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No. 23 I.KAO F.XFOSURK-UN-FU 1229 :tlon oiri. n,|* >}*IC 10 Dr. IX I- Sackctt. di.iirman, Department of r.ji;(U-iniolOi'y and Uiostati-tics, for cliseusMom that pro- . stimulus- to carry out this study, to Or. G. If. Hill, formerly professor of clinical epidemiology smd biosutlxtics, and .. 11 . i.'i, Health and Welfare Division, Statistics Canada, who :i the clii-Kjuaro tests of statistical significance and ottered . Vi' aid in age staiulaulizmc; and analysing the data, to Dr. -in-tom. visiting professor, McMastcr University. and Pro- -> Medicine and Epidemiology, Yale University, who helped f j>:t!.ili-/ation of the study and the data analysis, and to lVacorh for assistance. ` t dtii i? ter- I for | - in i ir.v for e is tltt: .les ml ! tit- 'n.fiils. #*y Re f e r e n c e s ;. r JP: Suntic.*! manpower: A comparison of operations and suf... . ji! the United States and in England and Wales. N Engl J MeJ l.'.MJ;. !V/li r. -*n HK'.Stnerlby ft, Uerfciuiaro R. eial: Hospital caseloads in l.iv.-I. New England". m! Uppsala: an international comparison. Lan- : *}9-S66. MS (.*. / lirituin. Ministry of Health. Report on Hospital In-Patient I: ..'!% for the year 1966. London. Her Majesty's Stationery Office, t .. nl.t. Dominion Bureau of Statistics. Surgical Procedures and Yreati-:.--1968 (Catalogue No 82-529). Ottawa, Information Canada. \t .sit. 1971 Hr. it Britain. Ministry of Health. Report on Hospital In-Vatient F.n.:. % tor t'icyear 1967. Parti. Tables. London. Her Majesty's Siationcrv t'-'->70 ' l States Department of Health. Education, and Welfare. Public 1l..lih Service. Notional Center for Health Statistics. International ('I'Mlieation of Diseases. Adapted. 1962 (Pi IS Publication No 719). 2 c.** Washington. DC. Government I'citilittg Office. 1965 c.r.-.it Dritain. Ministry of Health. Genera! Register Office. Code ofSurc.d bmcedures. London. Her Majesty's Stationery Office. 1956 8. Bradford Hill A: Principles of Medical Statistics. Eighth edition. New York. Oxford University Press, pp 201-219. 1967 9. Canada. Department f National llc.tlili and Wetfare. Medicosocial Statistics Office. Statistic* on the Supply and Distribution of Active l'hy - sicians in Canada 1969-J972 (Bulletin 1). Oeiolier. 1972 10. Great Britain. Department of Health and Social Security. Digest of Health Services Statistics for England and Wales 1969. London. Her Majesty's Stationery Office. 1969 11. Stevens R: Medical Practice in Modern England: Theimpact ofspccialiration and state medicine. New Haven. Yale University Press. 1966. pp 306-211 12.- Great Britain. Department of Health and Social Security. Health and Persona! Social Services Statistics. 1972. London. Her Majesty's Station ery Office. 1973 13. Statistics Canada: Hospital statistics: Ptefintinary annual report. 1971 (Catalogue No 83-217). Ottawa. Information Canada. 1973 14. Canada, Dominion Bureau of Statistics Hospital Statistics 196$. Yol I. Hospital beds (Catalogue No 83-210) Ottawa. The Queen's Printer, dune. 1970 15. Canada. Dominion Bureau of Statistics. Causes of Death: Canada provinces by sex and Canada by sex and age. I96S (Catalogue No 84203). Ottawa. The Queen's Printer. 1970 J6. Great Britain. Minhtry of Health. General Register Office. Statistical Review of England and Wales for thcyc.tr 1968. Parti. Table* - medi cal. London. Her Majesty's Stationery Office, 1970 17. Lewis CL: Variations in the incidence of surgery. N Engl J Med 281:880-884. 1969 18. Hurtado AV: Utilisation control and quality assurance at the KaiserPerni.inente Medical Care System. Portland. Oregon. Presented at the Medical Directors Conference. Health Maintenance Organization Ser vice. HSMH.VDHLW. Denver. Colorado. April 23->s. 1973 19. Hesbngv JFl'. Mott FIX Hewitt D. et al; An interim report on the Sault Ste. Marie Study: a comparison of |>crsonal health services utilization: a joint Canada-World Health Organization project. Can J Public Health 61:289-206. 1970 20. Weddell j: Cited by Cochrane AL: Effectiveness and Efficiency: Ran dom reflections on health services: the Rock Carling Fellowship 1971. London. Nuffield Provincial Ho>priaL Trust. 1972. p 32 he MEDICAL PROGRESS nc <0 i VULNERABILITY OF CHILDREN TO LEAD EXPOSURE AND TOXICITY (First of *1Vo Paris) Jan e S. Lin -Fu , M.D. T LAD poisoning in adults is largely an occupational o Lj haza,-d that can be kept under reasonable control, *' and the source and degree of exposure are generally known. I it recent decades, improvements in industrial y methods and in occupational health standards, such as irt'iiuuion of periodic examinations of exposed work<r et' tor early evidence of undue lead absorption, have redoa-d severe occupational (cad poisoning considcran kh. particulaily ;n the larger industries. In contrast, ' childhood plumbism generally occurs as accidental ! pti-tming amen? voung children who cannot be kept wider constant surveillance. Although peeling lead- 1 bawd paint in old houses has been implicated as the major source of severe exposure among children, the J *<iiro of poisoning, in many cases, remains undeter mined. i I :--m the Office ofClinical Services. Health Services Administration. PubL M-.'atih Service. U.S. Depunment of Health. Education, ami Welfare. UUille. Md. 20S52. I^cad poisoning caused by paint ingestion in infants and children was reported in the Australian literature around the turn of the century5 and gradually gained recognition in the United States as a public-health problem in the 1920's, when pica was linked to its oc currence.**' Despite the apjxiarance of scores of papers in the medical literature in the ensuing years describ ing hundreds of cases with a formidable mortality and morbidity,"'there was little systematic effort to deal with this problem. When titanium oxide began lo re place lead pigments in interior paints in the 1940's, man)- thought thal lead poisoning in children had be come a problem of the past, not realizing that millions of bouses still had lead-based paim on them, and that exterior lead paint and other lead sources may also pose a hazard.'"TM Thus, unlike industrial plumhism, the childhood lead-poisoning problem remained essen tially unchanged for about half a century, during which only a few cities made limited attempts to deal with GID350I0 J t visa THE, NF.W F.SC1AND JOURNAL OV MKMCIXti Hoc. fi, t'-rt ! [ i `; In the late 1960's, the public as well as health work ers suddenly awoke to the fact that lead poisoning was still taking a high toll among children in many areas."41 A long-neglected fact also became obvious: lead poi soning in children, as in adults, is in fact a preventable illness. After this awakening, many cities set up or ex panded screening programs for the detection and treat ment of children with lead poisoning. Much hud been well defined boundaries of these areas began to disap pear, It has also been suggested that with replacement of the old inner-city dwellings by urban renewal nul i oilier modern construction, the location of reported {; eases has moved outward to other parts of the cun*.- | furthermore, as screening programs were launcHd , J in smaller cities, it became apparent that absorption uf 4 excessive amounts of lead is not limited to children in ' 1 known about the epidemiology of childhood lead poi large urban areas. A 1971 Illinois survey involving [ soning by the late hut data collected since 6151 children one to six years old living in 14 cities of {, then have revealed some new facts that few were pre intermediate size (10,000 to 130.000 population) n- ,i pared for. A recent survey of 21 screening programs that tested vented that 18.6pcrcent had blood lead levels of 40 1:0 i ;\ per 100 ml or more -- a figure similar to that repotted j :.ji a total of 344,637 children between 1969 and 1971 re in large urban cities; 51 children (0.8 per cent) had I vealed that 8.8 to 32.9 percent had blood lead levels of blood lead levels of 80 pg per 100 ml or more.** j -/ 40 pg per 100 mi or more -- levels indicative of undue Nor is the problem prevalent only in the eastern part I . lead absorption.^ The overall average percentage of of the United States as some had thought. A 1971-19/.* ,* children found in these programs to have such lead lev survey of 27 cities in 23 states located in the Midww. ' j els was 26.1, which is not essentially different from that South, West, North and East of the country, invoh i;} .! reported earlier by a few programs.1' In this survey, 0 to 19.4 per cent of the children screened had blood lead levels of 60 pg per 100 ml or mote, anti 0 to 7.6 percent 2309 children, revealed that children with blood lead levels of 40 /ig per 100 ml or mot e were found in ail but four cities. In the cities where no such children, wnc < \ had levels of 80 pg per 100 ml or more -- levels des found, only a very limited number were tested.*' j ' ignated by the United States Surgeon General as Even children living in rural areas are not spared j constituting "unequivocal cases of lead poisoning" to from this health problem, though the prevalence an- f. be handled as medical emergencies.r`,J It should l>c noted that these figures arc based on testing of prese lected populations, most of whom arc from old and poorly maintained neighborhoods, but they do reflect the gravity of the problems of undue lead absorption and lead poisoning in children in many areas of the United States today. pears to be lower. A recent survey of 230 rural chikh.u [ one to five years old from Dutchess County, New York, and Litchfield County, Connecticut, revealed that JO. j*. or 9 per cent, had blood lead levels in excess of 40 jiy Y. per I00ml,andvahicsa.shghas70jugpcr 100ml w<tv :* found. Ninety-one percent of the children tested w< < white, and some came from middle-class and upp'i- Perhaps even more surprising to many is the recent middlc-class homes/* finding that these phenomena, earlier thought to be The importance of undue lead absorption in eh:!- found only in the ` inner cities" or "lead belts" or then has previously been reviewed.1It is lVec|t.n "urban slums," arc now reported to be no longer so the prelude to actual lead poisoning; unless further well confined. In Baltimore, screening results in the hazardous exposure is terminated, poisoning will ou :ii five-year period 1966 through 1970 showed 43.3 per in one to two months.ai-4!* Its recognition is therefore cent of children with blood lead levels of 60 pg per 100 vital to the prevention of lead poisoning. Moreover. ml or more came from outside the so-called "inner young children may be particularly vulnerable to lead - city." In 3971 and 1972, 38 per cent of the children toxicity, and deleterious effects may occur in the ahfound to have blood lead levels of 40 ng per 100 ml or sencc of overt clinical evidence of poisoning. Several re more came from such outer areas. Of 19 cases of child hood lead poisoning reported to the City Health De cent studicssuggcstcd that the frequency of intellectual impairment and other psychologic deficits appeared to ; partment during this period, 11 were from the inner be increased among children with evidence of undue city, and eight from other areas.* Philadelphia also lead absorption who were not thought to have f uii found roccntly that approximately 50 per cent of the poisoning,4*'41 Others reported that anemia is conmior reported eases of childhood lead poisoning arc located even in those with blood lead conocmrationsof 37 w ; outside what was formerly referred to as the ``lead pg per 100 ml -- levels that have often been accepted >- bells" or "inner city." Some came from census tracts harmless in the past.** where the property values were equal to or greater than Studies of blood lead levels in adults comparable that of the average property value of most dwelling those in children cited above arc not available. How'- units in the city of Philadelphia, indicating that this er, undue lead absorption is unlikely to be as prevail!' health problem is not necessarily found only in the among adults as in young children, except in those v iv ' "slums."* As these cities began to cover areas not con arc occupationally exposed. A 19G1 survey of bk ; ventionally thought of as "lead belts," die previously Sc Hu c Ut CiW: Hattinu'fc <`ii> i-atioivi. 'SoSofc'fv. Wi: f'liil.ttkJphw committtittitirttic. Department. jvruw.tl iviumuniof Public Health, personal lead levels among adults in six cities (New Oik ->r''Ualtas, Denver, Chicago, New York and Cinema. revealed that of 735 samples tested, 2.7 per cent w,v over 40 pg per 100 ml."4 in a survey of 106 person- w downtown Philadelphia, 2.8 per cent had such low!- CLD3S011 l .FAD KXl'OSl/RK--MN-I'U 12.il ^1 and uoitcd rilics.' nched lion of ren in ohing lies of n) >e- -10/1*ortcd i) hud ** (i pari 1-1972 dwest. olving d lead ill but i were pared cc ftpildren York, mi 20, 10 /g l were 1 were I|Jp<T- i cluttciitly uvthcr occur rclore rover, o lead :c flb- lylre- .-etual red u indue lead imivii to on ted as hie it* DWfV- . alertt v win* Mood leans, tmui! were 'its in rvcK v,rute of HI jjersons front suburban Philadelphia had ), .-elsexceeding 40 /<g per 100 nil.*" Among those oecu- ii idonaliy exposed, the figures varied front 12 percent it service-station attendants to 67 per cent in garage t cltanics in (his survc),.r''' i ,cad is a ubiquitous trace element in modern man's , t -.tronmem; exposure to it is inevitable, even for the ,born fetus.-'1-''* But what accounts for the much hijior prevalence of undue lead absorption among i- ung children? Can exposure to peeling lead paint in ,!! houses explain this phenomenon adequately, or arc ,1/hhen exposed to a number of other- hazardous lead .;>::rccs? Arc. children more vulnerable than adults to tit-* same type of exposure? And perhaps even more im- jv-riant, arc they more susceptible to the toxic effects of ;lii- potentially lethal element? If so, what might ac- riKint for it?'Flic following is an attempt to find at least ji.wiial answers to these questions. ^____ Le a d Ex p o s u r e in Cu h .d r k n ua l-Based Paint : he literature generally indicates that the source of Nj>smcih clifldhood lead poisoning is almost invaria nt-. lading lead paint and broken lead-impregnated ill.- -ter found in poc>rlyjnauHaincd old houses.A .-.ireful review of a number of reports, however, left Mui.i- eases unaccounted for. Christian reported that of '*y< children with lead poisoning seen between 1959 .urd 1964, only 575, or 62 per cent, were known to have :ii"`*sicd paint.'3 Of 1155 children treated for lead poi....;ng in Chicago between 19G7-1968, 78 per cent gave .i ji'-sitivc history of pica for paint and plaster.5' Some liii .lren with a negative history arc found to have posii\' abdominal x-ray studies and deliberate denial by -..> fills or failure to observe such ingestion must ac- it for such cases, but for a number of children, sources of c x j k j s u ic cannot be ruled out com- ;>l*-rely. 1 unlu rmorc, analysis of paint in homes of children wiiii lead poisoning has not consistently revealed a !;.i/.irdons lead content. Tyler reported that of 5466 'tunnies of paint obtained from the home environment *l' i'\Kl-poi?ordn< victims in Philadelphia between :'`f5 and 1962. only 57 per cent yielded positive find- . defirted as paint with more than 1 per cent lead.55 hi a poierdal source of lead was uncovered in ; }x t com v :::e paint samples obtained from New h" r. City dwellings in which children with lead poi- lived.'"'' Paint with 1 per cent lead cannot be '-.i-idcrcd safe, and the negative results may to some 'tout reflect a sampling problem, since repeat investi-'-`u .;i often yielded more positive results. Also, chvellh'-* other than the children's homes where they may *" - considerable time are often not known to the in- utors. But, again, the .possibility of oilier sources h- /arrlous exposure must be considered, i n- above data should not lie construed as incant ro- Me evidence that children with a negative history ' u t-stion or negative findings on housing inspection did not get poisoned from lead paint, but should serve to broaden perspective on the problem and stimulate investigation tntfl other possible .sources or hazardous exposure. Some sources occasionally implicated in'ChrdT'lead paint on furniture, toys and other items easily accessible to children, improperly glazed earth enware, lead fumes and ashes produced by burning lcnd-baltery casings, and other miscellaneous items.24-hi recent years it has also become in creasingly apparent that a number of sources other than those mentioned above mav contribute appreeia. bly to Hie lend intake of young childrea-mid-mav even be a means of poisoning. An outgfading io thcTXTTcmcly KTgfi lead content of street dirt and sur face soil in many cities. Dust and Dirt A 1971 Midwestern city survey found the average lead concentration in dirt collected from residential sites to be 1636 fig per gram, and that from commercial sites to be 2413 fig per gram.*2 In 1972, a study of lead content of street dirt in Washington, D.C., revealed an alarming concentration of 12,820 ppm (12,820 fig per gram) in samples collected from a very busy downtown intersection; lesser but still remarkably high concentra tions of 4000 to 8000 ppm were found in samples from many other sites.* Surface soil in some city parks'also lias very high lead content. Samples collected from MacArthur Park in 1-os Angeles, for example, were found to have a lead content of 3357 ftg per gram.** In Charleston, South Carolina, a survey showed that soil lead values varied widely from 1 to 12,000 ppm; values of over 1000 ppm were found in samples taken from the yards of 11 of 13 houses where childhood lead poi soning had occurred, suggesting a possible relation be tween lead in dirt and poisoning in children/' House hold dust samples in the Boston area have been found to contain 0.1 to 0.2 percent (1000 to 2000 ppm) lead.5' Sayre cl al. recently investigated house and hand dust as a potential source of lead exposure in children. They found not only that inner-city children have higher mean blood lead values than suburban children but that the lead contents ofdust collected from homes and hands of the former are significantly higher than that of the latter, and that there is a definite relation between individual hand and household dust lead con tents. These investigators suggested that among innercity children, hand-to-mouth activity could easily resultJiiJngcsuon of a considerable amount of lead/* ^ The importance of the high lead content of dust and */ \ dirt can be viewed in its proper perspective bv consul- ir cration of thcjdailv ncrirnssnnc intake ol lead for chil dren one to three years old, which was set at 300 ftg bv a iJ^ublicHcahh Service acf hoc committee in ]97L^-J This level was specified without benefit oflatcr flaiaindicaling a greater gastrointestinal absorption and rctentjon of lead m children than in adults. The average daily intake of lead from diet and air among young rKfitM.fi AJ: Persona! cominunicitlion. GLD35012 mi TJJK NIvW KNGLANO JOURNAL OF MLOIOINK Dee. G, !>?< Vo! children probably amounts to one-half to two-thirds of the daily permissible intake, thereby leaving a very narrow margin of safety." Recently, JJarltrop and Alexander suggested that the daily lead intake in young children be limited to less than 3QQ "Sucking clff'ty'fingeTSpcauiigVUTT'tinclcan hands, consumption of food items dropped on the ground and mouthing toys or ether objects coaled with dust or dirt am common practices among toddlers and young chil dren. For those who reside or play in an environment where rfust-and dirt of high lead content are readily available, it is not unrealistic to speculate that inges tion of an amount exceeding, and even many times, the daily permissible intake could be a common occur rence. For children with pica for dirt, the grave danger of exposure to din of high lead content is obvious. One should, however, not lose sight of the fact that lead con tent of dirt, expressed in parts per million, is relatively low as compared to that of old lead paint, which often amounts to 5 to *10 per cent or more of the final dried solids.* Ambient Air Ambient air is another source of lead exposure among urban dwellers. Ixad concentration in ambient air varies inversely with altitude,1and devices used in measuring air lead concentration arc rarely, if ever, placed at the height at which young children breathe. This fact is seldom given consideration in calculations of the-respiratory intake oflcad among young children. One study indicated that lead concentration at 20 me ters above the ground is only half the amount obtained at 1.5 meters.*-' Miscellaneous Sources A number of lead-comnimng items that may not be a source ofexposure among adults can be a real danger among young children with pica and those with in creased oral activity. Newspapers, magazines and chil dren's books with ink of high lead content arc good examples. A recent survey showed that certain yellow, red and orange colors used on newsprint yielded lead contents of 1000 ppm or more. One sample had a lead content of over 4000 ppm.^Clnldren with lead poison ing who gave a history of eating pieces of newspaper rather than paint have been cited.7* Other miscellaneous sources include lead in the paint coating of pencils, which poses a hazard for chil dren who habitually chew on their pencils, l^cad con tent as high as 12.5 per cent has been reported in such paint,7-* Chewing of toothpaste tubes and ingestion of toothpaste with high lead content have been cited as another mode of hazardous exposure among children. Surveys of toothpaste, toothpaste tubes, and coatings of the tubes have revealed lhat,thc lead content of the outer coatings of some tubes exceeded 5 per cent, and some toothpastes in contact with the tulles had lead The Pencil Makers Association. representing 90per cent of the U.S. pro ducers, has announced the e.t.t Nollmentora cottiliealion program to ensure that lead in member companies' pencil paint does not exceed I per cent. contents of 180 pg per gram or more.7 * 71 Some canned infant food and evaporated milk have also Ix'cn found to contain appreciable amounts of lead.*-'1'4 Re f e r e n c e s 36. 1. Lend: Aithome lead in perspective. Washington. DC. National Ac.u!e* my of Science's 1972 1 2. Chisolm H Jr. Kaplan E: I .end poisor.Vj i- childhood: comprehend.- management ami prevention, J Pediatr "3 *-2-950. l%8 3. Lln-ITi JS: Lead Poisoning In Chitdrer. ?;{.* Publication No 2|}>0i Washington. )X\ Government JVinlir.g C-Sre. 1?70 t 4. //cm: Preventinglead poisoning in chi'jr*;. C-:!d Today 2:2-6.36. I*)?; 5. GibsonJL: A plea for painted railings *ri painted walls ofrooms .tv th.. source oflcad poisoning amongst Qujer'i.'d children. Au'l Med thw 23:149-153. 1904 6. Bhekfan KD: Ixad poisoning in child.especial reference to lead as a cause of convulsions. Am J Med Svi iS3:877-8$7. 1917 7. Stroitn RA: Meningitis, caused by lead po.s.v.ina. iu a child of nineteen months. Arch Pediatr 37:532-537. 1920 8. Ruddock JO Lead poisoning in children with special reference to pica JAMA 82:1682-1684. 1924 9. McKhatm CP: Lead poisonine in children with notes on therapy. Am J D Child 32:386-392, 1926 JO. McKhann CF, Vogt UC: Lead poisoning in children. JAMA 101:1 [Ji ll 35, 1933 11. Donnally f((f. Schulz. CA. Nimetz A: Chronic lead poisoning in c.-rl. childhood. Va Med Mon 62:83-89. 1935 12. Nicholson \VW: Lead poisoning in children. Kentucky Med J 33'lxti 131. 1935 13. Bttcy PC. Buchanan UN: The simulation of intracranial tumor by Km,1 encephalopathy in children: with remarks concerning the surgical ik -.u - ntent of live latter. JAMA 105:244-250. I93S 14. Goctixch E. Mason JIM: Glycosuria in lead noisoninv. Am J Di* Chile 59:119-128.1940 15. KowatoiTI: Lead encephalopathy. Am J Dis Child 61:547-556. 16. Kaplan E. McDonald 3M: Blood lead determinations us a Health De partment laboratory service. Am J Public Health 32:481-486. 1942 17. McDonald JM.KaplanK: Incidence oflcad poisoning in ihccityof'lak .' timore. JAVIA 119:870-872. 1942 18. Byers RK. Lord F.E: Late eifeets oflcad poisonine on mental dc'v'vp 1 meat. Am J Dis Child 66:471-494. 1943 19. Stetson CA Jr: Pica: its relationship lo lead poisoning in children. I Maine Med Assoc 38:10-12. 1947 20. Feldman HT: Lead poisoning: salient features in its diagnosis and treat ment. Clin Pxr Child Hosp 7: >94-205. 1951 21. Chisolm JJ Jr. Harrison HE: The exposure t>fchildren to lead. Podia::** 18:913-958. 1956 22. McLaughlin AtC: Lent! poisoning in children in New York City. l,;i`l 1954: an epidemiologic study. NY State J Med 56:3711-3714195*' * 2J. JenkinsCl).MellinsRB: Lead poisoning in children: a study oftoil' ->' ; eases. Arch Neurol fttjvhiatry 77:70-7& 1957 < 24. Byers RK: Lead poisoning: review of the literature and report on 4: cases. Pediatrics 23:585-603. 1959 25. Cohen GJ. Ahrens WO: Chronic lead p<w.\<>rting: a rev icwof seven w.if' experience at the Children's Hospital. District of Colombia. J Peduu 54:271-284. I9S9 26. Ingalls TH. Tihoiii FA. Werrin At: lead poisonin'; in Philadelphia I9S5-I960. Arch Environ Health 3:575-579. 1961 27. Jacobztner H. Rayhin IIW: The cpidentiok'ay oflcad poisonine in - hi!- dren. Arch Pediatr 79:72-76. 1462 28. Griggs RC. Sunshine I.NcwiU V.Vct al: Fnvi.-.>i'.meni.il factors in hood lead poisoning. JAMA 187:703-70.'. 1964 29. Christian JK, Cetewyez RS. Andetman XL: A three-year study <v !.'.v poisoning jn Chicago. Ant J Public Health 54:1241-1251. I9M 30. Chisolm JJ Jr: Chronic lead inio\ie,tiion in children. Dev Med t la'- Neurol 7:529-536. 1%5 31. Jneoh/iner II: Lead poisoning in childhood: epidemiology. ntanit.-t-- lions, and prevention. Clin Pediatr 5:277-286. 1966 32. Perlstein MA. Attala R: Neurologic sequelae ofplmtibism in olfft-f-v Clin Pediatr 5:292-298. 1966 33. CotVmR. Phillips JL. Staples WI.et al: Treatment oflcad cneeph.t>"|v thy in children. J Pediatr 69:198-206. 1966 ig.; .w.1' 4! 45. 4:v: 4S. ii JI.-7 ;} ^ V. 54.'' 'Since January 1. 1973. there has been a co-operative I'DA-iWs-tn tpiality-assurancc program covering all evaporated-milk plants in tl- nation to limit lead content of such products to less thaw ft.5 ppm ' the recommendation t>f the I DA. the infant-food niamtfactorcf' Jft. actively developing methods to improve their cans ami reduce content of canned infant food. GUD35013 '^o bu 'c t >> l k a u r:xi*osuKi:-UN'-ar 1233 _____ ,yj Jr: 'I he it>cof chelating agents in the treatment ofacute and * lead intoxication in childhood. J PeJialr 73:1-38. 1968 \ (iT.I'u JS: Ci.itdhood lead pois<!>xug: an cradicaMc disease. Children ,-..'-7. I<270 . it.'tlKtfWW l-O. Lead p.'i>onin!' - the silent epidemic. N Engl J Med ;,?-.7(U-7V5. 1970 i, isint! J: r.flimjtcsnf the nature and extent of lead paint jxiRoning in i'.- United States (N5S 7N-746J. WasItirtgRnt. IX*. Department of i .mmerce. National Bureau of Standards, December 1972 j u JS: l-nditeahvirptlynoflead amongchildren n new look atari ,-V problem. N l.ngl J Med 2S>''.:?02-710. 1972 , M'dical aspect- of childhood lead poisoning. HSMItA Heutifi f<cp V net-143. 1971 I. PR. Thomas CSV. Sithe R.H ct at: Pediatric blood lead levels: a *, in 14 Illinois rities of intermediate population. MM A 221:1475- I ;**. 1972 l I.I.liuW Lead Poisoning: A .summary report of ft survey in 27 cities. ,!>!){,VV Publication No 73-t<j002). Washington. DC. Government looting OSlice. 1972 ; 1 epow MD: Testimony presented before hearings of the Senate Com merce Committee. Subcommittee on the Environment. May 8. 1972 iS.-n.tl No 92-75). Washington. IX'. Government Printing OJlice. W`2 fin-olm JJ Jr: Increased lead absorption: toxicological considerations. Pediatrics 48:349-352. 1971 VI.'.vriotMA. KowmidesOP, CJnytonBE, ct al: l.cad poisoning in chil dren. Arch Di> Child 39:M3. 196-1 David O. Clark J. Vocllcr K: Lead and hyperactivity. Lancet 2:900-90.2. I"*2 deli Ftiirde B. Choate MS Jr: Does asymptomatic lead exjvwure in chil dren have latent sequelae'* J Pcdialr 81:1088-1091. 1972 I'ue-chcl SM. Kapito L. Schwachman 11: Children with an increased tv-.ivt burden: a Screening and follow-op study. JAMA 222:462-466, K2 h. ; - PR. Astley R. RaiucDN: Lead intoxication in children in Birming ham. Hr Med j 1:402-406. 1973 |l. !ctUer DM. Cateott (:J. Keenan RG. ct al: The public health signiiie mce of atmospheric lead. Arch Environ Health 3:568-574. 1961 Survey of Lead in the Atmosphere ofThree Urban Communities (MIS Publication No 999-Ap-l 2). Washington. DC. Government Printing Of* tKv. 1965 Vedlerwau HL. Scanlon J: Getting the lead out. N Engl J Med 2s v .4<^-467, 1973 S..:nh>n J: Human fetal hazards from environmental pollution with cert.iai non-essential trace elements. Clin Pediatr 11: 135-141, 1972 Christian JK: Childhood lead poisoning: a major urban health problem. Vhr Med J 54:677-682. 1969 V-lt* HK. Rlunhwtia LA. Murray FK. ct al: Ambulatory treatment of Se.iJ pv'isoning: report of 1.155 cases. Pediatrics 46:389-396. 1970 55. Tyler RL: Philadelphia tvnihais "silent epidemic** in the ghetto: lead poisoning contiv'l. J Environ Health 33:64-71. 1970 56. Gurnee VF: Lead poisoning in New York City. Trans NY Acad Sc< 33:539-545. 1971 57. 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