentrations than those associated with anemia. Nervous system and renal effects of lead ara usually recognlxabla only during the phase of overt lead toxicity. In children with blood laad concentrations above 100 ug/100 ml of whole blood, the risk of i acute encephalopathy la high and the onset unpredictable. Adults with blood lead concentrations over 120 ug/100 ml ara regarded as having "dangerous" exposure with possible acuta symptoms and long-term sequelae. ! Serve conduction, aa measured by nerve Impulse amplitude, may be decreased .In the adaptive phase of laad toxicity, as shown by Fullerton and Harrison (1969) In workers with excessive exposure to laad. ' r >.f B |We kfHiWWPPffi***.*) l '^ A W |;ys|W.p4HpiW,I^Pgll l L.IA17454* psup^ -14- Clinical renal effects of lead toxicity--namaly, renal tubular dysfunction of Cho Fsneont syndrome type--occur only during clinical lead toxicity. Industrial workers with excessive lead exposure and Increased urinary excretion of lead but without signs of clinical lead toxicity have only minor increases in urinary eelno add excretion (Clarkson and Rench, 1956; Coysr et el., 1972). It la unllkaly, tberefore, that renal tubular function la impaired to a seaaurable degree during the adaptive phase. Nevertheless, Intranuclear Inclusion bodies (lead-protein complexes) occur In renal tubular lining cells of rata at a lover dosage of lead than any functional signs of lead toxicity. It Is suggested, therefore, that Inclusion body formation Involving the binding of renal lead In a nondiffusible lead-protein complex probably occurs during the adaptive phase of Increased exposure to lead. Overt clinical toxicity may be subdivided Into early, reversible, end Irreversible phases, "Reversibility" Is more useful than "acute" and "chronic," because the letter terns Imply time ea e factor. A child with acute lead Intoxication may have more significant Irreversible central nervous system sequelae than one with more prolonged but leas severe exposure to lead. And a child with neurologic sequelae of lead toxicity may have a normal blood lead content. 4.3 RECOGNITION 0T SUBCL1NICAL LEAD POISONING The closer the blood lead content gets to 60 wg/100 ml, the morn likely are clinical manifestations. The "Statement on Diagnosis and Treatment of Lead Poisoning in Childhood" Issued by the American Academy Q of Pediatrics In 1961 recommended that "two successive determinations of 40 Mg/100 ml of whole blood or higher should be obtained for a definite 1 'PPjWj WWWW^iWW||fflWBPW|P LIA17455 -15- diagnosis of lead poisoning." Chisolm (1965) later suggested Chat the Halt of "nomal" blood lead concentration should be lowered to 40 tg/100 ml-- a recoenendation Chat has been endorsed by Stelnfeld (1971). Although blood lead Concentrations of 40-60 wg/100 ml (in Che-early adaptive phase) are not usually associated with clinical or even bio chemical evidence of toxicity. It Is not necessarily true that Cher* are d o harmful effects. Two paths of Investigation -have been directed toward.demonserating that adverse health effects of lead mey occur -' with a blood laad content aa low at 40 ug/100 ml; ona concerns the biochemical effects of lead on beae-syntheslzlng enzymes, and the second involves detection of subcllnlcal central nervous system effects. Tbe most sensitive biochemical Indicator of an lncreaaa la blood lead Is in vitro assay of delta-salnolevullnlc acid dehydrate (T n) in stroma of circulating red blood cells. Bernberg and co-workers 0-970)^ hava recently shown that s decrease In ALAS activity Is correlated vlth '* Increased blood lead content and Is a particularly useful Indicator when the blood lead content is 40-50 ug/100 ml (Bernberg and Mlkkanen, 1972). Vhen the blood lead content la higher, the activity of the i enzyme Is too lew to be useful clinically. Whether the lead-assoclated decrease In ALAS represects any adverse health effect le uncertain. It must bn kept in mind that this test eeasures the in vitro activity of ALAD In blood heaolysats and does not necessarily reflect any Impair ment of this enzyme la the Intact red blood cell In vivo, because of the extreme sensitivity of this test. Its possible clinical significance deserves full evaluation. ilfiinffiiM ilflM i r'liinf iHifATi) ftilfiniWni LIA17456 18- gacent atudlae suggest Chat subtle effects on central nervoua function, particularly Intelligence and behavioral activity, art praaant la children with blood land concantratlona over 40 yg/100 ml. A comprehensive atudy of 53 asymptomatic children vlth blood lead coneantretlone over 50 yg/100 ml (or over 40 yg/100 ml vlth arise lead content exceeding 500 yg/24 hr after ethylenedlemlnetetreacetata provocation) vaa conducted by Pusschel and co-workers In Boaton (1972). A history of slid CSS ayo?terns, euch aa clumsiness end Irritability, vaa obtained In about one-third of the 58 chlldsen. HInor neurologic dysfunction and various torat of motor impairment vere detected by-.*' - ore elaborate testing In 22-27X of the children teeted. Chelation . therapy was administered. and Manures vere taken to laprove their ; l home environment. Eighteen months later, significant Increase la soma erase of intellectual performance vaa observed. Similarly, David and co-vorkera (1972) found higher blood end urine lead concentrations after challenge with a single dose of e chelating agent in hyperactive children than in nonhypsreceive children, suggesting e relation betveen Increased lead content In [ r 1 these body fluids and hyperactivity. Mors than half the hyperactive I Children (28 of 54) had blood lead concentrations betveen 25 end (5 yg/100 ml. These workers argue that any blood lead concentration over 24.5 yg/100 ml la dangerous end may produce central nervous r_ system effects. In addition, da le Burde end Choate (1972) shoved that 70 asymptomatic 4-yoar-old children with Increased blood lead concentrations (meen, 58 yg/100 ml; renge, 40-100 yg/100 ml) or e lead content of at least 50 yg/100 ml with positive radiographic findings of lead lines in long bones or metallic denticles in the Intestines had deficits In fine motor function end behavior. t. i 0 .wh wj wwswmb l>H.Pik!JHiJ IJJUM,1 IIIWWWIHIM^^J ^WWBp^j^w, LIA17457 17- In contrast with previous understanding, a recent English study suggests that anemia is cossaon in children with blood lead concentretions between 37 end 60 vg/100 ml (Betts et si., 1973). The common conclusion of esch of these studies Is that blood lead content over 40 yg/100 ml must be regarded as potentially hazardous to health. E 4.4 ESTIMATE or THE NUMBER Of 0. 8. CHILDREN VITH INCREASED BLOOD LEAD . The National Bureau of Standards has recently published the results of mathematical models vith the assumption* end date used to formulate them (Cllslnn, 1972). Estimates are given of the number of children who have Increased blood lead concentrations (> 40 ug/100 ml) In 241 Standard Metropolitan Statiatical Areas in the United States. Present estiastes based on these models suggest that approximately i'1 * 600,000 children would show increased blood lead content if tested. , The models end assumptions have been only partially validated. By using the National Bureau of Standards modal in conjunction with data froa the major screening programs, it is possible to con struct Table 3, which gives the estiastes of the numbers of cases of 1 childhood lead poisoning of various degrees that may occur annually in the United States (Anderson, D., J. Reed, end V. Heiden, personal communication). These estimates should be regarded as first approximation* that can serve only to suggest the general magnitude of the problem. Better date Mist await the results of well-designed epidemiologic etudle* conductad on e national scale. ! ! BlimpswmyMWfj w u m mwemw 'i" im''mnnw,e|s;'nwm' niS)|ei ' . en1 ".snm o. ; rjg&i&fe&stfksk:&& L. 1/4174 5 8 rpr**? m 0 i \ 0 3. METHODS OF COSTHOL OF LEAD POISOKIHC Lead poisoning Is e preventable disease Chat can be controlled la thraa wayat by eliminating the sources of lead; by controlling the Mans by which lead enters the body; or by finding and treating case* early. Elimination of the sources of lead Is certainly the most important approach over the long term and conforms with timehonored public-health practices directed at control -of the vectors of disease. The moat significant identifiable source of lead poisoning today is lead-containing paint in houses to which 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 that cosea from the uaa of lead-containing gasoline. A boat of other lead-containing substances around bouseholda have been identified aa potential eourcea of lead exposure, auch as the paint on pencils, evaporated-milk cans, toothpaste tubes, porcelain,and earthenware. Their contribution to the lead-poisoning problem la considered to be substantially leas than that of lead paint on walls sod woodwork of old bouses, old toys, and beds. It la unlikely that sourcea other than lead paints can be responsible themselves for the cases of increased blood lead content under discussion, but It is of course possible that they could stake a difference in borderline cases. Thus, control can be achieved by removing children from delapldated bousing In which peeling coats of leaded paint are available to them or by removing leaded paints from the interiors of such buildings. It may also be possible to reduce the tendency toward pica by dealing with the underlying social and environmental factors that have been 0 Mrnjm IWfWSSRRP J~ '* Si-Ul UJ `O r 1 i i 3, -------------- urn i ..... .. Jim ' LIA1745Q r shown Co have a role lo Chit behavioral anomaly. However, Chit Ccaoittea hat bean appointed co attlac In developing federal policies that vi.ll prevent future lead poieoning associated vith paints yet to be applied to surfaces accessible to children with pica; hence, the Conalttee Mit focus on future sources of exposure, not present or past. Recently, the Cosalttee on Environmental Retards of the American Acadeey of Pediatrics (1972) recooaanded that the*lead content of paints he reduced to less than 0.06Z. This reconsendatlon was based on tbs assunptlon that the risk of lead Intoxication In children Is Increased when the dally Intake, fro* sources other than food, exceeds ISO vg/dey. Estimates of dally Intake froe food, water, and air have also been nade by Barltrop, who gives a total of 1S6 ug of lead per day. Barltrop goes on to reduce the dally permissible Intake of 600. wg/day for an adult to 180 pg/day for a 2-year-old, and further corrects this nunbar for calorie requirements of a child, thereby ending up with a final value of 133 ug/day, which he suggests as a maximal permissible safe intake (barltrop, 1973). A maximal permissible lead content of paint (0.06Z of dried f11s) was than derived fros a d u e her of aaeuaptlons, Including: (a) that gastro intestinal absorption of lead Is the sane fros paint as fro* food; (b) rhat * child eats 1 la.^ of paint per day; end (c) that six layers of paint lw~vw accumulated. The validity of the recommended maximal lead content la sensitive to these and other aaeuaptlons In tha calculation. 3.1 LIMITATIONS IN THE AVAILABLE KNOWLEDGE 0 WHICH A STANDARD COULD BE BASED If a limit Is to he established on a rational baala, tha following questions should be answerable, particularly for children In tha sus ceptible age group. WMSLA UL.WHJBJS'A s ! i ik !Pgj|ji*>i.jg^^ " L I A17 4 6 0 20- () Vhat body burlwn of laul 1* aaaociattd with symptoms ot lead tcricity? (b) Bow it blood load related to body burden of lead and 1(0* ot symptoms of lead Intoxication! (e) Vhac dally intake of lead in paint will result la the permissible body burden of lead or the maximal permisalble blood lead content? (d) Bow much eorface area la nibbled by children? (a) What limit on the percentage of lead In paint would beep the blood lead content or the body burden of lead within acceptable llmlta? The following brief suoaarles of the etate of our knowledge with respect to each of these questions should serve to Illustrate the serious llnitallona In the present state of our knowledge. 5.2 ASSOCIATION OT BOOT BURDE* 0? LEAD VITH SYMPTOMS OF LEAD TOXICITY It should be emphasized that lead deposited In the skeleton Is only potentially toxic, as opposed to lead In soft tissues, such aa kidney, brain, and liver. Thus, the significance of e given body burden of lead will depend not only on the total amount of lead present In the body, but on its distribution between the skeleton and the soft tissues. Barry and Kotsman (1970) measured the lead concentrations la the tissues of 10 English children and 49 adults described aa having been exposed to a normal urban environment. Table 4 summarises their # date. The total lead body burden of the children renged from 0.5 to 3.L mg, with a mean of 1,5 mg. Approximately $41 of the lead was In the skeletons L IA1 7 A 6 1 ; : 21' ( of the children, cospared vlth 932 In tha adults. Tbs mean total body burden of tha 29 adult sales was about 160 t, compared with about 110 ag for tha 20 adult females. An Interesting consent sane by the authors is that "the relatively high proportion of lead In soft tissue, compared to the lead levels In bone of young children, say be accounted for by tha lack of hard, dense bone et this stage of life which, when developed la later life, appears to taka up and ratals lead. It la suggested that eMa aay account. In acne aaasure, for tha advarae reaponae la young children to severe lead, exposura," Tha ralation of altber clinical signs of lesd toxicity or changes la the early Indicators of abnormal lead exposure^ euch se blood lead concentration, erythrocyte ALAD, and free erythrocyte protoporphyria, to either the soft-tissue or the skeletal laad burden la poorly defined. Inasmuch ss lead concentrations In tissues arc not usually measured befora autopsy, there Is no basis for a correlation between signs and symptoms and the body burden, other than for fatal encephalopathy. Chisolm and Harrison (1956) and Kehoe et. *1. (1933) have measured the body burdens of lead In children who died of lead Intoxication. Their results Indicate that the associated soft-tissue body burdens ranged from 20 to 100 mg, or from about 35 to about 200 times the "norami" soft-tissue burden. The skeletal burden, as estimated from rib analysis, varied from 100 to 400 mg, or 100-400 ticsa tha "normal" skeletal burdan. Tha "normal" values were determined In England and nay not he applicable : to a D. S. population. In summary, only a few data are available to describe the normal % lead content In children's tissues, snd no data are available for cases e of land intoxication other than fatal encephalopathy. IjWBHIBWF1 sswimaSMB|l|WNW^ LI A17462 tlM W ilnSvitT -22- 3.3 BELATICS OF BLOOD LEAD TO BOOT BUKDCI QT LEAD AND TO SYTO>TO*S OF LEAD INTOXICATION The blood load concentration tan reflect either recent exposure or an equilibrium relationship to land la the akaleton and aoft tissues. To evaluate the former, It la necessary to understand the clearance rate* of lead from blood. Using laad-210 aa a tracer, it has been determined la the baboon that lead dears In three exponential com ponent# : approximately 731 of the blood lead 1 day after Injection la removed with a biologic half-time of 1.2 days, 24X with a biologic half time of 10 days, and 31 with a biologic half-time of 4 months (Cohen et al., 1970). No Information la available from which to estimate the reservoir of lead In the tissues of e person who has a blood lead concentration higher than normal, but who la removed from exposure. The relation of blood lead concentration to symptoms of Intoxication la not adequately defined. If the blood lead concentration does not exceed 40 vg/100 cl of whole blood, there are no clinically observable effects In adults or children, although erythrocyte ALAD activity stay 1 be leas at these concentrations than at blood lead concentrations below 40 pg/100 ml (Bermbcrg g. gi-, 1970). The term "asymptomatic increased lead absorption" has been coined i to designate the gray area of blood lead concentrations that are signifi cantly higher than the normal range, or from 40 Co 60 ug/100 ml of blood (HAS. 1972). The available Information concerning blood lead concentrations in relation to signs and symptoms, as sumarlzed by the NAS Committee On Biologic Effects of Atmospheric Pollutants In 1972, la given In -P4jWJ ^.SMlP^'B!Ul^i!:JUU|jlM^,^l^|JS^4<P!j^^.^j3IW8WipMI^PtPEHiWP^-j*l^<^'^WjWpPg<i^itl!W|ypil>!P|MlitLJ|l*JS^ LI Al74 63 -:>- Table S. It should be noted, however, that these data bava been obtained, for the aoit part, froa atudlaa on adults, 3.4 DAILY INTAKE OF LEAD IN PAINT THAT RESULTS I* HAXIHAL PERMISSIBLE BLOOD LEAD CONTEXT Concentrations of lead In tba blood of unexposed children (12-34 onthe old) have bean reported to range froa 13 to 40 Kg/100 al of whole blood, with a oedlan of 27 Kg/100 ml (Robinson et el., 1938). On the basis of Tapper's observations on adult Intake (1971), the total Intake of lead for a child would be 104-204 Kg/day. The contribution of Inspired air to tbs estimated totals for average lead intake Is approxi mately 3-61. On tba basis of a gastrointestinal-absorption factor of 10Z, approxlnately 95-183 Kg/day should be excreted In feces. In fact, CKlsola and Harrison (1956) and Barltrop and Klllala (1967) observed dally excretion of 120-175 Kg In feces, with a naan of 132 Kg/day. Tbe percentage of Ingested lead absorbed froa the gastrointestinal tract of children is one of the najor uncertalntlaa, Alexander et al. (1973) have recently reported, based on netabollc balance studies. In 8 children over a 3-day period, that absorption In children nay be as high as 30X with an average retention value of 18X, Lead concentrations la tlw elood of children of 40 Kg/100 ol or higher are considered evidence of undue absorption of lead. On the basis of data on excretion of lead In feces lsssedlately after the cessation of pica and of tbe results of balance studies (Kehoe, 1961) Involving tbe experimental Intake of soluble foros of lead. King (1971a) has esti mated that a dally Intake of 300 Kg of lead would not result in a signifi cant Increase in the blood lead concentration. Doubling of this Intaks over a period of 3-6 oonths would result In a blood lead concentration that could exceed the defined toxicity value of 60 Kg/100 ml. syj'w. iwfljsw1 l LI A17464 -24- 5.5 5U3EACI AREA KIBBLED BY CHILDBEX The quantity of lead ingested with paint la related to paint-chip Ixa, psrcsntags of lead in tha paint, and the tunbar of layara of paint on a particular chip. On tha baala of 6.5 og of paint par square canti na tar par Xayar of lntarlor paint and 16.0 mg of paint par aquara centi meter par Xayar of axtarlor paint, Table 6 llsta tha amounts of paint nacaaaary to obtain 200 ug of lead, or tvo-thlrda tha daily calculated parnlaalbla lntaka for different percentage* of lead In paint and different ousbera of layer* (ling, 1971b). For 0.06Z and six layara of interior paint, thl* would corraapond to a chip of about 9.5 cm* or 1.3 It ahould be noted that tha rata of absorption of lead froa paint chips is not known and aay in fact be highly variable. The Aserican Acadaay of Pediatrics report assumed a chip lntaka of 1 in?/day. This would be equivalent to about 3.5 ft^/yaar. There la no ba*la for stating whether this 1* a reasonable assumption, and it aay In practice be impossible to obtain realistic data. 5.6 LIMIT OH PERCENTACE OF LEAD IH PAINT THAI WOULD KEEP LEAD INTAKE BELOW DAILY PERMISSIBLE INTAKE Assuming a dally intake of L in? 'of six layers of paint per day, and 5-1Cl absorption of lead, 0.06Z lead in paint would keep the daily lead intake below the recosnended 300 ug. This was the line of reasoning adopted by the American Academy of Pediatrics. However, thie conclusion could be grossly modified by varying the assumption* noted above. 4. DISCUSSION It la apparent that there is not sufficient information on which to promulgate a standard based on knowledge of tha essential quantitative relation* that link tha lead content of paint to symptoms of intoxication However, this 1* not unusual in puhllc-heslth practice. Many useful m WPP uyimm L IA 1 7 3 C 0 -25- standards have been established by Informed people who neks judgments baaed oa whatever fact* are available. An alternative to a Halt bad on firm scientific evidence night ba ono founded on a d o re pragmatic approach. One night eetabllah a Halt on the basis of the lowest lead content of palate found la dwellings la which lead poisoning has been reported. The only etateaeat la the literature that deals with this question cooes from Chleola and BarrieoA (1956), who stated. In relation to their own experiencei "Vo case of lead Intoxication has been found where the only source of load contained less than IT of lead In the dried paint surface." Although this conclusion wan published 17 yeers ego. It has not been refuted Vy any subsequent publications. The painte used before about I960 con tained about 50X Iced on the average, and It la not surprising that a fiftyfold reduction in the lead contest would reduce the attach rata to the point where cases of lead Intoxication would not ba observed. This night serve ee e basis for setting a Halt. However, one cannot ba assured that effects of lead Intoxication so subtle as to escape atten tion do not occur at lead concentrations lower than IX. A third approach, and one that has been used in public-health practice, would be to require that the lead In Interior paints be reduced to the lowest practicable concentration. By "lowest practicable" is neent the loweat concentration that can ba achieved by existing tech nology. It le Inplled that the lowest practicable concentration will ba interpreted with restraint and with due recognition given to the eve11able scientific and nedlcal Information, ee well ea the adnlnlstratlve and economic factors. A decision could ba nada to prohibit conpletaly the use of lead in paints, but lead can ba expected to occur In trace quantities mm 1MWWI ^ww^B^iaPwx^iJjiL pwi'W LIA17301 "tnitrilfe 'milfit iH>mrii'ii'r~'i'iiir riV'S^yii' ni'-'Wenfr 'is'>ffndWi ~ 'r *--';. -16- ee aa industrial lnpurity in the Ingredient* that ara used to formulate paint*. This requires that the phras* "d o lead" be defined. If lead la Mt used la paint manufacture, soa* other aaterlala oust take Its place. A Judgment oust be sada as to whether the substitute ostetiala involve less risk to the public health. Finally, it is possible that each progressive reduction in the lead content of paint will Involve greater cost, and cocoensurste benefit to tbe public health should he ensured. Thus, reducing lead to the lowest practicsbls content aoat inevitably Involve a value judgment in which one balances the likelihood of health daaage at a given lead concentration against the likelihood of health damage from substitute materials, the effect of the change on the per formance of the paint, and the cost of making tbe change. The various approaches ere fundsaentally different. The first * two Involve interpretation of scientific data and * decision as to the lead content of paint that will keep lead poisoning froe developing , in the future. The "lowest practicable" approach requires value judgments In which scmlquentltatlve, almost Intuitive reasoning is used to arrive at n conclusion. A standard based on the first two approaches is dearly one that can best be developed by scientists. Bovever, scientists are not uniquely qualified to recoamend a standard based on the "lowest practicable" concept. * As has been noted, so insufficient body of information exists to permit establishment of s standard for lead in paint based on scientific facta. Although lead hee been known to be n toxic material for centuries and Is a major industrial chemical, there has been inadequate research. 9 Although lead la paint has been identified as an etlologlc factor in lead poisoning asong children vlth pica, there is a paucity of epidemiologic WMW..AIIW-.WIIP LI A. 17 3 0 Z -27- data with adequate u m histories by scans of which one could describe the essoclaclon of e given child's blood lead concentration to the coedIt Ion of the painted surfaces to which the child had been exposed. There should be sore lnforeatlon about the clinical significance of blood lead short of full-blown lead poisoning. Such Information cannot bs expected to cose Into being In lesa than e 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 e change on Manufacturing practices end on the quality and safety of the aodlfled products. The course of action ultimately selected should protect the public with e 0f dele terious effects, either on the economics of the Industry or on the quality of the products. Lead compounds art used In paints principally for three reasons: aa pigments, as driers, and as agents to prevent so-called loss of drying in storage. The use of lead In pigments requires such high concentrations In the paint formulation that current regulations setting a aaxiaua of 0.5X lead have for all practical purposes elreedy eliminated lead pigments in household points. Driers (metal salts or fatty acids) help to speed the oxidative hardening of the paint film when the vehicle contains imsaturated components, such as vegetsbla oils or alkyd resins (Stewart, 1969; Bikales, 1961, 1966, 1970). Lead driers (typically laad 2-ethylhexoata, lead naphthenate, or lead tallate used in lead concentrations of 0.2-0.AS based on weight of dried paint film) are particularly valued, because they effect relatively rapid drying throughout the mass of the film. Other driers--such as various fatty acid salts of calcium, cobalt, . jtassst ^ wfWPIIP LIA173C3 'nuawiMi 28 itnc, end zirconium--act conoonly used In conjunction with lead driers In empirics! formulation* designed to give the desired rats c od thoroughness of drying at vidsly varying taaparatura and humidity (Stevart, 19M). A further use of lead compounds la as additives to retard so-called loss of drying, l.e., the deterioration In drying properties of paints > that can occur In storage. Tor this use, proprietary lead complexes are apparently preferred and are added In concentrations shout equal to or somewhat lover than those of the lead driers (based on lead content). Kelatlvely little Information Is available on the types of compounds used or on the nechanlsa of their action (Stevart, 1969). A reduction in the permissible concentration of lead In paints to 0.061 would In sffect prohibit any Intentional addition of lead compounds to pigments, driers, or other paint additives. Paints based e on oleoreslnous substances would require reformulation to ellmlnats lead driers and all other lead compounds. Analytic procedures would be necessary to ensure that no accidental contamination by lead com 4 pound* had taken place during manufacture. Atomic-absorption spectrophotometry la particularly suitable for this purpose, and a slept* colorimetric method he* been devised to Indicate whether the proposed maximal concentration of C.061 has been exceeded (ASTM, 1973). It cam be expected that reformulation to the 0.06Z lead content and the associ ated tasting would require at least a year. The burden would be heaviest on the many small paint menufscturera that lack the necessary technical staff and resources. s?***SWW*OS(pi* *-1A 1 7304 a*. .: c^b^'w-- -29- f Household paints arc generally classified a* intended for Interior t or exterior uee. Interior palnta are likely to represent the greater tI potential hazard because of their greater accessibility and because children, at their nose susceptible age, are nore often left unattended when Indoors. At present, aost interior paint is based on aqueous emulsions; this type of.paint does not usually depend on euto-oxidatioa of unsaturated compounds to harden end therefore does not require any metal salts as drier*. Although emulsion-based paints normally produce surfaces with little gloss, new types that can give a sealglosay finish are now on the market. These era expected to make Inroad* Into tbs last Mjor use of oleoreslnous paints In the Interior of households-- surfaces with glossy finishes, because Interior paints usually dry under more controlled conditions and are not subjected to as severs weathering conditions as exterior paints, adequate points of both tbs emulsion and the oleoreslnous types can be formulated for interior use without any Intentional addition of lead compounds. ?aint* designed for application to exterior surfaces require s useful rate of drying end adequate durability under wide variations of climatic conditions. Ths combination of low temperature and high humidity (e.g., 50 Fend 70S KH) Is particularly stringent. The use of emulsion-based exterior paints, which require little or no drier, is Increasing rapidly, but oleoraslnous paints still account for e large part of ths market. Lead drlera play an Important part In the formulation of the latter type. Lead-containing primers are also useful on hsavlly chalked surfaces and to prevent staining by the water-soluble extractives present In some types of wood. I I 1 J mi inssse.iwsBwnwtmjWj ,gi ij|p4iuii^j;gji 4Hi|P, 11 i|j,i|WjiiJiJUWgi L I A 173 05 -JO- In th* formulation of paints, the lead drier* cannot usually be . '' ellmlnatsd by Bra substitution of an equal amount of another metal alt of a fatty acid. A combination of other metal drier* Bust be i fitted to each particular recipe, and there Is sons question as to whether paints so reformulated are equivalent In quality to thoee containing lead driers. The substitution of other driers for tha lead salts also raises the important question of the safety of the substitute aaterials. Coder current regulations, the Food ind Drug Administration permits the use of some driers for coatings that coae Into contact with food-- namely, soee fatty acid salts of alualnua, calcium, cerium, cobalt. Iron, lithium, magnesium, manganese, aloe, and xlrconlum (Code of Federal Regulations, Federal Food, Drug, and Cosmetic Act). As already pointed -out, several of these metal salts are normally added to paint In con junction with the lead compounds. It Is likely that paint manufacturers will use combinations of these same driers If the lead content must be I reduced to e maximum of 0.061. Zirconium-bated drlsra appear to be the moat useful single substitute. 'The cost of the substitute driers, being higher than that of the lead salts, would raise the rav-materlal cost of the reformulated pslnt by several cents a gallon. The Committee has been apprised of the fact that Chicago, Illinois, slresdy has s local ordinance calling for a naxlmal lead content In pslnt of 0.06Z of dry-weight solids. This regulation was effective on the let of July, 1972, end le applicable only to Interior surfaces of dwellings or dwelling units (doalclles). It specifically exeapts Varnishes, oil steins, floor paints, and coatings In aerosol cans. Conversations with Chicago city officials have Indicated that compliance L 1*173 06 MBJHWJWWW i vlch th* ordinance ha* b*cn successful in perhaps 902 of th* "off-theshelf" paint* tested. Furthermore, th cot of paint produced la th* Chicago area vs a reported to be no higher than th* national average. In tern* of paint already existing on vail surfaces, th* Chicago ordinance calls for a Halt of no more than 1 *g of lead per aquara centimeter of surface. At the present tine, there have not been enough epidemiological data collected to determine whether the 0.062 regulation has resulted in a change In the number of caaaa of Increased blood lead in children screened within the City of Chicago. It la hoped that; In tine, the experience of the City of Chicago la administering this ordinance will provide the CPSC with additional useful Information relative to many of the point* raised in this report. 7. CONCLUSIONS AND gECOJMESDATlOW (a) Although It would be desirable to erMteh a limit on the lead content of paints sold to consumers by a quantitative rational* that take* Into consideration the quantity of paint apt to be Ingested by children with pica, the rate of absorption of lead from the gastro intestinal tract, and the amount of absorbed lead that will produce Intoxication, the Committee concludes that there 1* at present Insufficient Information to permit arriving at a recoemendation on that basis. A broad program of research la required to understand better th* mechanisms Involved In lead Intoxication and methods by vhlcb the disease can b* controlled. National and local health education programs to alert parents to the health hatsrd to children are recooaended. (h) A more pragmatic approach would be to ascertain, through epidemiologic methods, the lowest concentration of lead In paint that has been associated with lead Intoxication among children with pica. The only statement in the literature that deal* with thl* question ..Hi- % gyijPwwiBWs^ji^HHxppwwgwfjiwilM^ 0 -12- LI A 173 07 f '^iV.T-fUf*1--'-- run . "m flj pgHJI. IJ m ip e e |MPV'w .IW mii mi published 17 yaars ago and stated that no case of laad Intoxication had bean found where tha only source of lead contained laaa than IS of lead in tha dried paint surface. Although this conclualon hat not aInca bean refuted, the Comalttea Is unable to conclude that subtle but nevertheless significant for** of lead Intoxication that nay hava aacapad clinical detection hava not occurred froa exposure to paint fllna with laad con- ceotratloaa lover then IX, * (c) The Coealttee haa learned froai repreeentatlvea -of the paint manufacturing Industry that the present requirement that tha lead con tent of paints be limited to 0.5X already precludes the use cf lead compounds aa pigments. However, lead driere are widely used et con centric Iona of 0.2-0.AX (based on lead content of the dried paint film), to help speed the oxidative hardening of the paint film whom the vehicle contains unsaturated component*, such as vegetable oils or a11yd resins. In particular, lead driers (typically lead 2-ethylhexoate* , lead naphtbenate, or lead tallate) used in lead concentration* of 0.2-0.*X are especially valued becauee they effect relatively rapid drying throughout the mass of tha film. Other lead compounds retard tha so-called loss of drying on storage. A redaction in the permissible concentration of lead In paints to 0.06X would prohibit the intentional use of lead compounds aa driers or ss additives to retard tha so-called loss of drying, (d) If the lead content of pelnta is limited to 0.06X, It would be necessary to reformulate laad driere for paints baaed on oleoreelnous substances. This would probably require substitution of metals other than lead. Although tha Committee has no reason to believe that the substitute eetals would introduce oew toxicologic problems, this possibility should be considered before sny steps ere taken that trill require substitution f of other metallic compounds. i;wau)Wu."i !}j.i iiiy ywjijpijni iwtpiujjupai^p ^pusesssB! mm IW IW P .wwt 'IIH'MVW 'U  !W|iPlpqjPIWPif!MtiP!ipWP3pifgp^ LIA17308 i < O w&r -33- () A prograa of reformulation of driers to neat a 0.061 lead requirement would take ec least a year to implement. (f) Evidence suds available to the Cosalttee nakes It clear that the Intentional Incorporation of lead into placenta and driers can ba eliminated for conauatar palnta applied to Interiors, toya, and furniture and that It nay ha poaalhlo to eliminate the deliberate uae of lead-in palate for outdoor uae. However, sco> lead nay nevertbeleaa be preaeat In theae products, owing to Its adventitious preaeoce In proceae materials. (g) Until nora scientific Information can be accumulated from the research programs recommended'in this report, the Comit tee suggests that It eight be vlaa for tbe Consumer Product Safety ComalsaloerYO' Institute aa Interia program of controls baaed on the concept that the lead in paint sold to conauaers be reduced to the lowest practicable concentration. The adnlnls tretloo of this concept should be Implemented irlth doe recognition of the need for balancing costa against baoeflta. It should also be recognized that the weighing of societal costs against societal benefits may not always involvs easily quantifiable considerations; It may be necessary to deflna the lowest practicable lead content oo the basis of the judgments of Informed people rather than scientific enalysls. Teste recently undertaken by the Americas Society for Testing Materials have shown that-"lead-free" paints contained as much aa 0.03X lead. This may be due to iapuritles In the materials used for paint manufacture and to the occasional carryover of lead from one Industrial process to the other or to uncertainties In the analytic procedures, Thera la oo assurance at present that the lead content of lead-free paints could not exceed 0.06^ owing to these factors. Thus, any regulation that govama the maximal lead content of paint products must be based on 0 LIA17309 Q i -34- eooaideration of the practicability of controlling the Iwd chat enters the proeees adventitiously and of the availability of raliabla analytic procedure*. (h) Tha Consumer Product Safety Commission should develop a national paint surveillance ayataa to ensure that established.standards are being sat. As part of the development of this surveillance network., it will be necessary to sponsor tbs development of better analytic . methods for Measurement of trace quantities of leed in off-the-shelf paint sajq4.es. (I) Any standard issued to limit the lead content of paint should be reviewed blannually in the light of whatever additional information becomes available. The limits may be ralaed or lowered, depending on circumstance*. Bovever, ample tine must be permitted for orderly reformulation of paints end driers, and no changes should be made without adequate consideration of the effects on the public health, of the coat, end of the effects on paint quality. The overriding considerations Bust of course be related to protection of the public health. (J) 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 pica has caused the Committee to recommend chat use of lead in paints be reduced to the greatest practicable extent. However, the Committee emphasises that there may he other uaee of lead, now and In the future, that could bring significant benefits to the consumer. In accordance with good public-health practice, more must be learned about the mecha nisms of lead intoxication, so that, as future applications for lead are developed, they may bo incorporated into consumer products without undue 1i 0 a efwwayitfffliw^ LIA17310 tui-uMw, -J>- risk. Th Co^alctea has Identified several research objectives ss having particular importance. S. KXSCAXCH MQUIkEMESTS (s) The "normal" body burden of lead In people of various ages should be better established for a variety of aodes of habitation and socioeconomic classes. (b) The absorption of lead fro* the gastrointestinal tract should be Measured in experimental animals and children having a normal dietary Intake of lead. The studies of children can be accoapllshed using the lead content of the normal diet. (c) Comparative studies of the sbsorptlon of lead froa the gastro intestinal tract of suitable experimental animals should be undertaken vith regard to lead in the normal diet and various paints and driers. (d) The clinical significance of Increased blood lesd content should be studied In children, with psrtleulsr emphasis on the adsptlve or subcllalcel phases. (e) Epidemiologic studies should be extended to Include the sequelae of overt lead Intoxication In children who survive ecuta toxic manifestations. (f) better analytic methods should be developed to measure lead w in off-the-shelf paint samples end body tissues, especially blood. (g) Health departments and hospitals of major urban centers should be encouraged to adopt mutually compatible protocols for mass screening of children end for Identification of the signs and symptoms of lead poisoning. Standard procedures should also be adopted for documenting the lead content of paint to which the children wore exposed. 5 BniihiMiWii BHiiisiaifc LIM73U -3h- (h) Xh Consumer Product S fty Comission should serve es a national registry foe. data accumulated In Ch screening progress and should ltsus consolidated annual reports of tbs findings of uch studies and the incidence of cooounlty lead poisoning In the United States. 1-1/17 3?? f~s t xsl s x kaavlta nf ScrMln| Trcrk** of Ilw4 La4 tvMntnilM* f CkllJrm n^) Living la balar lovat.4 Bnvalag la 0, *. Cttia. . C) City hltlMfi 0>lt(| Yeer ms 1969 1970 1947-70 9w"^r e Chlldreo 643 744 939 120,000 Tratllna .! Olllr,, vlll. Incr.a... Haog Lv.J. t 40 tc/100 1 30 60 l/100 *1 l/lQ0 ml SO xVlOO ml Ceeyacet 23.1 21.9 11.3 20 4 5.6 i.i 7.2 i.* 7.4 1.4 iu*la, mi RmN X<u<rk 1949-70 1970 1,197 394 29.* IS. 9 * 9.3 7.4 VaMngtM, D.C. Tack Ctty 1970 !1?0 1971 1,131 2 ,448 S4.J.J2 7,319 22.0 43.3 29.7 21.7 12 24.3 27.4 10.1 12.3 3.9 4.4 U CwlftM, 1979 KC1 Survey 27 title* 1971-71 1.J00 9.1-41.* fertleei, Km. 1973 90S 2.3 leltlcl ecreealeg for U-AU 0.34 ac/l .1 e tea in --------------------------------- - 703 u.j . j . 3.4 1.0 leltiel icrMU| for (sir U4 ICO c/g Svta (ro V. Catnra. K.D., Sure ( U*4 r.Uo.1.; Control. K<m York City r-yrrf-anT f Kvaltk DOT! Ml. fo. 71-10003 Cleck Mi ttallett 1971 f*CftcJfcl et f 1971 W/ r n^i^ijPRRipps^r. *l m, j ih mp v .iffih # >5 <p ak iMl iM LIA27312 HBMHPMw i IS- i TABUS 2 Balations of Various Me*uraoc* of Lead Toxicity to Category of Lead Effect (Modified from Coyer end thytug 1973) X Blood lasd pg/100 ml ' nr Primary A1A Primary CF Anemia Ptrvous eyetaa affect* bail effect* X Po. effect. <10 wj/100 ml II. Adaptive, 40-AO pg/100 ml b , Subcllnlcal| &0-80 yg/100 ml Dorntl slight increase in Cl laical Toxicity, >S0 pg/100 ml largt lacrease normal slight increase >3 fold moo* moo* moo* retlcolocytoeis decreased nerve conductloot none (inclusion hodiesT) usually staxla, cooa convulsionsi Faneonl ayndroo* chronic aaphropatby ALA " Delca-Aainolevullolc Acid. CF " coproporphyr in rtf freo erythrocyto protoporphyria ' J j1 j ____________________ /i' p<yajiiap|gjgBjg L I A1 73 13 - - -.-V--; *- .1{-<J~l-^..B.-^,t^-.J' ^-,:.-- .-< . ' - > .- -. -- 4 ./ * <<> ~ .- y^ - - TABLE } National Data on Incidence and Kedlcal Significance or cojwwiin c h il d h o o d l e a d roisomic Children In Susceptible Age Croup................... (undtr S years old) .20,000,000 Children at Itlak.............................................................................. (under 3 year* old, live In metropolitan areaa, families la poverty claaalfIcation) 2,300,000 Children with Increased Blood Lead Content.......... .. (blood lead content above AO wg/100 ml) 400,000 Children with Symptomatic Lead Poisoning per Terr................. 30,000 Children with Aaysptosatlc Lead Poisoning per Tear................... (all should be treated) 40,000 Children with neurologic Handicaps, Including Mental Ketardatlon................................................................................................ 4,000 Children InquiringLifetime Institutional Care......................... 130 Deaths per Tear................................... .................... .................................. (includes acuta and long-term consequences of lead poisoning) 200, - 9 The children la susceptible aga group and children at risk ere baaed on Bureau of Census data which have been rounded off. Children at risk are under 4 years old living In dilapidated housing containing hazardous concentrations of lead. m Of those at risk, 2*X are estimated to have blood lead concentrations of at least 40 tig/100 ml of whole blood. The percentage la the median values of surveys in Illinois and New Tork City. If other cltlee are used, the percentage la higher. There Is, however, little lnformetlom from theWest end from small cities. Lilly gm^gggpffWW^JPW"mi^^ 'Hi LI A 1 7314 TA&U 3 - continued -40* from current screening progress--such as those la Kev Tork. Philadelphia, sad Chicago--It appears that about 51 of the children vlth blood lead concentrations over 40 wg/100 ml have clinical algae or syeptoao--convulsions, onmla, craaps, etc. The estleete of asymptomatic children vlth blood leed coneeatrstions about 40 wg/100 ml of vtvols blood is 3.2Z of the population et risk. This estimate la based o q the resales of Illinois end Kev Tork City screening projects. Children vlth neurologic handicaps, including mental retardation, are estlnated at 2CZ of the cooes of symptomatic lead poisoning, on thn basin of follov-up studios In Chicago. i i r' ......  <MW|WgSi!!^pp^TPg|iaWUi^^ LI A17315 '*5oral" iMd Burden* tn the Skeleton And Sole Tlasuea of Adult* and Children* Suhlect* Age, Ho. Tear* Skeletal Lead burden, It Skeletal Lead, 1 o( Total Body Burden Soft-Tlaeo* Lead Burden, g__; Total Body Lead Burden, ' iS Children. both *exe* 10 <6 1.0 (0.21-2.37) 64 0.53 1.53 (0.12-1.58) (0.5-3.1) Adult male* 29 10-8CH- 153 (21-341) i 94 9.5 (5.3-21.1) 162.19 (27-332) Adult fenala* 20 20-80f 107 (12-237) 93 3.7 112.49 (2.6-8.4) (19-244) A. Note: Vusher* In parentheae* ere range*. All number a have been rounded off. *D*ta froe Harry and Hoaanaa (1970). I --i ! Bt.iy*wujntjesawiaiv.ajleM^yi.ewyB.W'Jmj<jiLsv^.e*) .< wawai.Ma " g. .. ... ^S^P^WjS^dP! BlWg^UPmimW.W'PW !Wjpaaiw LIA17316 iimiiwm--wn uni .............. .. m ...... ' 1 "-- .............. l'l --irTlTTriij npiujiji|ij|ii iinj rliiTrTJ'Lii>il',.r.nrij,ii.rja[i.iuii|Mi)niiiJpillffi LIA17317 Lead Content# t ' TABLE 6 Lead Content of feint* ' Lead per Sq. Cm. Per Layer (Microcrams) (IU30 MlUlcr3n*> No. Sq. Os. Co Contain 2(XJug ` Kon-Tood Lend: 2/3 DPI Per Liyer Per 6 Layers Sq. Oa. Sq. In. Sq. Cm. Sq. In. 2 I1.TERI0H PAINT (6.5 erg/ca /layer) 1.00* 0.50 0.20 ' 0.10 0.06 0.05 0.03 65.0ug 32.50 * 13.0 6.50 3.90 3.25 1.95 \ * EXTERIOR PAINT (16.0 ag/ca^/lcyer) 1.00 0.50 0.20 0.10 0.06 0.05 0.03 160ug 80.0 32.0 16.0 9.6 3.0 4.8 ' 3.1 6.2 15 30.1 51.3 61.5 102.6 0.43 0.96 2.32 4.7 8.9 9.3 15.9 0.51 1.0 2.5 5.0 8.5 10.3 17.0 0.08 0.15 0.39 0.77 1.3 1.6 2.6 1.2 2.5 6.3 12.5 20.8 25.0 41.7 0.19. 0.39 .93 1.93 .3.24 3.9 6.5 0.2 0.4 l.l 2.1 3.5 4.3 7.0 0.03 0.06 6.17 0.33 0.54 0.67 1.08 . Ho. Layers Paint in Surface Covering Containing 30uj Pb/Sq. Co. -- (0.03t- fb/Sq. Co.) Kit-Sr r Less than l 1 2-3 4-5 7-8 9 14-16 - Lest than 1 1 7 2 3 4 6 * Maximum Indicated in industry standard 2-66 -- assumed to be the lead content of paint applied since the 1940'e. King, .1971. . " if \ lignum LI 417318 Alexander, P. V,, a. P. Delves, end B. E. Clayton. Ths uptake and a aeration by child ran of iaad and othar contaminant*, pp. 319-331. In Proceeding* of latarnatlonal Sycpcslun on Environmental Haalth Aapecta of Laad. EU2 5004 d-a-f. Luxembourg! Coealaalon of tha European Cocnunities, 1973. American Acadeny of Padlatrie*, Subcoealtta* on Accidental Poisoning. Statanant on dlagnocls and treatment of load pol*onlng In childhood. Padla tries 27:676-MO, 1961. American Aesdeny of Padlatrlca, Coardttee on Environmental Batarda. Laad cootant of paint applied to surfaces accaaalbl# to young children. Padlatrlca 49:916-921, 1972. Aaarlcan Society for Testing and Materials, Beport of Coanltte* DOl, 2103. Phlladalphla, 1973. (Unpublished material) BariCrop, D., and K. J. P. Elllala. 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 Syaposlua on Environmental Health Aspecta of Lead. EDB 5004 d-e-f. Luxeabourg: Coandaaion of the European Cooaunltlaa, 1973. Barry, P. f. 1., and D. |. Meatmen. Lead concentrations In huann tissues. Brit. J. Indust. Hed. 27:339-351, 1970. Batts, P. I., B. Astlay, and D. M. Rslna. Laad Intoxication In children la Birmingham. Brit. Med. J. 1:402-406, 1973. Bikale*, K. M., Ed. Encyclopedia of Polyanr Science and Technology. Vol. 1, pp. 705-727 (1964)i Vol. 5, pp. 126-139, 216-234 (1966)| Vol. 13, pp. 4B6-333 (1970). Sew Torki Interscience Publishers. < j L I A 1 73 1 g r i --45-- ' Blankaaa, L. A., H. K. Sachs, E. P. Murray, and H. J. O'Conn* 11. Incidence of high blood lead level* In Chicago children. Pediatric* *4:061-667, 1969. British Medical Journal (Editorial). Diagnosis of Inorganic lead poisoning: A statement. Brit. Med. J. 4:501, 196B. Chlaola, J. J., Jr., and H. E. Harrison. the exposure of children to lead, Pedlatrlca 18:9*3-958, 1954. __ Chlaola, J. J., Jr. Chronic lead Intoxication In children. Develop. Hod. Child tleurol. 7:529-536, 1965. Chlaola, J. J., Jr, Screening technique* for undue lead exposure In children: Biological and practical consideration*. J. Pediatrics 79:719-725, 1971. Clark, A. J., and C. V. Hallett. Lead polaoolng survey - Portland, Maine, July-August, 1970. J. Maine Med. Assoc. 62:6-7, 1971. Clarkson, T. V., and J. E. tench. Drinary excretion of anlno acids by sea absorbing heavy Betels. Blochea. J. 62:361-372, 1956. Cohen, H., H. Elsenbud, and M. E. Vrenn. The Retention and Distribution of Lead-210 In the Adult R.iboon. Radioactivity Studies Progress Report KTO-3086-10. Voi. 1, 1970. Devld, 0., J. Clark, and K. Voeller. Lead and hyperactivity. Lancet 2:900-903, 1972. de la Burde, B., and M. S^. Choatc, Jr. Does asynptoaatlc lead closure In children have latent sequelae? J. Pedlatrlca 81:1088-1091, 1972. federal food. Drug, and Cost*tic Act. Ragulatlona, Part 121, Chapter I, Title 21, Code of federal Regulations, Subpart f. Paragraph 121.2514. Pina, f. R., C. W. Thomas, R. H. Suhs, R. E. Cohnberg, and B. A. flaahner. Pediatric blood lead levels. A study In 1* Illinois cities of lntaraedlat* population. JAMA 221:1*75-1479, 1972. Vi liHPniliaiaMHiir ' KWWUlTCjllljaMiU.ir:- .*T,r*l" ''"."TT* ",.. '""" <--iesgiiHBM'.wws wiig?npw LIA17320 ii.. -46- * -* ' \ Tullerton, P. K., and M. J. C. Harrieon. Subcllnleal lead neuropathy la nan. Electroeneephalog. Clin. Jtaurophyaiol. 27 (7):718-719, 1969. Cl Islt>n, J. P. Estimates of tbe Nature and Extant of Laad Paint Poisoning In the United Statea. (KBS Technical Note 746) Waehlngtoa, D.C.: Rational Bureau of Standards, 1972. 131 pp Coyer, t. A., and J. J. Chleolo, Jr. Lead (Chapter 3, pp. 57-93). In D. I. K. Lee, Ed. Metallic Ccmtanlnnnta end Human Health. Mew Tork: Academic Press, 1972. Coyer, K. A., and B. C. Rhyne. Pathological effects of lead. Internet, lev. Exp. Path. 12tl-77, 197J. Coyer, K. A., K. Tsuchlya, D. L. Leonard, and H. Kahyo. Aminoaciduria In Japanese workers In lead and cadmium Industries. Acer. J. Clin. Path. 57:635-642, 1972. Oulnae, 9. P. Lead poisoning. Amer. J. Med. 52:283-288, 1972. Bernberg, S., and J. Klkkanen. Effect of lead on 6-aslnolaevullnle add dehydratase. A selective review. Pracov. Lek. 24:77-83, 1972. Bernberg, S.. J. Klkkanen. C. Mellln, and H. Llllua. 4--aminolevulinic acid dehydrase as a measure of lead exposure. Arch. Environ. Bealth 21:140-145, 1970. Ingalls, T. H., E. A. Tlboul, and M. Verrln. Lead poisoning in Philadelphia, 1955-1960. Arch. Environ. Health 3:575-579, 1961. ' * Kehoe, E. A. The normal metabolism of lead. (Prom The Barben Lectures, 1960: The Metabolism of Lead In Man in Bealth and Disease) J. Boy. Inst. Pub. Health 24:81-97, 1961. Kehoe,*R. A. The metabolism of lead under abnormal conditions. (Prom The Barbeo Lectures) J. Roy. Inst. Pub. Heslth 24:101-120; 129-143, 1961. t; Kehoe, E. A. Present hygienic probleae relating to the absorption of lead. $ r" (Prom The Herben Lecteree) J. Roy. Inet. Pub. Bealth 24:177-203, 1961. LI A1732I mMpvw /* -47JUbo*, R. A., 7. Tha-jnn, and J. Cholak. Oo the norm! absorption and excistion of lead. IV. Lead abjarpcion and excretion in infant* and children. J. Indut. Hyg. 15:301-303, 1933. Ring, B. C. Maxima deily intake of I*d without excceelve body lead-burden In children* Aaer. J. Dl*. Child. 122:337-540, 1971-*. Ring, B. C. Kemorendua: Criteria for Evaluating Lead Retard of Painted Surface*. Bur. of Conamlty Environmental Management, May 1971-b. Raelp, T. J., and C. R. Laurer. Isotope excited x-ray fluoceacence. Analytical Chem. 44:57A-67A, 1972. Lin-Pu, J. S. Undue abeorptlor of lead anong children. A new look at an old problem. Kew Eng. J. Med. 286:702-710, 1972. 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Statement before th* Dally Permissible Intake ad hoc Committee meeting, Cinclnneti, Ohio, 1971, 9P eMWMiuuifje i ,'nw ' jWMWpw LI A17465 -4r- r* y, t. ' **o : : 'U-h Xt.ii, , 'd. Kir*. 8. c, j'*f . Ci t.h* n i ' ibao'pclcn rnl ' . < : . I". 11 < f-1 1, l-ld 10!. J-'V '< i 1 - - ` i s/ < *>cly .fid !> *'n u n;-:iO <: ' 1-In.' : ' .H Surfi'ifi. i Cu >a>n > .,/ -* g* it, -H*/ ;97l-fe. Koclp, T , ini ?. Ui.fn < *y flu.-r*c3c. Aal/tlcl Oi*^. 44;>'A*6 7A, 1972. Llp-fu, J. S. ','nd aHsc, /tlv. ut 1**4 *' . >6 cM Idc. 4 d m 3o c V t n ! 1 profc>!#a, '"<v 4.4 ,. Hsd ?i}A:7Q2 710, 1972. -41 s; j- ' -l'-i' ' *e 1-d ! -/ * 1 ' - .. , i-d i 1 >'* v' ' Aca.`---y of * -I .**, ;97i. 50 U . !9*<4 s ,1. - 7 '< :.hl24r*a ' cn (*jd ' -ii !>>.. . . : , i ' *.j M>s4c ' - , >.. Tr;ic.xi, *M < :! / JA 1* I' ,r. Til c4cotr{ * >t id b!.4 ini *w ;* `<t -I'i * sod -M14 ' > 1 '_* - i\ ' <1-/97, 1958. lntf'-l, 7. 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