Document 65j2oR9wb1vgYRwVpMbJgeXvo

J- in ir I i i ^T-n'r^ikd* REPRODUCED BY U.S. DEPARTMENT OF COMMERCE NATIONAL TECHNICAL INFORMATION SERVICE SPRINGFIELD, VA 22161 =. *f$,V5B5*sis`y ''" 's DISCLAIMER Mention of the name of any company or product does not constitute endorsement I / the Agency for Toxic Substances and Disease Registry. ii DUP040009434 THE NATURE AND EXTENT OF LEAD POISONING IN CHILDREN IN THE UNITED STATES: A REPORT TO CONGRESS Agency for Toxic Substances and Disease Registry Public Health Service U.S. Department of Health and Human Services July 1988 ) DUP040009435 (3) The costs of preparing and submitting the report required by this section shall be borne by the Hazardous Substance Superfund established under subchapter A of chapter 98 Internal Revenue Code of 1954. Since much of the data needed for this report was not readily available in an appropriate format in the peer-reviewed literature, but was developed specifically for this report, a postponement of the original deadline (March 1, 1987) was granted to ATSDR, The report has undergone extensive peer review by external peer reviewers1 and a Federal ad hoc panel.2 The ATSDR appreciates the efforts of the consultant authors and peer reviewers in developing this report; the final document, as a culmination of this process, is the sole responsibility of ATSDR in fulfillment of its Congressional mandate (see Acknowledgments, page xix). The ATSDR considers this report to be a significant milestone in the public's Understanding of the widespread distribution and effects of childhood lead poisoning. As with all reports to Congress, the recommendations within this report must be weighed against other competing priorities. 1External peer reviewers are listed on pages xx-xxi. 2Members of the Federal ad hoc panel are listed on pages xxii-xxiii. iv DUP040009436 PREFACE Section 118(f) of the Superfund Amendments and Reauthorization Act (SARA),/ of 1986 (42 U.S.C. 9618(f)) required the Agency for Toxic Substances and Disease Registry (ATSDR) of the U.5, Public Health Service to prepare a study of lead poisoning in children. Congress specifically requested that the following issues be addressed, as stated in SARA Section 118(f): (f) Study of Lead Poisoning in Children-- (1) The Administrator of the Agency for Toxic Substances and Disease Registry shall, in consultation with the Administrator of the Environmental Protec tion Agency and other officials as appropriate, not later than March 1, 1987, submit to the Congress, a report on the nature and extent of lead poisoning in children from environmental sources. Such report shall include, at a minimum, the following information-- (A) an estimate of the total number of children, arrayed according to Standard Metropolitan Statistical Area or other appropriate geographic unit, exposed to environmental sources of lead at concentrations sufficient to cause adverse health effects; (B) an estimate of the total number of children exposed to environ mental sources of lead arrayed according to source or source types; (C) a statement of the long term consequences for public health of unabated exposures to environmental sources of lead and including but not limited to, diminution in intelligence, increases in morbidity and mortality; and (D) methods and alternatives available for reducing exposures of children to environmental sources of lead.2 (2) Such report shall also score and evaluate specific sites at which children are known to be exposed to environmental sources of lead due to releases, utilizing the Hazard Ranking System of the National Priorities Li st. iii DUP040009437 CONTENTS (continued) Secondary Exposure Prevention Measures __________ ..... Secondary Nutritional Measures .................................. Extra-Environmental Prevention Measures ________...____ 6. A Review of Environmental Releases of Lead Under Superfund 7. Information Gaps, Research Needs, and Recommendations Information Gaps ........................... ...... ........ ......... .............. ........... Research Needs .--------- ---.........____ ............. Recoiumendations 1. Lead in the Environment of Children ....... .................... 2. Lead in the Bodies of Children ................ ...................... C. CONCLUSIONS AND OVERVIEW............................................... ...______... 1. Lead as a Public Health Issue ............____________ 2. Lead in the Environment of Chi1dren 3. Lead in the Bodies of Chi1dren........... .. 4. the Extent of Lead Poisoning in Children in the Urn ted States 5. The Problem of In Utero Lead Toxicity: The Extent of Fetal Lead Exposure in the United States ...... 6 Removal or Reduction of Lead in the Child1* Environment ............................................ .......... ............. 7. Future Directions of Lead as a Public Health Problem PART 3 CHAPTER II. INTRODUCTION AND DISCUSSION OF TERMS AND ISSUES ... A. INTRODUCTION .............. B. DISCUSSION OF TERMS AND ISSUES....................... ............. 1. Young Children and Other Groups at Greatest Risk for Lead Exposure and Adverse Health Effects ...____ 2. Monitoring Lead Exposure in Young Children and Other Risk Pbpulations .................... ................................ .. 3. Environmental Sources of Lead in the United States with Reference to Young Children and Other Risk Groups .... 4. Adverse Health Effects of--Lead in Young Children and Other Risk Groups and Their Role in Health Risk Assessment ................ . CHAPTER III. LEAD METABOLISM AND ITS RELATIONSHIP TO LEAD EXPOSURE AND ADVERSE EFFECTS OF LEAD...................................... .. A. LEAD ABSORPTION IN HUMAN POPULATIONS .................. .......................... 1. Respiratory Absorption of Lead in Human Populations . 2. Gastrointestinal (GI) Absorption of Lead in Human Populations ................................................. ................ 3. Percutaneous Absorption of Lead in Human Populations 4. Transplacental Transfer and Fetal Uptake of Lead in Pregnant Women ....... ................... ................................................. B. DISTRIBUTION OF ABSORBED LEAD IN THE HUMAN BODY........... .. 1. Lead Uptake in Soft Tissue ____ ______________ ___________ 2. Lead Uptake in Mineralizing Tissue .................. vi J-31 1-34 1-34 1-34 1-36 1-37 1-38 1-39 1-39 1-41 1-42 1-42 1-43 1-45 1-46 1-48 1-49 1-50 II-l II-l II-6 11-6 II-7 II-9 11-11 III-l III-l III-l 111" 2 ni-4 m-4 111-5 111-6 III-7 r DUP040009438 CONTENTS TABUES.................................................... ....................,............... ................. FIGURES ...-.* *...*.. ..a....:...,. ......... t AUTHORS AND CONTRIBUTORS ............___________________ _ ACKNOWLEDGMENTS ..................................................... ................... ........................... NONFEDERAL PEER REVIEWERS _____________________.________ _____________ FEDERAL AD HOC ADVISORY COMMITTEE......... .............................................. PART 1 EXECUTIVE SUMMARY ___________________ ________________ _________ _ RESPONSE TO DIRECTIVES OF SECTION 118(f) OF SARA .... .1. Section 118(f)(1)(A) 2 Section 118(f)(1)(B) 3. Section 118(f)(1)(C) 4. Section 118(f)(1)(D) 5. Section 118(f)(2) B. SUMMARY OF REPORT RECOMMENDATIONS C. ISSUES, DIRECTIONS, AND THE FUTURE OF THE LEAD PROBLEM 1, 1ssues ...... 2. Directions and Future of the Lead Problem ........ PART 2 CHAPTER I, REPORT FINDINGS, CONCLUSIONS, AND OVERVIEW......................... A. BACKGROUND INFORMATION TO THE REPORT ________________________ 1. Historical Perspectives and Discussion of Important Issues .............. 2. Lead Metabolism and its Relationship to Exposure, Risk Population Identification and Adverse Health EffeeLs ..........a................,-........**.*..,..... 3. Adverse Prenatal and Postnatal Effects of Lead in Children*. Relationship to Public Health Risk and Their Relative Persistence............................................... MAIN REPORT: QUANTITATIVE EXAMINATION OF LEAD EXPOSURE AND TOXICITY RISK IN CHILDREN AND PREGNANT WOMEN AND STRATEGIES FOR ABATEMENT ................................................................................................... 1. Ranking of Lead-Exposed Children by Geographic Area ... 2. Numbers of Lead-Exposed Children by Lead Source ....... 3. Number of Women of Childbearing Age and Pregnant Women ................ ................................ .. 4. The Issue of Low-Level Lead Sources and Aggregate Lead Exposure of Children in the United States ....................... 5. Lead Exposure Abatement Strategies and Alternatives ... Lean in Paint ........................................................................................ Lead :n Ambient 6 r Lead in Oust and Soi 1 ---------------------------------------------------------- Lead in Drinking Water.................... ................................ ....... Lead in Food .............. ......................... ...................... .. Nutritional Measures in Primary Prevention of Lead Page xi xvi xvii xix xx xxii 1 3 3 6 9 11 13 13 15 15 16 1-1 1-2 1-2 1-3 1-6 1-8 1-10 1-15 1-21 1-23 1-24 1-25 1-27 1-27 1-28 1-29 1-30 v DUP040009439 CONTENTS (continued) 4. Children with Potential Exposure to Lead Paint in the SHSAs ........ ........ ....... ........................ 5. Conclusions and Overview ............................................. .... CHAPTER VI. EXAMINATION OF NUMBERS OF LEAD-EXPOSED U.S. CHILDREN BY LEAD SOURCE A. GENERAL ISSUES 1. The Level of Exposure Risk in Human Populations by . Lead Source ............. ........................................................ 2 Relationships of External to Internal Lead Exposure on a Total Population Basis ...........___ _...... 3. Human Behavior and Other Factors in Source"Specific Population Exposures to Lead ......... 4. Organization of the Chapter ....... .............. NUMBERS OF CHILDREN EXPOSED TO LEAD IN PAINT 1. Estimation Strategies and Methods .......... 2. Resul ts ___ _______ _____..........____ C. NUMBERS OF CHILDREN EXPOSED TO LEAD FROM LEADED GASOLINE 1. Estimation Strategies and Methods .................. 2. Resul ts ............ ........................ ....................... NUMBERS OF CHILDREN EXPOSED TO LEAD FROM STATIONARY EMISSION SOURCES ............................. . 1. Estimation Strategies and Methods _____ ........___ 2. Results .......... ....... ...........________ _________ _ E. NUMBERS OF CHILDREN EXPOSED TO LEAD IN DUSTS AND SOILS ... 1. Estimation Strategies and Methods ........... ........ . 2. Results .......................................................... ............. ........ NUMBERS OF CHILDREN EXPOSED TO LEAD IN DRINKING WATER ... 1. Estimation Strategies and Methods ..... 2. Results ............................. .......................... G. NUMBERS OF CHILDREN EXPOSED TO LEAD IN FOOD 1. Estimation Strategies and Methods ..... 2. Results ............................... .....------ ------H* SUMMARY AND OVERVIEW_______ _____________ _ 1. Paint Lead as an Exposure Source ....... 2. Gasoline Lead as an Exposure Source .... 3. Lead from Stationary Sites as an Exposure Source 4. Lead in Dust and Soils as an Exposure Source ... .5. Lead in Drinking Water as an Exposure Source ... 6 lead in Food as an Exposure Source --........ . 7. Ranking of Lead-Exposed Children by Source ------- CHAPTER VII. EXAMINATION OF NUMBERS OF LEAD-EXPOSED WOMEN OF CHILDBEARING AGE AND PREGNANT WOMEN ...................... A. STRATEGIES AND METHODS ............. .................... .............. . 1. Methods.......... ......... ............................... . 2. Results ............... ......................... ............ ...... Page V-48 V-49 VI-1 VI-1 VI-1 VI-3 VI-8 VI-9 VI-10 VI-11 VI-13 VI-17 VI-21 VI-22 VI-23 VI-26 VI-27 VI-29 VI-31 VI-33 VI-33 VI-36 VI-37 VI-44 VI-46 VI-48 VI-48 VI-49 VI-51 VI-52 VI-52 VI-52 VI-53 VI-53 VII-1 VII-1 VII-2 VII-5 viii D U P040009440 CONTENTS (continued) ,. LEAD EXCRETION AND RETENTION IN HUMAN POPULATIONS _____ _____ 0 METABOLIC INTERACTIONS OF LEAD WITH NUTRIENTS AND OTHER ACTIVE FACTORS IN HUMAN POPULATIONS .. .......... ................. IE. LEAD METABOLISM AND SOME KEY ASPECTS OF LEAD EXPOSURE AND TOXICITY .......... .......... . 1. Lead Metabolism and the Nature of Lead Exposure and Toxicity ..................... .................. ....................... 2. Lead Metabolism and the Identification of Risk Populations for Lead ........................... 3. Lead Metabolism and Biological Exposure Indicators ..... CHAPTER IV. ADVERSE HEALTH EFFECTS OF LEAD: RELATIONSHIP TO PUBLIC HEALTH RISK AND SOCIETAL WELL-BEING .................... ................. A, THE EXPOSURE (DOSE) INDEX IN ASSESSMENT OF THE ADVERSE HEALTH EFFECTS OF LEAD IN HUMAN POPULATIONS) ........................... B. MAJOR ADVERSE HEALTH EFFECTS OF LEAD IN CHILDREN ............. . 1. Effects of Lead on Heme Biosynthesis, Erythrocyte Physiology and Function,, and Erythropoietic Pyrimidine Metabolism......................................................... 2. Neurotoxic Effects of Lead in Children ___ ______ 3. Other Adverse Effects of Lead on the Health of Young Chi l dren ................... ....... ........... ........................ e. DOSE-EFFECT/DOSE-RESPONSE RELATIONSHIPS FOR; PEDIATRIC LEAD EXPOSURE _____ .............. ..................................................... ............. x>, PERSISTENCE OF ADVERSE HEALTH EFFECTS FROM LEAD EXPOSURE IN YOUNG CHILDREN................. ............................................................ CHAPTER V. EXAMINATION OF NUMBERS OF LEAD-EXPOSED CHILDREN BY AREAS OF THE UNITED STATES............. ............... ....................... .......... . A. ESTIMATED NUMBERS OF LEAD-EXPOSED CHILDREN IN SMSAs BY SELECTED BLOOD LEAD CRITERION VALUES..................................... 1. Estimation Strategies and Methods ................................. 2. Results ..... ........................................................................... B. NUMBERS OF LEAD-EXPOSED CHILDREN BY COMMUNITY-BASED SCREENING PROGRAMS ................................................ ...................... 1. Lead Screeni ng Programs............ ............................... .......... 2. The NHANES II Study ............................................. .................. C. RANKING OF CHILDREN WITH POTENTIAL EXPOSURE TO PAINT LEAD IN HOUSING...... ....................... ............................................................ 1. Strategi es and Methods ............ ............................... ........... 2. Results........ ................. ........................................... ................ 0. SUMMARY AND OVERVIEW ................................................... ............ 1. Lead-Exposed Children in SMSAs ...____ .........-----------2. Numbers of Lead-Exposed Children Detected by Screening Programs ............................... ........ ................................... . 3. Comparison of Prevalences Found in NHANES II Updated Prevalences and U.S, Screening Programs .............. .......... Page III-7 III--9 '' III-10 III-IO III-12 III-13 IV-1 IV-2 IV-3 IV-3 IV-7 IV-17 IV-20 IV-21 v-i V-2 V-3 V-7 V-16 V-16 V-31 V-33 V-33 V-34 V-44 V-44 V-46 V-47 vii DUP040009441 CONTENTS (continued) APPENDIX B. TABLES OF INDIVIDUAL SMSAs WITH A POPULATION OF LESS THAN ONE MILLION SHOWING NUMBERS OF YOUNG CHILDREN BY THE AGE OF THEIR HOUSING AND FAMILY INCOME ....... APPENDIX C, TABLES OF INDIVIDUAL AND MERGED SMSAs WITH POPULATIONS OF LESS THAN 500,000 SHOWING NUMBERS OF YOUNG CHILDREN BY THE AGE OF THEIR HOUSING AND FAMILY INCOME ....... APPENDIX D. SMSAs RANKED BY NUMBER OF YOUNG CHILDREN IN PRE-1950 HOUSING AS OF 1980 ............................. ........................... . APPENDIX E. LEAD-CONTAMINAtED SOIL CLEANUP, DRAFT REPORT......... APPENDIX F. FINAL AND PROPOSED NATIONAL PRIORITIES LIST WASTE SITES . WITH LEAD AS AN IDENTIFIED CONTAMINANT ............................. APPENDIX G. METHODOLOGICAL DETAILS OF BLOOD LEAD PREVALENCE PROJECTIONS FROM NHANES II DATA ........................ C~1 D-l E-l F-l G-l x DUP040009442 CONTENTS (continued) Page CHAPTER VlII. THE ISSUE OF LOW-LEVEL LEAD SOURCES AND AGGREGATE LEAD EXPOSURE OF U. S. CHILDREN................... ........................ A. NATIONAL/REGIONAL SURVEYS OF BLOOD LEAD LEVELS: BASELINE LEVELS AND SOURCE-RELATED CHANGES IN SURVEY BASELINES EL USE OF SOURCE-SPECIFIC TRACING METHODS ..................... C. THE USE OF SOURCE-BASED DISTRIBUTIONS OF LEAD INTAKE AND SOURCE-BLOOD LEAD RELATIONSHIPS IN ASSESSING AGGREGATE INTAKE AND POPULATION RISKS........... .................................. . 0. BI0KINETIC MODELS OF THE IMPACT OF LEAD SOURCES ON BLOOD LEAD ..............----------- --,......------------ ...... ];. SUMMARY .............. i.............................. VIII-l y VIII-2 VI11-4 VIII-5 : VI11-6 VIII-13 CHAPTER IX. METHODS AND ALTERNATIVES FOR REDUCING ENVIRONMENTAL LEAD EXPOSURE FOR YOUNG CHILDREN AND RELATED RISK GROUPS . A. PRIMARY PREVENTION MEASURES FOR LEAD EXPOSURE ___ ______ 1. Primary Prevention Using Environmental Measures .... 2. Primary Prevention Using Combined Environmental and Biol ogi cal Measures ........................ ...................... B. SECONDARY PREVENTION MEASURES FOR LEAD EXPOSURE -----1. Environmental Lead Control ____ ____________ 2. Environmental/Biological Prevention Measures 3. Extra-Environmental Prevention Measures .... IX-1 IX-4 IX-4 IX-18 IX-20 IX-20 IX-24 IX-24 CHAPTER X. A REVIEW OF ENVIRONMENTAL RELEASES PF LEAD AS EVALUATED UNDER SUPERFUND ..................................................:------ .... A. NPL SITES -- PROPOSED AND FINAL ..................................... Exposure of Children to Lead at NPL Sites.................... B. URBAN AREA SITE ................................. . -............... HRS Scoring at the Boston Urban Site ................. C. REVISION OF THE HAZARD RANKING SYSTEM.......................... D. SUMMARY____ _______________ _________ __________ _______ X-l X-2 X-2 X-4 X-6 X-10 X-ll CHAPTER XI. LEAD EXPOSURE AND TOXICITY IN CHILDREN AND OTHER RELATED GROUPS IN THE UNITED STATES: INFORMATION GAPS, RESEARCH NEEDS, AND REPORT RECOMMENDATIONS...................... A. INFORMATION GAPS ________ ________________________ ...-----------B. RESEARCH NEEDS ................. .................................................................. C. RECOMMENDATIONS ............. ................ ................. ........ ..................... 1. Lead in the Environment of Chi1dren ......... ........ 2, Lead in the Bodies of Children................ ........ ............ . XI-1 XI-1 XI-4 XI-5 XI-6 XI-8 REFERENCES.................................................................................. ........................ R-l ONE MILLION SHOWING NUMBERS OF YOUNG CHILDREN BY THE AGE OF THEIR HOUSING AND FAMILY INCOME -------- ---------- A-l ix DUP040009443 Table 1-1 1-2 1-3 1-4 1-5 1-6 1-7 III-l IV- 1 IV-.2 IV-3 IV-4 V- l TABLES Page Relative persistence of adverse health effects in infants and chi 1 dren X--9 Estimated numbers of children, who are projected to exceed 15 pg/dl Pb-B, by family income and race, in all SHSAs, 1984 .................... v.................................... .......... .......... 1-12 Summaries of estimated numbers of children 6 months to 5 years old in all SHSAs who are projected to exceed selected levels of blood lead, by urban status, 1984 ........ 1-13 Cincinnati, Ohio-Kentucky - SHSA census count of children of all races, 6 months to 5 years old, by family income, urban status, and age of housing, 1980 ----------------- ......------------- - 1-16 Categories of estimation methods for children exposed to lead by source .,____ _________________ _________ 1-17 Estimated number of women of childbearing age and estimated number of pregnant women and projected numbers above four selected Pb-B criterion values, by race and age, in all SMSAs, 1984 .......................... ......................... ............. 1-22 Categorical tabulation of the elements of primary and secondary prevention of lead exposure in children and related risk groups of the United States .........-------.... 1-25 Comparative dietary lead metabolism in infants and III-8 Effects of lead on the heme biosynthesis pathway in humans ......................................... ....................... IV-5 Summary of major findings from prospective studies of early developmental exposure to lead ....................... . IV-1Q Lowest observable effect level for effects in children IV-21 Relative persistence of adverse health effects in infants and children ............................................. ............... IV-24 Projected percentages of children 0.5 to 5 years old estimated to exceed selected Pb-B criterion values by family income, race, and urban status, who live "inside central city" of SMSAS, 1984 .................................. .....--........... V-7 xi DUP040Q09445 Table V-2 V-3 V-4 V-5 V-6 V-7 V-8 V-9 v-io V-ll V-12 V-13 V-14 TABLES (continued) Projected percentages of children 0.5-5 years old esti mated to exceed selected Pb-B criterion values by family income, race, and urban status, who live "outside central ci ty" of SMSAs, 1984 ................. ..................... .........._______ Projected percentages of children 0.5-5 years old estimated to exceed selected Pb-B criterion values by family income and race who live in small SMSAs, 1984 .................___ Estimated numbers of children 0.5-5 years old, who are projected to exceed three levels of blood lead by family income and race living inside central cities i n SMSAs, 1984 Estimated numbers of children 0.5-5 years old, who are projected to exceed three levels of blood lead by family income and race living not inside central cities in SMSAs, 1984 ................................................................... . Estimated numbers of children 0.5-5 years old, who are projected to exceed three levels of blood lead by family income and race in small SMSAs, 1984 ..................__________ ... Estimated numbers of children 0.5-5 years old who are projected to exceed 15 pg/dl Pb-B, by family income and race, in all SMSAs, 1984 ..............-------- ...____.... Summary of estimated numbers of children 0.5-5 years old in all SMSAs, who are projected to exceed selected levels of blood lead, by urban status, 1984 ................ CDC lead screening classification scheme, 1978-1985 ........ CDC lead screening classification scheme as of January 1985, using the hematofluorometer ___ ______________ C0C lead screening classification scheme as of January 1985, using chemical analysis of EP................... ..................... Results of screening in U.S. childhood lead poisoning projects, FV 1981 . Lead poisoning screening of children reported by 27 state and local agencies, FY 1983 ................................ Current (1985-1986) lead screening activities reported by state and local programs to ATSDR ............ ................... Page V-8 V-9 V-10 V-il V-12 V-13 V-14 V-18 V-19 V-19 V-21 V-23 V-24 xii DUP040009444 Table VI-8 Vi-9 VI-10 VI-11 VI-12 VI-13 VI-14 VI-15 VI-15 VI-17 VI-18 VI-19 VII-1 VII-2 VII1-1 TABLES (continued) Estimated numbers of U.S. children falling below indicated Pb-E levels as a result of Pb-gasoline phaseout____...._ Geometric mean Pb-B levels by distance from smelter for children near Idaho smelter Extrapolated pediatric population estimates for stationary lead sources: TBC/LIA and EPA approaches .................................. GCA/OAQPS estimates of total and child populations exposed to stationary Sources of lead ................... Ramblers of children living in housing classified by housing,age Children potentially at risk for lead exposure by house hold plumbing, by age............. ............................. .............,........ Estimated numbers of children at greatest risk of exposure to lead in household plumbing ......................................................... Persistence of aging housing stock in occupied U.S. housing i nventory' .* ^ .* Lead levels in water samples obtained from water fountains/coolers.at naval facilities in Maryland ....------... Percentage of variably collected water samples exceeding 20 pg/T of lead at different pH levels and by age of hOUSe ........ . .*....' a ........... . . .. Daily mean dietary lead intake by percentiles ............... Mean dally dietary lead intake in preschoolers classified as total or normalized daily intake ............................. .. Estimated percentages of women of childbearing age exceeding selected Pb-B values, their geometric means and standard deviations by race and age, for populations in al 1 SMSAs, .1984 .................. Estimated number of women of childbearing age and estimated number of pregnant women and projected numbers above four selected Pb-B criterion values, by race and age, in all Estimated contributions of leaded gasoline combustion to blood lead by various pathways ...............--............ Page VI-23 VI-24 VI-28 VI-28 VI-38 VI-38 VI-39 VI-39 VI-42 VI-43 VI-45 VI-46 VI1-5 VI1-6 VIII- Table V-15 V-16 V-17 V-18 y-19 y-20 V-2I vi-i VI-2 VI-3 Vl-4 VI-5 VI-6 VI-7 TABLES (continued) Impact of new CPC lead exposure screening guidelines on the number of lead toxicity cases in New York City .............. Temporal variation of lead toxicity cases in selected lead poisoning screening programs, 1973-1985 ................ Lead screening statistics for the Chicago Department of Health, 1981 to 1985, by CPC Classification II, III, or IV Rate of first hospitalization and associated mean Pb-B in "asymptomatic" children in Newark, Nj, by year of first admission .................-------- .........------- ............ Blood lead levels in U.S. children by race and age, 1976-1980 ....... ........... .................................... ................................. Ranking of 1980 census SMSAs by number of children 0.5-5 years old living in pre-1950 housing, and total number of young children in SMSA .......... .................................... Cincinnati, Ohio-KY-SMSA 1980 census count of children of all races 0.5-5 years old by family income, urban status, and age of 'housing . Categories of estimation methods for children exposed to 1 ead by source ....... ................................ ................................... . Summary of Pb-B levels of a relatively homogeneous white population in the United States ................. .......................... National best estimate and upper bound of numbers of children under 7 years old in lead-based painted U.S. housing by age of units ................................ Numbers of U.S. children residing in unsound and leadbased painted housing ranked by age and criteria for deterioration...... ........... ............................ Regional best estimate of numbers of children in unsound lead-based painted housing by age and numbers of peeling pai nt urn ts Estimated numbers of U.S. children living in unsound, lead-based painted housing above indicated Pb-B cri terion values ............... ............... ..................... .......... ...... Recent consumption of lead in gasoline............................. .. m V-27 V-29 / V-30 V-31 V-32 V-35 V-43 VI-4 VI-8 VI-13 VI-14 VI-15 VI-17 VI-18 xiu DUP040009447 FIGURES figure 1-1 Percent of U.S, Residences Constructed Before 1940 ,___ _ 11*1 Pathways of Lead from the Environment to Man and Body Disposition of Lead ____ .,___... *____ IV-1 Effects of Lead (Pb) on Heme Biosynthesis ..................... . IV- 2 Multi-Organ impact of Reductions of Heme Body Pool by Lead ........ ........................................................ IV-3 Dose-Response Curves for Elevation of EP as a Function of Blood Lead Level ......................___ ..........,,. VI-1 IIlustrative Log-normal Pb-B Distribution Curve .......... VIII-1 8 8-28 Parallel Decreases in Blood Lead Values Observed in the MHANE5 II Study and Amounts of Lead Used in Gasoline in 1976 I960 .................. Schematic Model of Lead Metabolism in Infant Baboons with Cpmpartmental Transfer Coefficients ___ VII1-3 Comparison of Distribution of Measured Blood Lead Levels in Children 1-5 Years of Age, Living Within 1 Mile of E. Helena, MT., Lead Smelter vs. Levels Predicted by Uptake/Biokinetic Model ___ .......______ Page I-4 II-2 IV-4 IV-6 IV-22 VI-7 VIII-3 VIII-7 VIII-11 xvi DUP040009448 Table VIII-2 VIII-3 VII1-4 VII1-5 IX-1 IX-2 IX-3 lx-4 IX-5 IX-G X-1 TABLES (continued) 111ustrative modeling balance schemes for average lead intake and uptake in 2-year old children under three scenari ds ^ ^^ n <. * -* Comparison of integrated Pb uptake/biokinetic model predictions to 1983 measurements to East Helena, MT Children's blood lead levels measured in Omaha, NEE, 1971-1977 vs, integrated upiake/biokinetie model pre dictions and including source levels ........................................... Children's blood lead levels measured in Silver Valley, ID, 1974-1975 vs. integrated uptake/biokinteic model predictions........................................................................................ , Categorical tabulation of the components of primary and secondary prevention of lead exposure in children and related U. S. risk groups ............... ......... ................... ...................... Abatement costs and no. of units for different site categories at a 1eaded paint threshold of 1.0 mg/cm2 in public housing ...... .................................. Estimated abatement costs and no. of units for different site categories at a lead paint threshold of 1.0 mg/cm2 in single-family FfiA housing units............................................... ,. Summary of total pre-1940 lead-painted housing versus deleading activity in selected Massachusetts communities for 1982-June 1986 ..................... ..........................................,....... ......... .... Percentage of lead-soldered cans in all U.S. manufactured food carts from 1979-1985 ............. ........................................................ Age- and sex-dependent diet lead intakes in the United States at two time periods _______________ _______________ _______ _ Most common activities associated with lead waste at NPL sites with lead release ...................... .......... ................................ .. Page VIII-9 / VI11-12 . VII1-13 VIII-14 IX-2 IX-8 IX-9 IX-10 IX-17 IX-18 X-5 xv DUP040009449 Lester D. Grant, Ph.D. Environmental Criteria and Assessment Office (MD-52) U.S. Environmental Protection Agency Research Triangle Park, NC 27711 Sandra Lee, Ph.D. Office of Solid Waste and Emergency Response (WH-548A) U.S. Environmental Protection Agency Washington, DC 20460 Ronnie Levin Office of Policy Analysis (PM-221) U.S. Environmental Protection Agency Washington, DC 20460 David C. Moore, Ph.D. Innovative Technology and Special Projects Division - Room 8232 U.S. Department of Housing and Urban Development Washington, DC 20410-6000 Roberts. Murphy, M.S.P.H. Division of Health Examination .Survey - Room 2-58 National Center for Health Statistics Centers for Disease Control Hyattsville, MD 20782 Joel Schwartz, Ph.D; Office of Policy Analysis (PM-221) ll.S. Environmental Protection Agency Washington, DC 20460 Staff of the Division of Vital Statistics National Center for Health Statistics Centers for Disease Control Hyattsville, MD 20782 xviii DUP040009450 AUTHORS AND CONTRIBUTORS Principal Authors Paul Mushak, Ph.D. Consultant and Adjunct Professor University of North Carolina/Chapel Hill 811 Onslow Street Durham, NC 27705 Annemarie F. Crocetti, Dr.P.H. Consultant and Associate Adjunct Professor New York. Medical College Apt. 11-A 31 Union Square West New 'fork, NY 10003 Contributors Michael Boliger, Ph.D. Center for Food Safety and Applied Nutrition (HFF-156) Food and Drug Administration Washington, DC 20204 Jeanne Briskin Office of Drinking Water (WH-550) U.S., Environmental Protection Agency Washington, DC 20460 Jeffrey Cohen, M.S.P.H. Office of Air Quality Planning ami Standards (MO-12) U. S. Environmental Protection Agency Research Triangle Park, NC 27711 J. Michael Davis, Ph.D. Environmental Criteria and Assessment Office (MO-52) U.S. Environmental Protection Agency Research Triangle Park, NC 27711 Henry Falk, M.D. Center for Environmental Health and Injury Control Centers for Disease Control Atlanta, GA 30333 xvii NONFEDERAL PEER-REVIEWERS Carol R. Angle, M.D. Collegfe of Medicine University of Nebraska 418 South 82nd Street Omaha, Nebraska 68114 Charles D. Brokopp, D.P.H. Bureau of Preventive Medicine Idaho Department of Health . Boise, Idaho 83720 O. Julian Chisolm Jr, M.D, Johns Hopkins University School of Medicine and Kennedy Institute 707 N. Broadway Baltimore, MD .21205 Jerome Cole, Sc.D. International Lead-Zinc Research Organization 2525 Meridian Parkway P. 0 Box 12036 Research Triangle Park, NC 27709 Devra Lee Davis, Ph.D, Board of Toxicology and Environmental Health Hazards National Academy of Sciences 2101 Constitution Ave. Washington, DC 20418 Claire Ernhart, Ph.D. Department of Psychiatry Cleveland Metropolitan General Hospital Cleveland, OH 44109 Patricia Field, Ph.0. Toxicology Laboratory . > State Laboratory of Hygiene 465 Henry Mall Madison, Wisconsin 53706 Robert A. Goyer, M.D. Pathology Department University of Western Ontario London N6A5C1 Canada ^ John W, Graef, M.D. Lead/Toxicology Clinic Children's Hospital Medical Center , 300 Longwood Avenue ; Boston, MA 02115 Philippe Grandjean, M.D., Ph.D. Department of Environmental Medicine Odense University J. B, Winslowsvej 19 5000 Odense, Denmark Paul Hammond, D.V.M., Ph.D. University of Cincinnati Institute of Environmental Health Kettering Laboratories 3223 Eden Avenue Cincinnati, OH 45267 Philip Landrigan, M.D., M.S.C. Environmental Health Sciences Laboratory Mt. Sinai School of Medicine New York, NY 10029 Donald Lynam, Ph.D. Department of Air Conservation Ethyl Corporation 451 Florida Blvd. Baton Rouge, LA 70801 Herbert Needleman, M.D. Department of Psychiatry Children's Hospital of Pittsburgh Pittsburgh, PA 15213 xx DUP040009452 ACKNOWLEDGMENTS The Agency for toxic Substances and Disease Registry (ATSDR) gratefully ackncwledges the efforts of the consultant authors, Drs. Paul Mushak and Annemaxie F. Crocetti, for their authorship of the interim and final drafts of this report to Congress. The Agency also acknowledges the generous contributions of Dr, Joel Schwartz, Office of Policy Analysis, U.S. Environmental Protection Agency (EPA), in carrying out the prevalence modeling for segments of this report and Dr, Lester Grant, Dr. J, Michael Davis, and Ms. Vandy Bradow of EPA's Environ-^ mental Criteria and Assessment Office (ECAO), Research Triangle Park, N.C., for their contributions. The Agency thanks Dr. Sandra Lee of EPA's Office of Solid Waste and! Emergency Response for preparation of Chapter X of the report, A number of Federal agencies contributed data, data analyses, and data interpretations for the report, and the Agency particularly wishes to thank Jeanne Briskin* Ronnie Levin and Jeff Cohen of EPA, Dr. David Moore Of U.S. Department of Housing and Urban Development (HUD), Dr. Michael Bolger of the Food and Drug Administration (FDA), Robert Murphy of the Center for Disease Control's National Center for Health Statistics, and Staff of the Division of Vital Statistics, National Center for Health Statistics. Thanks also are due to Drs. Henry Falk and James Pirkle of the Center for Environmental Health and Injury Control, Centers for Disease Control (CDC) and Dr, Kathryn Mahaffey, National Institute for Occupational Safety and Health, CDC, (NIQSH), for helping with preparation of the report. The Agency wishes to thank those Federal and nonFederal peer reviewers of the report who reviewed the various drafts and offered constructive and valuable comments, and also to thank ATSDR staff member Susan Baburich, who directed gathering of the most recent screening information and who also assisted Dr. Frank Mitchell in overseeing the preparation of the earliest drafts. Thanks and appreciation are extended to those persons at ECAO/EPA, Research Triangle Park, N.C., who worked diligently in the production of the various drafts of the report: Ivra Bunn, Linda Cooper, Chip Duke, Douglas Fennell, Varetta Holman, Allen Hoyt, Carolyn Norris, Deborah Staves, and especially Miriam Gattis and Lorrie Godley. xix FEDERAL AD ROC ADVISORY COMMITTEE Michael Bolger, Ph.D. Center for Food Safety and Applied Nutrition (HFF-156) Food and Drug Administration Washington, DC 20204 Barry L. Johnson, Ph.D. Agency for Toxic Substances and Disease Registry Atlanta, GA 30333 Jeanne Briskin Office of Drinking Water (WH 550) U.S. Environmental Protection Agency Washington, DC 20008 . Sandra Lee, Ph.D. Office of Solid Waste and Emergency Response (WH-548A) U.S. Environmental Protection Agency Washington, DC 20460 ': Rufus Chaney, Ph.D U.S. Department of Agriculture Building 008 BARC - West Beltsville, Maryland 20705 Ronnie Levin Office of Policy Analysis U.S. Environmental Protection Agency Washington, OC 20460 Jeffrey Cohen, M.S.P.H. Office of Air Quality Planning and Standards (MD-12) U.S. Environmental Protection Agency Research Triangle Park, NC 27711 Jane S. Lin-Fu, M.D. Division of Maternal and Child Health - Room 6-17 Health Resources and Services Administration Rockville, MD 20857 J.. Michael Davis, Ph.D. Environmental Criteria and Assessment Office (MD-52) U.S. Environmental Protection Agency Research Triangle Park, NC 27711 Kathryn R, Mahaffey, Ph.D. National Institute of Occupational Safety and Health C enters for bisease Control Cincinnati, OH 45226 Henry Falk, M.D, Center for Environmental Health and Injury Control Centers for Disease Control Atlanta, GA 30333 David C. Moore, Ph.D. Innovative Technology and Special Projects Division - Room 8232 U.S. Department of Housing and Urban Development Washington, DC 20410-6000 Lester 0. Grant, Ph.D. Environmental Criteria and Assessment Office (MD-52) U.S. Environmentai Protection Ageney Research Triangle Park, NC 27711 Robert S. Murphy, M.S.P.H. Division of Health Examination Survey - Room 2-58 National Center for Health Statistics Centers for Disease Control Hyattsville, MO 20782 Vernon N. Houk, M.D. Center for Environmental Health and Injury Control Centers for Disease Control Atlanta, GA 30333 David Otto, Ph.D. Clinical Studies Division (MD-58) U.S. Environmental Protection Agency Research Triangle Park, NC 27711 xxii DUP040009454 Sergio Piomel]i, M.D. Pediatric Hematology - Oncology College of Physicians and Surgeons Columbia University 630 West 168th Street New York, NY 10032 Routte J. Reigart, M.D. Department of Pediatrics Medical University of South Carolina 171 Ashley Street Charleston, SC 29425 John F. Rosen, M.D. Division of Pediatric Metabolism Albert Einstein College of Medicine Montefiore Medical Center 111 East 210th Street Bronx, New York, NY 10467 Samuel Schwartz, M.D. Minneapolis Medical Research Foundation 501 Park Avenue Minneapolis, Minnesota 55415 Ellen Silbergeld, Ph.p. Environmental Defense Fund 1525 18th Street, N.W, Washington, DC 20036 (Listing of nonfederal peer reviewers does not necessarily denote each reviewer's agreement with all the report's content.) xxi DUP040009455 James Pinkle., M.D, Center for Environmental Health and Injury Control Centers for Disease Control Atlanta, GA 30333 Rebecca. J. Schilling, D.V.M., M. P.H, Center for Environmental Health and Injury Control Centers for Disease Control Atlanta, GA 30333 Joel Schwartz, Ph,D. Office of Policy Analysis (PM 221) U.5. Environmental Protection Agency Washington, DC 20460 James Simpson Center for Environmental Health and injury Control Centers for Disease Control Atlanta, GA 30333 John Zipeto, P.E., M.P.H. EPA Region 1 JFK Building Boston, MA 02.11$ xxrn DUP040009456 The report comprises three parts: Part 1, consisting of the Executive Summary; Part 2, consisting of Chapter J. "Report Findings, Conclusions, and Overview," which provides a more detailed overview of information and conclu sions abstracted from the main body of the report; and Part 3, consisting of Chapters II through XI, which constitute the main body of the report. Before addressing the specific directives of Section 118(f), ityis important to point out that childhood lead poisoning is recognized as a major public health problem. In a 1987 statement, for example, the American Academy of Pediatrics notes that lead poisoning is still a significant toxicological hazard for young children in the United States- It is also a public health problem that is preventable. In recognition of evolving scientific evidence of the harmful effects of lead exposure, Congress directed ATSDR to examine (1) the long-term health implications of low-level lead exposure in children; (2) the extent of lowlevel lead intoxication in terms of U.S. geographic areas and sources of lead exposure; and (3) methods and strategies for removing lead from the environment of U.S. children. The childhood lead poisoning problem encompasses a wide range of exposure levels. The health effects vary at different levels of exposure. At low levels, the effects on children, as stated subsequently in this report, may not be as severe or obvious, but the number of children adversely affected is large. Moreover, as adverse health effects are detected at increasingly lower levels of exposure, the number of children at risk increases. At intermediate exposure levels, the effects are such that a sizable number of U.S. children require medical and other forms of attention, but usually they do not need to be hospitalized, nor do they need conventional medical treatment for lead poisoning. For these children, the only appropriate solution, at present, is to eliminate or reduce all significant sources of lead exposure in their environment. At high levels, the effects are such that children require immediate medical treatment and follow-up. Various clinics and hospitals, particularly in larger cities, continue to report such cases. Lead exposure may be characterized in terms of either external or internal concentrations. External exposure levels are the concentrations of lead in environmental media such as air or water. For internal exposure, the most widely accepted and commonly used measure is the concentration of lead in blood, conventionally denoted as micrograms of lead per deciliter (100 ml) of whole blood -- abbreviated pg/dl. For example, when ATSDR estimated the number 2 DUP040009457 PART 1 EXECUTIVE SUMMARY Exposure to lead continues to be a serious public health problem -- particularly for the young child and the fetus. The primary target organ for lead toxicity is the brain or central nervous system, especially during early child development. In children and adults, very severe exposure can cause' coma, convulsions, and even death. Less severe exposure of children can produce delayed cognitive development, reduced IQ scores, and impaired hearing -- even at exposure levels once thought to cause no harmful effects. Depending on the amount of lead absorbed, exposure can also cause toxic effects on the kidney, impaired regulation of vitamin 0, and diminished synthesis of heme in red blood cells. All of these effects are significant. Furthermore, toxicity can be. persistent, and effects on the central nervous system (CNS) may be irreversible. In recent years, a growing number of investigators have examined the effects of exposure to low levels of lead on young children. The history of research in this field shows a progressive decline in the lowest exposure levels at which adverse health effects can be reliably detected. Thus, despite some progress In reducing the average level of lead exposure in this country, it is increasingly apparent that the scope of the childhood lead poisoning problem has been, and continues to be, much greater than was previously realized. The "Nature and Extent of Lead Poisoning in Children in the United States: A Report to Congress" was prepared by the Agency for Toxic Substances and Disease Registry (ATSDR) in compliance with Section 118(f) of the 1986 Superfund Amendments and Reauthorization Act (SARA) <42 U.S.C. 9618(f)). This Executive Summary is a guide to the structure of the document and, in partic ular, to the organization of the responses to the specific directives of Section 118(f), It also provides an overview of issues and directions to the U-5, lead problem. DUP040009458 1 Valid estimates of the total number of lead-exposed children according to SMSAs or some other appropriate geographic unit smaller than the Nation as a whole cannot be made, given the available data. The only national data set for F'b-13 levels in children comes from the National Health and Nutrition Examina tion Survey II (NHANES II) of COC's National Center for Health Statistics, Jhe NHANES II statistical sampling plan, however, does not permit valid estimates to be made for geographic subsets of the total data base. In this report, the numbers of white and black children (ages 6 months to 5 years) living in all SMSAs are quantified according to selected blood lead levels and 3Q socioeconomic and demographic strata. Within Targe SMSAs (those with over 1 million residents each) for 1984, an estimated 1.5 million children had Pb-B levels above 15 pg/dl. In smaller SMSAs (with fewer than 1 million residents), an estimated 887,000 children had Pb-B levels above 15 pg/dl. In short, about 2.4 million white and black metropolitan children, or about 17% of such children in U.S. SMSAs, are exposed to environmental sources of lead at concentrations that place them at risk of adverse health effects. This number approaches 3 million black and white children if extended to the entire U,Si. child population. If the remsinirig racial categories are included in these totals, between 3 and 4 million U.S. children may be affected. The numbers of children in SMSAs with blood lead levels above 20 and 25 pg/dl are 715,000 (5.2%) and 200,000 (1.5%), respectively. These figures, however, are for all strata Combined; many strata (e.g., black, inner-city, or low-income) have much higher percentages of children with elevated Pb-8 levels. Although these projected figures, based on the NHANES II survey, provide the best estimate that can now be made, they were derived from data collected in 1975-1980 (the years of NHANES II) and extrapolated to 1984. With respect to bounds to the above projections, variables in the methods used to generate these figures contribute tp both overestimatipn and underestimation. The major source of overestimation is the unavoidable omission of declines in food lead that may have occurred in the interval 1978-1964 and that would have affected the results of the projection methodology. On the other hand, two significant factors contribute to underestimation. One Is the restriction of the estimates to the SMSA fraction of the U.S. child population, some 75% to 80% of the total population. The other is the unavoidable omission of children of Hispanic, Asian, and other origins in the U.S. population. In a number of SMSAs in the West and South west, children in such segments outnumber black children. In balancing all sources of overestimates and underestimates, including variance 4 DUP040009459 of children considered to be at risk for adverse health effects, the Agency used blood lead (Pb-B) levels of 25, 20, and 15 pg/dl to group children by their degree of exposure. These levels are not arbitrary. In 1985 the Centers for Disease Control (CDC) identified a Pb-B level of 25 pg/dl along with an elevated erythrocyte y protoporphyrin level (EP) as evidence of early toxicity- For a number of practical considerations, CDC selected this level as a cutoff point for medical referral from screening programs, but it did not mean to imply that Pb-B levels below 25 pg/dl are without risk. More recently, the World Health Organization (WHO), in its 1986. draft report on air quality guidelines for the European Economic Community, identified a Pb-B level of 20 pg/dl as the then-current upper acceptable limit. In addition, the Clean Air Scientific Advistory Commit tee to the U.S. Environmental Protection Agency (EPA) has concluded that a Pb-B level of 10 to 15 pg/dl in children is associated with the onset of effects that "may be argued as becoming biomedically adverse", In this connection, the available evidence for a potential risk of developmental toxicity from lead exposure of the fetus in pregnant women also points towards a Pb-B level of 10 to 15 pg/dl, and perhaps even lower. These various levels represent an evolving understanding of low-level lead toxicity. They provide a reasonable means of quantifying aspects of the childhood lead poisoning problem as it is currently understood. With further research, however, these levels could decline even further. A. RESPONSE TO DIRECTIVES Of SECTION 118(f) of SARA Section 118(f) and its five directives give ATSDR the mandate to prepare this report. These directives are identified in the five subsections below. 1. Section 118(f) (IMA) This subsection requires an estimate of the total number of children, arrayed according to Standard Metropolitan Statistical Area (SMSA) or other appropriate geographic unit, who are exposed to environmental sources of lead at concentrations sufficient to cause adverse health effects. Chapter V, "Examination of Numbers of Lead-Exposed Children by Areas of the United States," and Chapter VII, "Examination of Numbers of Lead-Exposed Women of Childbearing Age and Pregnant Women," respond to this directive. 3 DUP040009460 older housing in which they live is likely to contain paint with the highest levels of lead and is, therefore, likely to pose an elevated risk of dangerous lead exposure. A noteworthy finding concerns the distribution of children in older housing according to family income. Actual enumerations (not estimates) show that children above the poverty level constitute the largest proportion of children who reside in older housing. The implication, consistent with the conclusion based on projections from NhANES II data that was stated above, is that children above the poverty level are not exempt from lead exposure at levels sufficient to place them at risk for adverse health effects. Children above the poverty level are the most numerous group within the U.S. chilcl population. Although Section 118(f)(1)(A) does not explicitly request such information, an accurate description of the full childhood lead poisoning problem requires an estimate of the number of fetuses exposed to lead in ute.ro, given the susceptibility of the fetus to low-level lead-induced disturbances in develop ment that first become evident at birth or even some time later during early childhood. Accordingly, in a given year, an estimated 400,000 fetuses (within SMSAs alone) are exposed to maternal Pb-B levels of more than 10 pg/dl and are therefore at risk for adverse health effects, this number pertains to a single year; the cumulative numbeir of children who have been exposed to undesirable levels of lead during their fetal development is much greater, particularly in view of the higher average levels of exposure that prevailed in past years. 2. Section 118(f)(1)(B) This subsection requires an estimate of the total number of children exposed to environmentai sources of lead arrayed according to source or source types. Chapters VI ("Examination of Numbers of Lead-Exposed Children in the United States by Lead Source") and VIII ("The Issue of Low-Level Lead Sources and Aggregate Lead Exposure of Children in the United States") respond to this directive. The six major environmental sources of lead are paint, gasoline, stationary sources, dust/soil, food, and water. Dust/soil is more properly classified as a pathway rather than a source of lead, but since it is often referred to as a source, it is included. (Figure 11-1 in the main report shows how lead from these sources reaches children.) The complex and interrelated pathways from 6 UP040009461 it) the projection model itself, the projections given are probably close to the actual values. A breakdown of the above estimates according to national socioeconomic and demographic strata shows that no economic or racial subgrouping of children is exempt from the risk pf having Pb-B levels sufficiently High to cause adverse health effects. Indeed, sizable numbers of children from families with incomes above the poverty level have been reported with Pb-B levels above 15 pg/dl. Nevertheless, the prevalence of elevated-Pb-B levels in inner-city, underprivi leged children remains the highest among the various strata. Although the percentage of children with elevated Pb-B levels is not as high in, for example, the more affluent segment of the U.S. population living outside central cities, the total number of children With these demographic characteristics is much greater than the number of poor, inner-city children* Consequently, the absolute numbers of children; with elevated Pp-B levels are roughly equivalent for some of these rather different strata of the U.S. child population. In this report, ATSDR has also used data from lead screening programs and 1980 U.S. Census data on age of housing to estimate SMSA-specific numbers of children exposed to lead-based paint. In December 1986, ATSDR conducted a survey of lead screening programs. Of 785,285 children screened In 1985, 11,739 (1.5%) had symptoms of lead toxicity by one of two definitions. Because CDC criteria for lead toxicity changed in 1985, some programs were still using the 1978 CDC criteria (Pb-B 530 pg/dl and EP 550 pg/dl) in 1985, whereas others used the new 1985 CDC criteria (Pb-B 525 pg/dl and EP 535 pg/dl). Differences in the estimates of children with lead toxicity become apparent when using the NHANES II data and the childhood lead screening program data. Estimates derived from screening program data very likely underestimate the actual magnitude of childhood lead exposure by a considerable margin. This is especially evident when the percentages of positive test results from screening programs are compared with the much higher NHANES II prevalences of elevated Pb-B levels in strata corresponding to screening program target groups, for example, poor, inner-city children in major metropolitan areas. An analysis of 318 SMSAs, based on 1980 Census data on age of housing, showed that 35 SMSAs had 50% or more of the children living in housing built before 1950, A total of 4,374,600 children (from these 318 SMSAs alone) lived in pre-1950 housing. The percentage of these children with lead exposures sufficient to cause adverse health effects could not be estimated, but the 5 DUP040009462 o The estimated number of children potentially exposed to U.S. stationary sources (e.g., smelters) is 230,000 children. The estimated number of children exposed to lead emissions from primary and secondary smelters sufficient to elevate Pb-B concen trations to toxic levels is about 13,000; estimates for other stationary sources are not available. o The number of children potentially exposed to lead in dust and'' soil can only be derived as a range of potential exposures to the primary contributors to lead in dust and soil, namely, paint lead and atmospheric lead fallout. This range is estimated at 5.9 million to 11.7 million children. The actual number of children exposed to lead in dust and soil at concentrations adequate to elevate Pb-B levels cannot be estimated with the data now available. o Because of lead in old residential plumbing, 1.8 million chil dren under 5 years old and 3.0 million children 5 to 13 years old,, are potentially exposed to lead; for new residences (less than 2 years old), the corresponding estimates of children are 0.7 and 1.1 million* respectively. Some actual exposure to lead occurs for an estimated 3,8 million children whose drinking water lead level has been estimated at greater than 20 pg/l. EPA, in a recent study, estimated that 241,000 children under 6 years old have Pb-B levels above 15 pg/dl because of elevated concentrations of lead in drinking water. Of this number, 100 have Pb-B levels above 50 pg/dl, 11,000 have Pb-B levels between 30 and 50 pg/dl, and 230,000 have Pb-B levels between 15 and 30 pg/dl. o Most children under 6 years of age in the U.S, child population are potentially exposed to lead in food at some level. Actual exposure to enough lead in food to raise Pb-B levels to an early toxicity risk level has been estimated to impact as many as 1 million U.S. children. Despite limitations In the precision of the above estimates, relative judgments can be made about the impact of different exposure sources. Some key findings are: o As persisting sources for childhood lead exposure in the United States, lead in paint and lead in dust and soil will continue as major problems into the foreseeable future. 8 DUP040009463 these sources to children severely complicate efforts to determine source- specific exposures. Consequently, exact counts of children exposed to specific sources of lead do not exist. The first step in approximating the number of children exposed to lead from each of the six major sources is to define v/hat Constitutes exposure. For each lead source, approximate exposure categories are defined and range from potential exposures through actual exposures known to cause lead toxicity. Because the type and availability of data for each lead source vary consider ably, definitions of exposure categories also differ for each lead source. The total numbers of children estimated for each source and category are therefore not comparable and cannot be used to rank the severity of the lead problem by source of exposure in a precise, quantitative way. Furthermore, because of the nature of methods used to calculate the numbers of children in these exposure categories, it is not possible to provide estimate errors. Some numbers are best estimates, but others may represent upper bounds or lower bounds. One should not overlook the limitations and caveats for these calculations, lest the estimates be misinterpreted and misapplied. In addition, source-based exposure estimates of children have different levels of precision. The estimated number of children potentially exposed to a given lead source at any level is necessarily greater than the number actually exposed at a level sufficient to produce a specified Pb-B value, Source-specific estimates of potentially and actually exposed children, based on the best available informa tion and reasonable assumptions, are summarized as follows: o For leaded paint, the number of potentially exposed children under 7 years of age in all housing with some lead paint at potentially toxic levels is about 12 million. About 5,9 million children under 6 years of age live in the oldest housing, that is, housing with the highest lead content of paint. For the oldest housing that is also deteriorated, as many as 1.8 to 2.0 million children are at elevated risk for toxic lead expo sure. The number of young children likely to be exposed to enough paint lead to raise their Pb-B levels above 15 pg/dl is esti mated to be about 1.2 million. o An estimated 5.6 million children under 7 years old are poten tially exposed to lead from gasoline at some level. Actual exposure Of children to lead from gasoline, was projec ted, for 1987, to affect 1.6 million children up to 13 years of age at Pb-B levels above 15 pg/dl. 7 DUP040009464 subset of the population of concern, not because of direct risk to their health, but because of the vulnerability of the fetus to lead-induced harmful effects. Direct, significant impacts of lead on target organs and systems are evident across a broad range of exposure levels. These toxic effects may range from subtle to profound. In this report, the primary focus has been on effects that are chronic and that are induced at levels of lead exposure not uncommon in the United States, Cases of severe lead poisoning are, however, still being reported, particularly in clinics in our major cities. > The primary target organ for lead toxicity is the brain or central nervous system (CNS), especially during early child development. Other key targets in children are the body heme-forming system, which is critical to the production of heme and blood, and the vitamin D regulatory system, which involves the kidneys and plays an important role in calcium metabolism. Some of the major health effects of lead and the lowest-observed-effect levels <in terms of Pb-B concentrations) at which they occur can be summarized as follows: o Very severe lead poisoning with CNS involvement commonly includes coma, convulsions, and profound, irreversible mental retardation and seizures, and even death. Poisoning -of this severity occurs .in some persons at Pb-B levels as low as 80 pg/dl. less severe but still serious effects, such as peripheral neuropathy and frank anemia, may start at Pb-B levels between 40 and 80 pg/dl. o Numerous epidemiologic studies of children have related lower levels of lead exposure to a constellation of impairments in CNS function, including delayed cognitive development, reduced IQ scores, and impaired hearing. For example, peripheral nerve dysfunction (reduced nerve conduction velocities) have been found at Pb-B levels below 40 pg/dl in children. In addition, deficits in IQ scores have been established at Pb-B levels below 25 pg/dl. Preliminary data suggest that effects on one test of children's intelligence may be associated with childhood Pb-8 levels below 10 pg/dl. o Adverse impacts on the heme biosynthesis pathway and on vitamin D and calcium metabolism, all of which have far-reaching physio logical effects, have been documented at Pb-B levels of 15 to 20 pg/dl in children. At levels around 40 pg/dl, the effects on heme synthesis increase in number and severity (e.g., reduced hemoglobin formation). o Of particular concern are consistent findings from several recent longitudinal cover a period of years epidemiologic studies showing low-level lead effects on fetal and child development, including neurobehavioral and growth deficits. 10 DUP040009465 o As a significant exposure source, leaded paint is of particular concern since it continues to be the source associated with the severest forms of lead poisoning. o Lead levels in dust and soil result from past and present inputs from paint and air lead fallout and can contribute to signifi cant elevations in children's body lead burden (i.e., the accumulation of lead in body tissues). o In large measure, paint and dust/soil lead problems for children are problems of poor housing and poor neighborhoods, o Lead in drinking water is a significant source of lead exposure in terms of its pervasiveness and relative toxicity risk. Paint and dust and soil lead are probably more intense sources of exposure. o Greater attention must be paid to lead exposure sources away from the home, especially lead in paint, dust, soil, and drink ing water in and around schools, kindergartens, and similar locations, o The phasing down of lead in gasoline has markedly reduced the number of children impacted by this source as well as the rate at which lead from the atmosphere is deposited in dust and soil, o Lead in food has been reduced to a significant degree in recent years and contributes less to body burdens in the United States than in the past, o Significant exposure of unkown numbers of children can also occur under special circumstances: renovation of old houses with lead-painted surfaces, secondary exposure to lead trans ported home from work places, lead-glazed pottery, certain folk medicines, and a variety of others unusual sources. 3. Section 118(f) (1)(C) This subsection requires a statement of the long-term consequence for public. health of unabated exposure to environmental sources of lead. Chapters III ("Lead Metabolism and Its Relationship to Lead Exposure and Adverse Effects of Lead") and IV ("Adverse Health Effects of Lead") address this issue. Infants and young children are the subset of the U.S. population considered most at risk for excessive exposure to lead and its associated adverse health effects. In addition, because lead is readily transferred across the placenta, the developing fetus is at risk for lead exposure and toxicity. For this reason, women of childbearing age are also an identifiable, albeit surrogate, 9 DUP040009466 period, the earlier GDC (1978) criteria (see Section B, Chapter V). The five highest prevalences are 11,0% (St. Louis), 9.0% (Augusta and Savannah, GA), 4.9% (Harrisburg, PA), 3.5% (Washington., DC), and 3.5% (Merrifiiac Valley, MA [program within the Maternal and Child Health project^). The majority of the risk prevalences were below 2%. Over the years, various characteristics of the lead exposure screening efforts in different, communities have been changing: the definitions of y toxicity risk, the administrative organization of the programs, aad the level of funding of the programs, among other factors, have varied considerably. These changes make it difficult to determine such factors as estimated time trends for more recent years, actual prevalences now being obtained, and what they mean compared with results of prior program screening, Whatever these difficulties, some points are worth noting. 1. Trends in lead toxicity prevalence rates over time, at least in the years of control by CDC and possibly later, suggest a moder ate decline in positive toxicity risk numbers from 1973 onwards, even taking into account changes in risk classifications. 2. Recent 'changes in the CDC toxicity risk classifications appear to be producing an increase in the numbep of positive toxicity cases, at least in one major city program.! 3. In coming years, changes in toxicity prevalences will presumably represent changes in the criteria for toxicity and declines in Pb-B levels associated to some extent with decreases in environ mental lead Inputs. 4. Compared with prevalence projections based on NHANES II data, screening results provide generally lower prevalences, even though children in these programs are "high risk" subjects. Reasons for the discrepancies include the high false negative rate for subjects who are first screened for EP, limited cover age of screening programs, and use of clinic contacts versus home visits. In the case of false EP negatives, any elevated Pb-B levels in these children are lost to accounting. This difficulty did not occur in the NHANES II survey, where direct Pb-B testing was done. 5. Communities that find the highest prevalences of toxicity cases among their children may not have an exceptional lead exposure situation. It may simply be that communities with a more sys tematic approach are turning up the highest rates, a possibi lity that requires centralized screening administration for investigation. 1-14 DUP040009467 TABLE 1-3. SUMMARIES OF ESTIMATED NUMBERS OF CHILDREN 6 MONTHS TO 5 YEARS OLD IN ALL SMSAs WHO ARE PROJECTED TO EXCEED SELECTED LEVELS OF BLOOD LEAD, BY URBAN STATUS, 1984 Characteristic Base Population Blood Lead Level (ucj/dl) >15 >20 >25 In SMSAs 1,000,000 7,251,000 1,493,400 459,500 128,200 In Central City 2,886,200 Not In Central City 4,364,800 901,800 591,600 301,700 157,800 86,200 42,000 In SMSAs <1,000,000 3,536,400 483,000 142,400 40,300 In Central City 1,504,800 Not In Central City 2,031,600 301,100 181,900 93,800 48,600 27,500 12,800 In Small SMSAs 3,052,600a 404,200 113,600 31,200 National Total 13,840,000 2,380,600 715,500 200,700 aTotal includes 6,800 children who could not be stratified by income and were not included in estimates for three Pb-B levels. Originally, the U.S. screening effort was administered by the CDC. At the end of Fiscal Year (FY) 1981, more than 60 programs were operating under CDC. After FY 1981, Federal support was folded into block grants to the various states, and administrative control is now in the hands of state health offi cials. Given the nature of the state-specific block grant mechanisms and how screening efforts would be funded within them, it is difficult to contrast data from the current programs with earlier programs under CDC. Section 8 of Chapter V presents a detailed discussion and tabulation of various past and present screening programs, the numbers of children screened, and the numbers of positive toxicity cases detected. In FY 1981, the last year of CDC management, 535,730 children were screened, with a positive toxicity rate of 4.1% or 21,897 children. In FY 1983, reports from the state agencies indicated that 676,571 children were screened, and 9,317, or 1.6%, had elevated lead exposure of 30 yg/dl and EP 50 pg/dl. In the most recent collection of screening data, carried out by ATSDR in December 1986, 785,285 children were screened in about 40 programs. Of these, 11,73-9 children, or 1.5%, had elevated Pb-B levels that met CDC's toxicity classification. This recent survey data base includes positive toxicity cases that range from 0.3% in four programs to 11.0% for the City of St, Louis program, based mainly on the 1985 CDC criteria but also using, for part of the 1-13 DUP040009468 I 9X-I A ft.** 0i?og- o0 ]* IS 1 OMHOt*-4cAr* *ge*Q O' .O 4k *1 *. _ to 4MH0*4A* W* fll 1s _ 40 .i 10 3 g 4* COM Si " VSoK Ugg^Mo OO ls . SO CD N :fN N.W1N* 9 j* . O* O >J -O O .O OOO fib M M <s m 0 01' -> u 0-00 OOO 0 Ul fs> M-* 0 0 M00 CO 4 *4 M fO O> ro 4(0 0 ggg ,W ro Ul 0 0M Ni V^ilo O 0 0.0 .O .000 10 M* tft ' 0 O m *- CVM >1 000 -OOO 000 O O SO A 0 O rsjoco 0MM40 M O Kyi O fS >4 M 404 roo .000.400000 M w O 0.0 g OOO OOO 0 (- Ut Ut CD O 0 0 00 .0 0 ,0 0 0 OOO 0 U*fS*fS p 4.H 0 <4 vp Ob 0IM0 M O O p 4k CD O 00H 3E. H OTIC (A X to .0e0 * >a 0 T X </i * j0g3 .V) V) O i*H.O </> z iiXk'-n . fl!rXs 1.0 M* im rOS mm m1e0"0n M/..3* !jM >0O o r> oco mSA O -J n sz 0 01 < o P" 0 DUP0400Q9469 Section C of Chapter V examines the numbers of children living in SMSAs by the age of their housing. Age of housing, particularly for the oldest category, can be taken as a reasonably good indicator of the level of poten tial exposure to paint lead (as detailed in Chapter VI). Also examined is the effect of family income on the distribution of young children by housing stock of varying age. The detailed SMSA-by-SMSA numbers of children in the oldest housing, i.e.., housing vffth paint of highest lead content, are tabulated in Section C of Chapter V and in Appendices A, 8, and C. Rankings of SMSAs by numbers of children in variably aged housing and by family income are given for all 318' SMSAs in Section D and Appendix D. The number of children living in pre-1950 housing was Obtained from the actual 1980 U.S. Census enumeration. Tabulations in Chapter V (and supporting data in Appendices A-C) indicate that young children are least often found in the most recently constructed housing, i.e., 1970-80 units. This is probably because young families are least likely to be able to afford newer housing, particularly new housing inside central cities. Table 1-4 presents an illustrative housing and income profile for strati fied groups of children in the SMSA for Cincinnati, Ohio-Kentucky. As shown in the table, children in families with incomes of $15,000 Or more very often constitute the majority of those in each of the "age of housing" categories. Poorer families constitute a small enough proportion of the total population that the highest income group usually predominates in the three "age of hous ing" categories. It is especially important to keep in mind that leaded paint in old housing remains as an exposure source for successive waves of young children who occupy such housing. In other words, the count of children at a specific point in time, such as the 1980 census, is actually multiplied manyfold over an extended period if the exposure source remains unabated. The cumulative tally over 3 to 5 decades for infant and toddler exposure in a residence with S unabated leaded paint will be at least five- or ten-fold greater than the numbers presented in Chapter V and supporting Appendices. 2. Numbers of Lead-Exposed Children by Lead Source In Chapter VI, the numbers of children exposed to lead are described in terms of different lead source categories. Since exact counts of children 1-15 DUP040009470 Source Category 5, Lead in drink- ing water 6. Lead in food TABLE 1-5. (continued) Level of Precision Method of Exposure Measurement Actual exposure Summing of corresponding actual exposure numbers from first three actual exposure categories, or'' use of multimedia regres sion equations (not pos sible with present data) Potential exposure Numbers of young children ' in homes with either old lead plumbing or with lead solder in new home Actual exposure that is measurable but not highest toxicity risk Numbers of young children in homes with lead levels in drinking water above 20 pg/liter Actual exposure at or near toxic levels .Number of children esti mated from NHANES II prevalences of projected toxic Pb-B levels (see Chapter VI for descrip tion) Potential exposure at or near toxic levels Tally of children within selected age group Actual exposure Fraction of those poten tially exposed children whose food lead intake may raise Pb-B high enough to cause concern exposed to lead on a source-specific basis do not exist, these numbers had to be estimated. Table 1-5 contains an outline of the various estimation strate gies. Since Section 118(f) did not specifically define the level of sourcespecific exposure to be considered, methods of varying levels of precision were used to estimate actual exposure risk. Table 1-5 sets forth the ap proaches by the six major categories: lead in paint, lead from gasoline combustion, stationary source lead, lead in dus.t/soil, and lead in food and in water. In some cases, numbers of children in proximity to a source are given. 1-18 DUP040009471 TABLE 1-5. CATEGORIES OF ESTIMATION METHODS FOR CHILDREN EXPOSED TO LEAD BY SOURCE Source Category Level of Precision Method of Exposure Measurement 1. Lead in paint Potenti a I exposure Determination of numbers of children in housing with highest likely leadpaint burdens; complements Chapter V data Potential exposure with a better indication of actual exposure risk Number of children esti mated to be in lead-paint housing with deteriora tion: peeling paint, broken plaster, damage Likely actual exposure Use of a specifically determined prevelenee for an NHANES II stratum matching such children; other, regional survey data 2. Lead in gasoline Potential exposure (Pb-B changes) in a subset of U.S. urban child population Total number of young children in 100 largest cities of the U.S. Actual exposures based on leaded gasoline combustion Logistic regression analysis to estimate numbers of children falling below selected Pb-B criterion values 3,. Lead from sta tionary sources Potential exposure Total of young chi1dren in communities within certain proximity of lead opera tions Actual exposure Prevalence of indicated Pb-Bs at or above some criterion level in actual field studies of station ary sources 4. Lead in dusts and soils Potential exposure Summing of potential exposure numbers from the above three categories (continued on following page) 1-17 DUP040009472 f, For lead in dust and soil, it is necessary to use source- specific numbers for the generators of this source, i.e,, paint lead in old housing, lead fallout from leaded gasoline combustion, and stationary emissions. With regard to potential exposure of children, these primary source Surrogates for dust and/or soil lead amount to a range of 5.9 to 11.7 million children. Actual exposures of children to soil/dust lead sufficient to raise Pb-B levels to the range of toxicity risk, cannot be estimated at this time, but the actual numbers may be considerable. g, Virtually all children are potentially exposed to some level of lead in drinking water, b. About.3.8 million children are exposed to residential drinking water containing the proposed EPA level of 20 pg/liter or higher, I. Children under 6 years old and exposed to lead in residential drinking water at levels high enough to result in toxic Pb-B levels number 241,000 (at >15 pg/dl). Broken down by Pb-B levels, they number 230,000 (at 15 to 30 pg/dl), 11,000 (at 30 to 50 pg/dl), and 100 (at >50 pg/dl). j. Children of school age have potential exposure to lead in drink ing water in school buildings. Numbers cannot be estimated at this time, k. Essentially all U.S, children of age 5 years or younger may have some level of food lead exposure. l. The number of children having food lead exposure sufficient to elevate Pb-B concentration to a level of some concern amounts to about 1.0 million as an upper bound. This is an overestimate arising from the fact that it is based on food lead data for the 1970s, when levels were higher than for more recent years. The above source-specific estimates represent a variety of estimation methodologies, data bases of differing age and specificity, and differing levels of estimate error, much of which remain unquantifiable. Consequently, each source should be considered in terms of relative exposure estimates within the source. Once cannot simply add these numbers together to obtain total source-specific exposures. Given the above qualifications, it is inadvisable to rigidly rank the importance of the described sources purely on a numerical basis. Other points about these source-specific exposures are discussed later in this chapter. Although it is not possible to rigidly rank source-specific exposure, conclu sions may be drawn about their relative impact, as set forth in Section C, Conclusions and Overview. 1-20 DUP040009473 In other cases, actual prevalences of Pb-B levels in a source-specific Manner can be used. The level of estimation error for each of the Source categories cannot be stated. In some cases actual counts of individuals are used, but in other casds elements of an estimation analysis are combined, with each having variable and relatively undefined precision. Some estimates are judged to be upper bounds, and others lower bounds for actual values. For purposes of summary and discussion, each source-based estimation analysis is presented separately. Summary of Source-Specific Exposures and Ranking of Lead-Exposed Children by Source The various source-specific estimates of numbers of children having different levels of lead exposure are presented below as summary statements: a. Children under 7 years old who are potentially exposed to paint surfaces containing lead concentrations of 0.7 mg/cm2 or higher number about 13.6 million, of whom about 5.9 million live in the oldest, highest paint lead residential units. Of these chil dren, about 4,4 million live in U.S. SMSAs. Children in deteri orated, old housing number 1.8 to 2.0 million, b. Children living in old and deteriorated housing and estimated to have Pb-6 levels above certain selected criterion values due mainly to paint lead exposure amount to; 1,2 million (at >15 pg/dl), 0.5 million (at >20 pg/dl), and 0.2 million (at >25 pg/dl). c. Children potentially exposed to lead from combusted gasoline and residing in the 100 largest cities of the United States are estimated to total about 5,6 million. d. Children 13 years old and younger who are sufficiently exposed to gasoline lead to show declines in Pb-B levels in response to the phasedown of leaded gasoline amount to: 1.6 million fall ing below 15 pg/dl and about 0.6 million falling below 20 pg/dl. These estimates are seen to be unrelated to any specific Pb-B levels. e. For stationary sites, namely primary and secondary smelters, the potential exposure estimate is about 230,000 children. Of this number, up to 13,000 children will have Pb-B levels above approximately 20 pg/dl. j-19 DUP040009474 TABLE 1-6. ESTIMATED NUMBER OF WOMEN OF CHILDBEARING AGE AND ESTIMATED HUMBER OF PREGNANT WOMEN AND PROJECTED NUMBERS ABOVE FOUR SELECTED Pb-B CRITERION VALUES (pg/dl). BY RACE AND AGE, IN ALL SMSAs, 1984 Race/Age (years) Women in SMSAsa Base Population ____Pb-B (ug/dl) >10 >15 >20 >25 y White 15-19 20-44 5,478,000 29,740,000 504,000 27,400 2,884,800 535,300 5,500 119,000 1,600 29,700 Black Total** 15-19 20*44 1.098.000 4.984.000 41,300,000 90,000 981,800 4,460,600 14,300 184,400 761,400 2,200 34,900 161,600 500 ' 10,000 41,800 Pregnant Women in SMSAsa White 15-19 20-44 433,000 2,380,000 39,800 230,900 2,200 42,800 Black 15-19 20-44 187.000 595.000 15,300 117,200 2,400 22,000 Totalb 3,595,000 403,200 69,400 aMethod of calculating explained in text of Chapter VII. ^Totals by addition, not estimation. 400 9,500 400 4,200 14,500 100 2,400 100 1,200 3,800 above 10 pg/dl. About 9% of the women aged 1$ to 44 were pregnant in 1984, and projection of the estimated prevalences yielded about 403,000 pregnant women with Pb-B levels above 10 pg/dl, which signifies that their fetuses were at risk for abnormal prenatal as well as postnatal growth and development (see Section A and Chapter IV), Since the individuals who are pregnant vary from year to year, the popula tion at risk is constantly changing and is not readily identifiable. In other words, it is not a single, fixed group of pregnant women who constitute a one time exposure risk to their fetuses. Over a 10-year period, for example, in the absence of effective exposure abatement the cumulative number of individual fetuses at risk would be greater than 4 million, even assuming multiple preg nancies in some women in this pool. 1-22 DUP040009475 3. Number of Women of Childbearing Age and Pregnant Women Although not specifically required in Section 118(f), this report includes a quantitative assessment of lead exposure of human fetuses via lead exposure of pregnant women in the O.S. population. In utero exposure results in post* natal consequences and therefore is considered within the spirit of Section 118(f) and requires Inclusion in this report. In pregnant women, lead readily crosses the placental barrier and does so early in gestation (see Chapter III), In utero exposure, therefore, occurs at periods of development when.important organs and organ systems can be affected adversely by lead uptake. Such adverse in utero effects have been known for many years and still remain as a public health problem in the form of low-level lead effects, as documented in Chapter IV and in U.S. EPA (1986a), Based on the evidence cited above, in utero exposure appears to produce effects of concern at Pb-B levels of 10 to 15 pg/dl and possibly lower. The implication is that every pregnancy potentially represents a fetus at risk if the mother is found to have a blood lead level of about 10 pg/dl or more. Since pregnant women are not a stable population segment, the total population of women of childbearing age must also be considered when trying to assess the size of this part of the public health problem associated with lead exposure. The methodology to estimate the numbers of lead exposed women is basically the same as that employed for the numbers of young children projected in Chapter V, For reasons indicated earlier for children, primary attention was placed on that segment of the female population living in SMSAs. After deriving the number of women of childbearing age for 1984, as well as the number of pregnancies for that year (live births plus fetal deaths and legal abortions), the estimated numbers of these women with Pb-B concentrations above four reference blood lead, levels (>10., >15, >20, and >25 pg/dl) were calculated. Prevalences for the Pb-B criterion levels were determined by application of logistic regression analysis of the NHANES II data for four race/age categories of women and adjusting for the effects of the phasedown of lead in gasoline. Table 1-6 shows the findings for 1984. About 41,300,000 women were of childbearing age; this represents about 45% of the total female populations in all SMSAs. Of these, about 4,460,000 would be expected to have a Pb-B level 1-21 source is possible, then the latter action is still useful. By doing so, one can drop the Pb-B level from 25 to 20 pg/dl, that is, below the given "toxidty" level selected for this illustration. Several approaches to the problem of the aggregate impact of lead from a variety of low-level sources are examined in Chapter VIII. National or regional surveys of Pb-B levels would, of course, reflect the total, integrated amount of lead absorbed from all sources across national or regional popula tion groups; such surveys could set baselines for observing changes. Methods for tracing the contributions of specific sources to blood lead need to be better developed, and the impact of lead distributions from cumulative sources (e.g.,, on young children in a given region) needs to be analyzed. Quantitative metabolic models of lead intake, uptake, and systemic distribution that permit the factoring of all inputs to blood lead, even when such inputs vary across pediatric groups, need to be developed or further refined. Further data on the distribution of lead between the fetus and the mother would be of particu lar value. Chapter VIII addresses each of these topics in some detail, with particular emphasis on the use of comprehensive metabolic/kinetic models that would be of use to regulators examining multisource lead inputs to human populations. Such models enable one to consider the incremental inputs of individual sources to blood lead as well as the result of removing or reducing a specific exposure scurce. '5. Lead Exposure Abatement Strategies and Alternatives In Chapter IX, exposure control approaches are described in general, and lead exposure control approaches in particular, A basic question underlying such past and ongoing exposure abatement efforts is the degree to which reduc tion should be attempted- For example, is it enough simply to reduce exposure so that Pb-B levels fall below some official index of toxicity, or should some margin of safety be sought? Questions of this sort shape the full scope .of abatement efforts. Lead exposure prevention cap be described along various categorical lines, as presented in Table 1-7. Prevention efforts can be defined as either primary or secondary, i.e. direct intervention applied globally prior to identifica tion of health risk, or intervention after the fact of identified health risk. 1-24 DUP040009477 Women of childbearing age, 15 to 44 years, have a smaller uptake of airborne lead than children on a body weight basis, and unlike children, they obtain the major portion of the total body burden of lead from food and water rather than from leaded paint chips, dust, and contaminated soil. Abatement limited to external exposure sources of significance for children may not necessarily achieve comparable improvement of lead exposure in women. 4. The Issue of Low-Level lead Sources and Aggregate Lead Exposure of Children in the United States Chapter Vi qf the main report, which deals with single-source exposures, provides estimated numbers of children exposed to lead in some dominant source or cluster of sources, such as dust and soil. This is possible because of the high concentrations of lead in these sources. It is not possible, however, to assess the impact of low-level lead sources such as food or water without simultaneously considering other lead inputs that may also be moderate in relative impact, because multiple, low-level inputs can accumulate to a potentially significant aggregate exposure. Lead entering the body from a variety of source? presents a unified toxicological threat that is independent of the source pf exposure. With multiple, low-level aggregate intake and uptake, it is essential to have ways to examine changes in levels of these sources as they relate to changes in Pb-B levels. This imperative is the rationale behind considering low-level sources, the subject of Chapter VIII. The cumulative exposure approach also requires us to examine various parameters associated with different body organs and functions (e.g., lungs versus the gastrointestinal tract) in the same population group or among various groups (e.g., children versus adults). Details of the metabolic factors appear in Chapter III.. The issue of aggregate exposure to lead has both scientific and regulatory policy aspects. With respect to policy, these aspects include the degree of remediation and feasible abatement level possible for various lead sources. For the purposes of illustration, consider a childhood Pb-B level of 25 pg/dl as an index of toxicity risk. If Source A contributes an equivalent of 20 pg/dl, or 80% of this burden, and Source B contributes 5 pg/dl or 20%, then one can remove the major source of the lead, 80% and have left 20% or 5 pg/dl. If this major source is not abatable, but abatement of the minor 1-23 DUP040009478 the legally allowed level of lead in paints to 0.06% net weight. CPSC has no pandate to control leaded paint produced before this date or to address the problem of leaded paint already in housing. Preexisting leaded paint problems are the responsibility of the Department of Housing and Urban Development (HUD). HUD can only regulate leaded paint in public housing or federally assisted dwellings. ^ Although HUD had some earlier responsibility over the paint lead problem, the bulk of HUD's activity is now in the form of three specific regulations. These three regulations, now in effect, differ in scope, level of control, and, likely effectiveness. For public housing, housing inspections and the finding of children with elevated Pb-B levels are trigger mechanisms for leaded paint abatement. Various FHA programs now require paint lead abatement in FHA- assisted sales or purchases. Refinancing of community-based grant programs, such as Urban Development Action Grants (UDAGs), will require evidence of removal of paint lead exposure problems. At this time, it is not clear what the total impact of these recent HUD regulations will be, since limitations are attached to their scope and applicability. State and municipal actions for the reduction of exposure to paint lead have consisted of statutes with limited application and have received variable enforcement. Among the states, Massachusetts banned lead in any unit in which young children live, but organized opposition from real estate interests and limited funding for enforcement essentially reduced the measure to one of secohdary prevention, that is, intervention only after demonstrated instances of Ipad poisoning have been found. In Chapter IX, Table IX-4, it can be seen that Cities in Massachusetts have tens of thousands of pre-1940 units painted with high lead-content paint, but the multi-year abatement counts total only in the hundreds or less. Certain U.S. cities took actions against leaded paint sale and use well before Federal or state agencies became involved. In 1951, Baltimore, MD prohibited the use of leaded paint for the interiors of dwellings and, in 1958, required warning labels on cans of such paint. In the early 1970$, Philadelphia implemented a primary prevention ordinance against leaded paint, but more recently, prophylactic removal has been discarded in favor of abate ment only after demonstrated toxicity in children. 1-26 DUP040009479 TABLE 1-7. CATEGORICAL TABULATION OF THE ELEMENTS OF PRIMARY AND SECONDARY PREVENTION OF LEAD EXPOSURE IN CHILDREN AND RELATED RISK GROUPS OF THE UNITED STATES Type of Prevention Method Components of the Measure I. Primary A. Environmental 1. Lead in paint 2. Lead in ambient air (a) Leaded gasoline combustion (b) Point source emissions 3. Lead in dust/soi1 4. Lead in drinking water 5. Lead in foods B. Environmental/0iological Source controls augmented by passive community nutrition interventions for calcium and iron II. Secondary A. Environmental 1. Case finding 2. Screening programs 3. Environmental follow-up 4. Event-specific exposure abatement E!. Environmental/Biological Nutritional assessment and follow-up on ad hoc identi fication basis C. Extra-environmental Legal actions and strictures Primary prevention efforts for lead exposure include purely environmental approaches as well as a combination of environmental and biological approaches. A similar duality can also be used in secondary prevention, with the added use of extra-environmental steps, such as legal actions and strictures. With re spect to primary prevention. Chapter IX examines regulatory and other measures on a source-by-source basis, since such have been the avenues by which Federal and other governmental actions have been carried out. Lead in Paint Paint lead exposure abatement has been attempted through various govern mental actions. In 1977, the Consumer Product Safety Commission (CPSC) reduced 1-25 DUP040009480 effective means of lead abatement in areas larger than a single home or several homes. Mobility of lead in dust and soil prevents simple extrapolation to a neighborhood or even larger area. Field surveys need also to define the relationship between blood lead and primary sources. The 1986 Superfund Amendments and Reauthorization Act provided for the funding and establishment of a demonstration project as a mechanism to begi6 to address the problem of area-wide soil (and dust) lead in urban tracts. In response to this, EPA conducted an experts' workshop on the design and scien tific operation of soil lead abatement projects in early April 1987 at Research Triangle Park, N.C. Such matters as methods of environmental monitoring, methods of biological monitoring, and statistical design of the population surveys were discussed. A workshop report is currently in preparation. The Region I office of EPA, in Boston, MA, with the assistance of the Harvard University School of Public Health recently carried out an examination of soil lead removal options. Their conclusions, at least as applied to Boston, indicate that specific soil lead abatement alternatives are a function of the amount of lead present, the disposal methods available, and relative costs. The draft report is presented as Appendix E and is summarized in Chapter IX, Lead in Drinking Water EPA is required by the 1974 Safe Drinking Water Act (SDWA) to set drinking water standards, with two levels of protection spelled out in the legislation. Of interest here are the primary standards for drinking water, which define contaminant levels in terms of maximum contaminant level (MCL) or treatment requirements. MCLs are limits enforceable by law and are to be set as close as possible to maximum contaminant level goals (MCLGs), which are levels essen tially determined by the relevant toxicologic and biomedical considerations, independent of feasibility. Congress recently Ordered EPA to revise the drinking water standards for various substances as necessary, including that for lead, the current MCL for lead is 50 pg Pb per liter of water (yg Pb/liter). It is expected that the revised standard will be somewhat more stringent, possibly 20 yg Pb/liter or even lower. At 20 yg Pb/liter, EPA estimates that about 20% of the tap water levels for homes on public water systems would exceed the proposed standard. 1-28 DUP040009481 Lead in Ambient Air I-PA has had regulatory authority over the use of lead in gasoline since 1973. The statutory specifics of such authority are embodied in Sections 108, 109, and 211 of the Clean Air Act. These collectively cover lead emissions to ambient air. Due to regulations concerned with lead and other pollutants, use of leaded, gasoline has been declining since the 1970s, as documented in a number of chapters in this report. With recent phasedown action to reduce the lead content of gasoline to 0.1 grams per liquid gallon by January 1, 1988, there is expected to be, and already has been, a significant impact on body lead burdens in the U.S. population. For example, in the section describing source-specific exposures it is projected that the gasoline lead phasedown will lower Pb-B levels to less than 15 pg/dl in millions of children between now and 1992. Gasoline lead phasedown also affects further input into ecological com partments, although past depositions (fallout) of lead onto soil from the widespread use of leaded gasoline will remain. Reductions in emissions from stationary sources, with measurable benefits to neighboring communities, have been achieved by the EPA-promulgated ambient air lead standard. In 1978, this standard was made more strict at 1.5 pg lead/m3 of air; currently, the standard is under consideration for possible further reduction. Lead in Dust and Soil The primary prevention measures for exposure to lead-contaminated dust and soil are usually directed at the generators of lead for these sources, that is, lead from paint, gasoline combustion, and stationary emitters. Such measures may reduce or eliminate further inputs from these sources but will not influence amounts already present. Currently, no particular body of regulatory action seems to be directed at controlling lead in dust and soil, although, as discussed in Chapter X, several Superfund sites containing lead in soil are due for cleanup. Reasons for the absence of specific regulatory action include lack of awareness of the problem, the complexity of the problem, and lack of data for inputs from primary con tributors on a site-by-site basis. At present, field studies are needed to provide evidence that ''macro*1 rather than "micro" control strategies are 1-27 DUP040009482 control dates back to the appearance of lead"containing pesticide residues on sprayed fruits. FDA actions from the 1970s onward have been aimed at reducing total lead intake pr known significant sources of lead inputs into foods. In 1979, FDA mad its goal the reduction of the daily total lead intake by children 1 to,, 5 years old to less than 100 pg/day. this would be the maximum permissible intake, and not a mean intake. Attention was focused on; (1) establishing permissible lead residues in evaporated milk and evaporated skim milk; (2) setting action levels {guidelines for reduction) for lead in canned infant formulas, canned infant fruit and vegetable juices, and glass-packed infant foods; and (3) establishing action levels in other foods. FDA maintains a program to monitor lead levels' in the U.S. food supply, but the program Is limited and requires expansion. FDA also monitors and enforces controls on such materials as pottery and food utensils with Teachable lead; published reports have documented lead exposure from improperly glazed pottery. The percentage of food cans that are lead-soldered continues to decline. In 1979 the percentage was very high--over 90%; but 1986 figures are expected to be about 2(}%. FDA has estimated that about 20% of all dietary lead was from canned foods and that about two-thirds of this was from lead soldering. Recent data provided to FDA by the National Food Processors Association indicate about a 77% reduction ip canned food lead in the period 1980-1985. Note that imported canned foods may still come id lead-soldered cans. The number of cans being imported is not known but may be considerable. Recent FDA surveys, from 1982/1983 to 1984/1985, suggest significant declines in daily dietary lead intake across all ge groups and fo;r males and females. On average, the decrements in dietary lead intake amounted to approximately 40%. These surveys involved relatively small samples; tftey need to be expanded con siderably in their coverage. Nutritional Measures in Primary Prevention of Lead Exposure Several biological factors can suppress lead uptake by the body or enhance its excretion, particularly nutrients that have well-established interactive relationships with lead uptake and toxicity. Supplemental dietary micro- and macro-nutrients may therefore be used to reduce internal exposure. When used on a prophylactic, community-wide basis, nutritional measures constitute one form of primary prevention. When these factors are exploited on aft ad hoc basis 1-30 DUP040009483 In addition to the pending rule on lead in drinking water per se, the 1986 amendments to the SDWA ban the use of lead spider and other lead-containing material in plumbing connected to public water supplies. States must enforce the ban by 1988 or be subject to a loss of Federal grant funds. Since EPA is concerned with tap water lead levels, as well as lead burdens/ in processed water leaving treatment facilities, the agency roust specify the "best available technologies" for preventing the entry of lead into drinking water. Two approaches are those of corrosion control, i.e., treating potable water to raise its pH and alkalinity with lime and sodium hydroxide, and the addition of orthophosphate to develop a protective film inside pipes. Further more, EPA is considering the removal of lead service connections and gooseneck connectors in its determination of best available technology. The fraction of the U.S. population that has corrosive drinking water is not precisely known, but such water is common to high-density population areas; thus the number of children involved is rather substantial (Chapters VI and IX). On the basis of studies from both the United States add Scotland, commu nity water treatment as a primary measure to minimize plumbosolvency is known to reduce exposure for children and other groups. In the United States, Boston water authorities began to reduce corrosivity in the 1970s, because of the density of old housing with lead in plumbing. These efforts considerably reduced the amount of lead in tap water (see U.S. EPA, 1986a). U.S. EPA (1986b) has estimated that the costs of water treatment to reduce corrosivity would be just 25% of the value of health benefits derived from reducing all exposures to lead in drinking water to less than 20 ppb, that is, a benefit-to-cost ratio of 4:1. Therefore, one would expect that extending similar actions under EPA regulations would have a widespread positive impact on children exposed to lead in drinking water. Lead in Food Lead from food and beverages is a significant exposure source for a portion of children, considering the distribution of lead intakes within populations of children (see Chapter VI) and the fact that the entire U.S. child! population encounters some lead in food. Therefore, primary prevention measures that limit lead exposure from this universal pathway are important. Regulating lead contamination in foods has been the responsibility of the U.S. Food and Drug Administration (FDA) for several decades. This regulatory 1-29 DUP040009484 chronic exposure and lower grade toxicity appear to be more persistent. Persistence of these problems is predictable, given the levels and types of lead exposure remaining in the United States. In 1981, Federal resources for screening were put under the program of the Maternal and Child Health Block Grants to States, Although the States' use of Federal funds for lead screening programs was estimated by one source to have been reduced initially by 25% (Farfel, 1985), a precise figure cannot be readily given since allocations of the block grant funds for particular projects are determined by the States according to their priorities, and data are not systematically collected on these State funding allocation decisions. The evidence of the national impact of this initial reduction in Federal resources appears to be mixed. While it appears that the total number of Screening program units in the nation has decreased from 60 to between 40 and 45 (Chapter V), there is also evidence in some States and localities that the number of children currently being screened has increased since 1981 (CDC, 1982; Public Health foundation, 1986). However, based on a study using data from the period prior to implementation of the block grants (Schneider and Lavenhar, 1986), it is likely that those areas that choose to decrease the efficiency of their lead screening services can expect to experience increases in the number of children with lead poisoning. Screening programs, especially those supported at levels that allow blanket screening, are particularly cOst-effecttve. To demonstrate this point, the costs of treating lead-poisoned children who were not detected in earlier screening were compared with the costs of community screening programs. In one report, the cost of repeat admissions to Baltimore hospitals for 19 leadpoisoned children was $141,750, or ati least $300,000 in 1986 dollars. For the 1985-1986 program year, the city of St, Louis listed budgetary support of $303,453 from the city and $100,000 from the State of Missouri for lead screening. Concurrently, agencies in the St. Louis program tested 12,308 children, of whom 1,356 or 11.02% were positive for lead exposure as indexed by blood lead levels. These figures are a low boundary for the number of positive cases, because newer, lower guidelines of CDC were only implemented in mid-1985. For the screening period in which its various components detected 1,356 positives, the St, Louis program cost $403,453 or less than $300 per affected child. In contrast, the estimated average cost, in 1986 dollars. 1-32 DUP040009485 in children or families where lead poisoning has occurred, their use becomes a secondary prevention measure. Only a few nutrients can realistically be viewed as having a role in preventive community medicine in high-risk populations. Of particular interest are iron and calcium as nutritional supplements. Numerous studies have shown that" calcium status and iron status in young children are both inversely related to the level of lead absorption, that is, as either calcium or iron levels go down, lead levels tend to go up. The reestablishment of optimal nutrition ip high-risk children exposed to any level of lead is not only necessary byt particularly effective. However, use of optimal nutrition, alone, without environmental abatement measures, is not likely to reduce Pb-B levels sufficiently. For the purposes of reducing lead uptake, nutrition monitoring and maintenance are probably best done in a ' program of nutritional care, such as the Women, Infants and Children (WIC) nutrition program. The level of funding and other support for such programs obviously determines their potential for reducing net lead exposure. Con versely, poor nutrition in those at high risk will enhance toxicity in that population. Secondary Exposure Prevention Measures This topic comprises (1) environmental measures, (2) combined environmental and biological measures (nutrition), and (3) extra-environmental measures. The most representative purely environmental measures are community screening pro grams and associated efforts to identify and abate specific hazards. Features of the various screening programs and the data derived from them are summarized above and discussed in Chapter V. Here, the focus is on their relative roles as secondary prevention instruments. The lead screening programs administered by the U.S. Centers for Disease Control resulted in about 4 million children being tested nationwide and about 250,000 children being diagnosed as lead poisoned by various criteria. On the average, the screening programs surveyed only about 30% of the high-risk chil dren. Furthermore, the detection rates for positive toxicity were considerably below those of NHANES II. Case finding and cluster testing, followed by targeted screening, also produce much higher positive response rates. Early screening and detection of lead exposure and toxicity have no doubt reduced the rates of severe poisoning. For a number of reasons, however. 1-31 DUP04Q0Q9486 Therefore* an effective response to the dust aspect of the problem could well be as important as removing paint film. Secondary Nutritional Measures As a secondary prevention method, the approach of combining environmental and biological (metabolic) measures through improved nutrition overlaps that' described for primary prevention strategies. In this case, however, nutri tional optimization to reduce overall toxicity risk is mainly directed to high-risk segments of the population or to children beginning to show elevations in their Pb-B levels. In addition, nutritional approaches used in this way would probably also require the affected family to take a more active role in monitoring the child's nutrition. Extra-Environmental Prevention Measures This report considers legal sanctions as a means of forcing the removal of lead from designated sites where there is documented evidence of lead poison ing. It is not easy to draw conclusions from the available information, but it may be useful to examine the experience of a screening program with a legal component. In its summary of screening activities submitted to ATSQR, the City of St. Louis described its dealings with landlords and others who own housing or public facilities where lead poisoning had been found. The main legal device at the City's disposal for forcing lead removal of leaded paint appears to be the imposition of minor fines. It is not clear that minor fines as legal sanctions have influenced the city's lead screening toxicity rate, which in the most recent survey was 11%, a rate that has remained about the same since 1978. This case does suggest, however, that the continuing high rate of lead toxicity has not resulted in more effective legal measures. 6. A Review of Environmental Releases of Lead Under Superfund Section 118(f)(2) requires the scoring and evaluation of sites at which children are known to be exposed to environmental sources of lead, using the Hazard Ranking System of the. National Priorities List. EPA has both listed and discussed facilities with releases of lead that have already been scored 1-34 DUP040009487 for the Baltimore children requiring multiple hospital admissions* was $16,000 per child. Over an extended period* additional costs in the development and care of these children occur and can be large. The effectiveness of screening children for lead poisoning is well demonstrated in terms of deferred or averted medical interventions, and in most settings is quite cost-effective. Ip April 1987, the Committee on Environmental Hazards, American Academy of ' Pediatrics, issued its "Statement on Childhood Lead Poisoning.11 It includes this statement: ",..to achieve early detection of lead poisoning, the Academy recom mends that all children in the United States at risk of exposure to lead be screened for lead absorption at approximately 12 months of age.... Furthermore:, the Academy recommends follow-up...testing of children Judged to be at high risk of lead absorption.'1 These guideTines from America's pediatric medicine community probably cannot be effectively implemented or coordinated with the current levels or existing type of program support at local, State* and Federal levels. When cases of toxicity were found in the course of mass screenings for lead poisoning, efforts were routinely made to find the causes, A careful examination of the information on reducing lead exposure by completely or partially removing lead paint clearly shows that, at best, the benefit is debatable. At worst, the problem may be exacerbated. One longitudinal study showed that when children return to "lead abated" structures after hospitaliza tion for treatment, their Pb-8 levels invariably returned to unacceptable levels. This is not a case of endogenous reexposure from the release of bone lead, because children with equally high Pb-B levels before such treatment retained lower blood levels when returned to housing already free of leaded paint. Information has accumulated to show that removal of leaded paint is hazardous to the workers doing the removal and that lead from the paint contin ues to be hazardous to the occupants because residual material has been moved to other areas that children contact. Several recent studies have shown that lead-poisoned children's exposure was exacerbated in various ways when leaded paint removal was being done or had been done in their homes. One difficulty is the relative mobility of powdery leaded paint, which enters cracks and crevasses, settles on contact surfaces, and readily sticks to children's hands. 1-33 DUP040009488 additional data have been gathered, and is used to help determine what sort of risk management action must be taken to reduce the risk from the facility to a reasonable level. The Hazard Ranking System was developed to prioritize actual and potential hazards to public health and the environment from hazardous waste disposal sites. It is used by EPA as a screening and prioritizing tool to determine which sites will be candidates for Superfund financial remedial response.. Of necessity, it is applied early in the site evaluation process, ' before many actual data have been collected, thereby requiring that assumptions be made about the site based on available data and on what is known about similar sites with similar releases* The criteria for setting priorities are based on relative risk or danger, taking into account the size of the population at risk* the hazard potential of the chemicals or substances found or known to be at the facility, and the potential for contamination of drinking water supplies, all of which are factors present at most hazardous waste disposal sites, but not necessarily present in urban residential settings. The Superfund Amendments and Reauthorization Act of 1986 directed EPA to modify the Hazard Ranking System so that "to the maximum degree feasible, it accurately assesses the relative degree of risk to human health and environmen-:" posed by sites. EPA was specifically directed to assess human health risks associated with actual or potential surface water contamination, damages from an actual or a threatened release tp natural resources that might affect the human, food chain, actual or potential ambient air contamination, and those wastes described in Section 3001 of the Resource Conservation and Recovery Act . (*..{}., fly ash, bottom ash,, slag waste, and flue gas emission control waste). EPA was also directed to give high priority to facilities where a release has resulted in closure of drinking water wells or has contaminated a principal drinking water supply. EPA is in the process of addressing these concerns in its update of the Hazard Ranking System. It expects to propose for comment a new Hazard Ranking System in the summer of 1988. 7. Information Gaps. Research Needs, and Recommendations In preparing this report, it was apparent that adequate information did not exist to fully answer many questions about childhood lead poisoning in 1-36 DUP040CI09489 using the Hazard Ranking System; it has also collected data on an area in Boston where children have been exposed to soil contaminated by lead-based paint and perhaps lead from past automotive emissions from combustion of leaded gasoline. It was necessary to obtain these data because no such site had ever been submitted for ranking under the Hazard Ranking System. The facilities that have been listed or proposed for listing on the ^ National Priorities List have all scored above 28,5, the cutoff point under the Hazard Ranking System for listing on the National Priorities List. All were facilities where lead has been pr is being smelted of otherwise processed* and all emit or have emitted lead from such processing. All have significant amounts of lead in the soil from such emissions. EPA has examined records to determine whether there is any evidence of children having been exposed to lead from these sources, since children are not an identified.population under the Hazard Ranking System. In some cases, especially around primary smelters, earlier studies had shown that children were indeed exposed to the air emis sions from the facility and to the .contaminated soil, due mostly to the fallout from air emissions from the facility. Those cases are discussed in Chapter X. The site in Boston for which EPA has gathered data specifically for scoring under the Hazard Ranking System consists of several residences. These residences are located in areas identified by the city as Emergency Lead Poisoning Areas, where a large number of children have been found to have elevated blood lead levels. Soil around these residences contains high levels of lead, much of it apparently from lead-based paint that has weathered and flaked from the houses into the surrounding soil. Some of the lead has most likely come from past automotive emissions resulting from the burning of leaded Only one residence was scored under the Hazard Ranking System for this report, since the data collected at several houses were similar and would result in approximately the same score. The Hazard Ranking System score for the house selected is 3,56 out of a possible 100. This score is the highest possible score for any of the houses, because of its proximity to a surface water source, and because it is within the range of industrial wells. The direct contact score is not used as part of a site's score for purposes of placing a site on the National Priority List. The Hazard Ranking System is not a risk assessment of the hazards to be found at a facility. Such an assessment occurs later in the process, after 1-35 DUP040009490 Research Needs A minimum inventory of research needs in the areas covered by this report includes the following: (1) Comprehensive studies of the relationship between exposed populations and various sources of lead, and the geographic distribution of these risk^ populations, are needed for high-level sources, as well as those currently viewed as "background" or "low-level." As part of this effort, censustaking instruments should include survey questions related to environ mental exposure to toxicants. (2) Development of quantitative biokinetic/aggregate uptake models for reli ably predicting body lead burdens should be continued. Such models could reduce the need for expensive future population surveys. (3) Both the scope and number of prospective studies of lead exposure and toxicity in U.S. and other populations should be expanded. (4) Further research on the relative strengths and shortcomings of biological indicators of systemic exposure, particularly in vivo measures of lead accumulation in the mineral tissue of young children are needed. A related need is more research on the relationship between fetal lead exposure and the body burden of lead in pregnant women. (5) In the difficult area of lead exposure prevention by primary and secondary means, research is required on several fronts: (a) Further field studies of the, efficacy of lead removal from children's environments at a tract or neighborhood level. Efforts would include before-and-after evaluation of Pb-B levels. EPA-sponsored studies are now underway to address these problems systematically via demonstration projects. (b) Field studies of the type detailed above that also permit specific assessment of how such procedures are related to primary contributors, such as paint lead versus urban air fallout of lead. Here, also, the EPA demonstration projects will be helpful , if source-dependent studies are made of these variables. (c) Assessment of removal technology for site debridement of paint and related sources. Since paint lead alone con stitutes an aggregate burden of millions of tons, removal is not an inconsequential problem. Moving the lead may also mean shifting exposure to another population, if adequate precautions are not taken. 1-38 DUP040009491 1 tha United States. These gaps in information and the research needed to fill them are summarized below. In addition, recommendations for further action are presented. Information {Saps (a) Comprehensive, current, and accurate data on the numbers of children and other risk groups having lead exposure by specific areas of residence do not exist as such. Therefore, this report was- confined to using, as best as possible, available data, (b) there is surprisingly little information on the actual numbers of young children exposed to lead in source-specific ways. Data that do exist are highly variable in their quality and level of detail. (c) Additional data are needed on the relationships between dust/ soil lead and both paint and air lead, especially when air levels are changing. In this report, we could not separate these media'-specific exposures in order to derive estimates for separate totals of exposed children. (d) More specific information is required on the actual distribution of lead concentrations in the tap water of households containing young children as well as lead in water of schools, day-care centers, etc, (e) Information on dietary lead intakes by infants and toddlers needs to be updated. Information is also needed on the distri bution of intakes in the U.S, child population. (f) Much remains to be learned about the adverse effects of lead in young children and other risk groups. (g) The area of lead exposure abatement approaches and strategies is plagued by a number of unknowns with respect to both their qualitative and quantitative aspects, (h) Information is needed on the full range of options, in terms of their technology and costs, for removing paint, dust, and soil lead from the environment. (i) A lack of knowledge exists about support approaches for any assault on lead exposure. These approaches include maintaining optimal nutrition in risk populations and effective legal mea sures to enforce compliance with abatement programs, (j) There is no good data base to assess how changes in the organ ization of screening'programs have affected the scope and effec tiveness of these programs in high-risk areas. It is particu larly desirable to know the level of undetected toxicity among target populations for screening. 1-37 DUP040009492 <1) Leaded paint continues to cause most of the severe lead poisoning in children in the United States. It has the highest concentration of lead per unit of weight and. is the most wide spread of the various sources, being found in approximately 21 million pre-1940 homes. (2) Dust and soil lead, derived from flaking, weathering and chalk ing paint plus air lead fallout over the years, is a second major source of potential childhood lead exposure. (3) Drinking water lead is intermediate but highly significant as an exposure source for both children and the fetuses of pregnant women. Food lead also contributes to exposure of children and fetuses. (4) Lead in drinking water is an example of a controllable exposure source for which state and local agencies should be encouraged to enforce strictly the Federal ban on the use of leaded solder and plumbing materials. A second initiative is the examination of the full scope of lead exposure risk from lead-leaching plumbing and fountains/coolers in schools. Strong efforts should also be made to reduce exposure to lead-based paint and dust/soil lead around homes, schools, and play areas. (b) Efforts at reducing lead in the environment should be accompanied by scientific assessments of the amounts of lead in each of these sources through strengthening of existing programs that currently attempt such assessment. The largest information gap exists in determining which housing, including public housing, contains leaded paint at hazardous levels. A similar gap exists for information in distributions of soil/dust lead on a regional or smaller area basis. Systematic monitoring of lead exposures from food and water is urgently needed. The Food and Drug Administration should seriously consider increasing support for its Total Diet Study to broaden population coverage. The data currently collected do not yield sufficient Information on the high risk strata of the population to support intervention measures. (c) Use of precise and sensitive methodologies is essential for environmental monitoring of source-specific lead. Mpre sensitive and precise techniques are required for in situ field testing of lead in painted surfaces, (d) Major improvements in the collection, interpretation, and dissemination of environmental lead data on a national basis are required and recom mended to assess the extent of remaining lead contamination and to . identify trends. Data from screening programs should be compiled nationally and made uniform so that geographic differences in lead toxicity rates can be determined. 1-40 DUP040009493 (d) Examination of the efficacy of high-risk lead screening programs both for their scope and effectiveness and for the relationship between key factors (e.g., resources made available, screening methodologies, end mechanisms to report data) and their impact on efficiency of identifying children at risk. (e) Assessment of the relative costs of effective, if expen sive, alternatives to the piecemeal abatement, enforcement, and follow-up approaches that appear to constitute present remedial actions. Would it be less expensive, in human and resource terms, to relocate populations as opposed to allowing them to remain in exposure settings? (f) Research that explores the feasibility of better indicators of lead exposure for screening purposes, particularly at low levels where, for example, erythrocyte protoporphyrin (EP) is less useful. This permits elucidation of those lower effect levels of lead in children not easily identified by EP testing. RECOMMENDATIONS In view of the multiple sources of lead exposure, an attack on the problem of childhood lead poisoning in the United States must be integrated and coordinated if it is to be effective. In addition, such an attack must incor porate well-defined goals so that its progress can be measured. For example, the lead exposure of children and fetuses must be monitored and assessed in a systematic manner if efforts to reduce their exposure are to succeed. A com prehensive attack on the lead problem in the United States should not preclude focused efforts by Federal, state, or local agencies with existing statutory authorities to deal with different facets of the same problem. Indeed, it is important that all relevant agencies continue to respond to this important public health problem, but to do so with an awareness of how their separate actions relate to the goals of a comprehensive attack. Specific recommendations to support the general objective of eliminating childhood lead poisoning are presented below: 1. Lead in the Environment of Children (a) Efforts should be implemented to reduce lead levels in sources that remain as major causes of childhood lead toxicity. 1-39 DUP040009494 (e) The 1987 statement of the American Academy of Pediatries calling for lead screening of all high risk children should be implemented. (d) In vivo cumulative lead screening methods should be used as soon as they become feasible. A quick, accurate.noninvasive screening test would result in greater acceptance by parents., resulting in many more children screened, (e) Screening should be extended to all high-risk pregnant women, with parti cular emphasis on urban teenaged pregnant women, and prenatal medical care providers should be involved in this effort, (f) The prophylactic role of nutrition in the amelioration of systemic lead toxicity should be determined, (g) Further use should be made of already developed metabolic models and research should be conducted to refine them, so that their ability to pre dict contributions to the total body burden can be utilized for varying environmental source contributions of known lead levels, (h) It is recommended that longrterm prospective studies of lead's effects on child growth and development be supported through appropriate mecha nisms, beginning with the relationship of maternal lead burden to in utero toxicity and Including children with neurological disabilities and genetic disorders, such as sickle cell anemia. (i) Nationwide assessments of lead toxicity status in U,S, children on a con tinuing basis are recommended, Efforts such as the planned NHANES ill survey should be supported to maximize the data collected on lead expo sure levels. Support should be provided for geographically more focused surveys as well, e.g,, at the level of Metropolitan Statistical Areas (MSAs). C. CONCLUSIONS ANO OVERVIEW 1. Lead as a Public Health Issue Lead poisoning has been Identified by the American Academy of Pediatrics as one of the most important toxicological hazards facing young children in the United States. In one form or another, lead poisoning has had this status for many decades. 1-42 DUP040009495 (e) the need ip examine fully the extent of lead contamination in all. parts of the child's environment remains. Emphasis Should be placed on examining the presence of lead in elementary schools, day cafe centers, nurseries, kindergartens, and similar facilities, with particular focus on the lead in drinking water, paint, dust, and soil. (1) All attempts at source-specific lead reductions in children's environments should be accompanied by an assessment of the long-term effectiveness and efficiency of such actions (see Section 2 of Recommendations also), (2) Lead is ubiquitous and persistent. Planned reductions of lead in one environmental compartment must be evaluated in terms of impacts on other compartments so that fruitless ''shifting" of the problem from one source or medium to another is avoided. For example, when leaded paint or soil is removed ffom a child's environment, consideration must be given to ultimate safe disposal. (3) The evidence is strong that Jjn utero exposure of the developing fetus occurs at potentially toxic levels in some proportion of the pregnant women of the United States, This at-risk popula tion must be given close attention in terms of assessing and reducing their most significant sources of lead exposure. This should especially include consideration of occupational exposure sources, (4) Lead pollution is a health issue that involves almost all seg ments of U.S. society. Extra-environmental or legal measures should be explored to reduce lead levels in the environment by both public and private sectors. 2. Lead in the Bodies of Children (a) Children are being exposed to and poisoned by lead while environmental lead reduction is underway. There is an urgent need for screening programs at levels sufficient to make a real and measurable impact in the prevention of childhood lead poisoning. (b) There is a need to maintain screening programs extant in some states that currently identify children at risk from lead exposure at or above 25 pg/dl. There is also a need to develop screening tests that will identify children below 25 pg/dl, since current erythrocyte protoporphyrin (EP) tests, used as an initial screening measure, cannot accurately identify children with blood lead levels below 25 pg/dl. 1-41 DUP04G009496 found in old paint, dust, soil, drinking water, food, and ambient air. Sites of such exposure of children include the interiors of Homes, outside play areas, and kindergarten, day-care, and elementary school facilities. A number of such sources can produce simultaneous exposures, raising the question of how one identifies and then ranks the contributions of lead from each source. By and large, control measures for lead in various media have been historically allocated to various public agencies, directed and guided by media-specific ' legislation. Section 118(f) Implies in its language that one can readily identify a sole or major source of lead exposure for individual children and that these exposure numbers can then be summed and the total estimates ranked by source. In actuality, this report alloys that (a) too many large gaps in data exist to quantify precisely source-specific lead exposure of young children; (b) siz able region-based differences in source-specific exposure would probably be diluted or lost in any national rankings; .(c) sources with the highest concen trations- of lead may not always have the greatest impact; (d) simultaneous exposures to a number of sources occur; (e) relative contributions of a number of lead sources are changing with time; and (f) it is not possible to rigidly rank exposure by source of lead. Concern for the health of the public and the need for prudent initiatives must cause Congress and society-at-large to ask what conclusions can be drawn from the data presented in this report. Although some of the estimates presented here have limitations and uncertainties attached to them, they still provide a number of key conclusions about source-specific lead exposure of U.S. children: (a) Lead in paint and lead in dust/soil have been and will remain as major exposure sources for U.S. children, (b) Leaded paint remains as a major source because of the huge amount of lead in this form--about 5 million tons or more--and the total dispersal of the source among 21 minion individual residential units and large numbers of old public buildings. This is the most important source in terms of reservoirs of lead and ubiquity of exposure. Post 1940 housing can also contain high levels of lead in paint. (c) Dust and soil remain as major sources of lead exposure for children because of the rather high levels of lead in these media, their ubiquitous distribution, and young children's behavior in relation to this source, i.e., mouthing behavior and ingestion of non-food items. 1-44 DUP040009497 While severe acute and chronic lead poisoning of children was the typical for of the disease at one time, this hazard is now viewed in terms of a cluster of low-level effects collectively known as the "silent epidemic." It must be remembered, however, that unacceptable numbers of severely poisoned children continue to be identified and treated in clinics and hospitals of the nation's urbah areas. The persistence of lead poisoning in U,$, children belies the basic fact that lead intoxication is a fully preventable disease. The level at which actual prevention is attempted, however, has been defined by the level of public attention and the degree of societal commitment at any given time. With downward revisions in the definition of unacceptable lead toxicity risk in U.S. children, options for prevention of unacceptable lead exposure likewise have changed, Severe 1ead poisoning of past years, the only form of v the disease then considered important, was often considered as manageable by secondary prevention methods, i.e., by identifying the lead-poisoned, child and then providing hospitalization and treatment. The present concern is with low but still important levels of lead exposures associated with subtle health effects occurring at Pb-B levels of 10 to 25 pg/dl, Hospitalization for treatment by chelation therapy, which is acceptable for children with higher jPb-B levels, is not without risk and potentially undesirable sequelae. It is neither appropriate nor feasible for the treatment of the huge number of children at lower Pb-B levels. Therefore, since no acceptable or feasible medical treatment exists at this time, the only option remaining is the removal of lead from the environment of children. Equally valid concerns can be expressed for options in avoiding fetal exposure in pregnant women at levels above 10 pg/dl. As a public health issue, lead poisoning involves (a) a persistent, ubiquitous toxicant whose environmental distribution produces (b) unacceptably large numbers of children with unacceptably high body lead burdens that require (c) environmental lead removal or reduction as the only exposure abatement option. 2. Lead in the Environment of Children It is now recognized that potentially hazardous levels of lead can be found in many of the environmental media or pathways that serve as exposure routes for young children. Lead at potentially significant levels may be 1-43 DUP040009498 as Pb-B level (dose) rises, so do the number of adverse effects and the severity of any given effect, A crucial point in the understanding of dose-effect relationships for lead is the propensity of this toxicant to accumulate in target tissues of young children and other risk groups. This insidious characteristic complicates interpretation of a Pb-B value, because the latter represents a combination of not only current lead uptake but release of accumulated lead from lead storage areas such as bone. The possibility that accumulated lead may be abruptly mobilized-back into the blood stream is especially important for potentially increased exposure of the fetus in pregnancy. Blood lead levels can be reliably employed to index early effects from low-level exposure to lead, but extreme care must be used for the collection and measurement of blood lead samples at such low levels. The report concludes that a definition of unacceptable lead toxicity risk continues to undergo downward revision by the scientific and public health com munities. Current information indicates that disturbances in various measures of neurobehavioral development, other neurological indices, developmental milestones, and non-neurological systemic functions are seen at child or maternal Pb-B levels in the range bf 10 to 25 pg/dl, and possibly even lower than 10 pg/dl. Strong support for these conclusions continues to be provided by well designed and executed longitudinal studies under way in a number of areas of the United States and elsewhere. These most recently identified effects, while they potentially affect largo fractions of the U.S. child population, should not deflect public attention from the fact that unacceptable numbers of children still are treated for severe lead poisoning in the hospitals of the nation's urban areas. These serious injuries involve the central nervous system and the blood-forming system, and can even constitute threats to life itself. 4, The Extent of Lead Poisoning in Children in the United States This report describes several approaches to Congressionally mandated assessments of the numbers of young U.S, children having Pb-B levels high enough to pose adverse health risks. Results of these assessments provide a number of key conclusions: 1-46 DUP040009499 (d) Lead in drinking water is currently a potentially significant source of lead exposure, but one that is now being given more regulatory attention. Prinking water in homes, public schools, kindergartens, day-care centers, etc,, may have been contam inated by lead in solder, flux, or other components of plumbing systems and devices supplying potable water. (e) Significant exposure of children can occur from sources away from the home, such as leaded paint, dust/soil lead, and drink- ing water lead in day care and school facilities. (f) The phasedown of lead in gasoline has markedly reduced input from this source to human body burdens, which at one time amounted to 40-50% of the burden reflected, in Pb-B levels. The accumulated quantities of soil/dust lead from leaded gaso line combustion and atmospheric fallout will only slowly diminish, however, <g) Food lead has been reduced as a population-wide source of lead exposure in children, especially for infants and toddlers. It is not clear to what extent further reductions will be possible. In addition to these purely environmental aspects of source-specific lead exposure, this report also draws attention to the fact that leaded paint is the form of childhood exposure that has been associated with the most severe lead poisonings. Other lead sources* e,g., drinking water or food, are judged 5 to provide a continuum of exposure for the populations at risk and to contribute to generally less severe lead poisonings. The difficulty ip judging source-specific contributions to the total body burden of lead and its consequent toxicity poses problems for source-specific regulatory initiatives and for lead abatement strategies. Which source should be first controlled to provide maximum benefit with the minimum expenditure of societal resources? As the report states, rapid reduction of a small fraction of the total body lead burden to below a risk level may be more desirable than removal of a large fraction of body lead that can only be accomplished at a much slower, costlier pace. 3. Lead in the Bodies of Children Various sources of lead contribute to total body lead burden in a way that is reflected in the most common index of such a burden, the blood lead value. A measurement such as Pb-B level not only integrates multi-source/multi-media exposure but also defines the degree of toxicity risk to be expected when spe cific Pb-B levels are encountered. This is termed the dose-effect relationship; 1-45 DUP040009500 (fo) The prevalences of elevated Pb-B levels obtained through screen ing data and those for various NHANES II strata are seen to be quite different in the report. This i$ especially so for those NHANES II strata that can only be compared to the high-risk populations examined in screening areas, i .e., inner-city, un derprivileged children. (1) The report concludes that screening versus stratified national sampling results are different for such reasons as (1) major flaws in the methodology of screening programs (resulting In marked underestimates), (2) nonintensive coverage of the target population, and (3) differences in program protocols among different screening programs with respect to which children should be screened. (j) The distribution of U.S. SMSA children among residences differ ing in age and therefore in degree of leaded paint exposure was also examined on an SMSA-by-SMSA basis. In all 318 SMSAs, about 4.4 million children live in the oldest housing (pre-1950) and are therefore exposed to the highest levels of lead in paint. The report concludes that the major socioeconomic category of children in the oldest housing, by far, are those above the poverty level. Leaded paint in old housing is not just a problem for poor families in inner-city areas. (k) Housing and income results complement the NHANES II projections and total exposed population estimates, in that they also show that many strata of children in exposure risk areas are affected, not just inner-city underprivileged groups. S, The Problem of In litero lead Toxicity: The Extent of Fetal Lead Exposure in the United States In Chapters III and IV, the report concludes that a strong case is to be made for identification of the human fetus as a high-risk population. Fetal exposure (for which the population of pregnant women is the surrogate risk group), leads to a number of potentially adverse effects jn utero and these may well persist during postnatal development. Examination of the extent of lead exposure among fetuses in the United States, via pregnant women's exposure, was carried out for 1984 as the reference year. Projection estimates were employed using the methodology already identi fied for childhood lead exposures. The important conclusions to be drawn from these findings include: (a) Over 400,000 fetuses in 1984 were exposed to lead at maternal Pb-Bs above Ip pg/dl, a level associated in recent studies with early developmental effects. Furthermore, over 4 million women of childbearing age were so exposed. 1-48 DUP040009501 (a) Sufficient methodology exists to attempt at least a stratified national assessment of children with unacceptable Pb-B levels. In the main approach used to define lead exposure in terms of a geographic index, a combination of census counts of young children plus vital statistics data were matched up with projected Pb-B prevalences to yield numbers of children in socioeconomic/demographic strata who have Pb-B levels above; selected values. (b) A crucial result from this assessment is that approximately 2.4 million, or 17%, of black and white children who live in SMSAs are estimated to have had. Pb-B levels above 15 pg/dl in the reference year of 1984; the criterion level of 15 pg/dl is judged in the report to be associated with health effects in young children. For the entire nation, this estimated number of children would probably lie between 3 and 4 million if all racial and residential categories were included. (c) The estimates presented here include children from all socio economic strata, e.g., urban/suburban children above the poverty level as well as the expected strata of inner-city children from families in poverty. (cl) Prevalences of elevated Pb-B levels are highest for inner-city, underprivileged black children, while rates for other strata of city children, both black and white, are intermediate. Suburban children above the poverty level have the lowest prevalences. (e) Tptal numbers of lead-exposed children in nearly all strata are significantly high. The largest base populations have lower prevalences while the smallest population base has the highest prevalences of elevated Pb-B levels. When combined, the results are large numbers in most strata. (f) The above approach contains uncertainties that may produce both underestimates in the numbers as well as overestimates. Sources of underestimation include restriction of the estimates to only SMSA-based children. Such individuals represent only 75 to 80% of the entire U.S. child population. The projected estimates are restricted to those groups in the original NHANES II survey, black and white children for whom prevalences could be calcu lated validly. Therefore, the numbers in the report do not include Hispanic and "Other Race" children. The main source of overestimation is the use of a projection model for Pb-B prevalences that did not include downward changes in food lead in the logistic regression analysis. The projections should therefore be considered as "tlie best estimates consistent with available scientific data." (g) The report also examines results of past and present lead screening programs in yarious communities of the United States, For 1985-1986, ATSDR determined through an extensive survey of operating programs that about 1,5% of screened children were at or above GDC action levels for Pb-B and erythrocyte proto- porphyrin (EP), using either earlier or more recent CDC classi fication schemes. 1-47 DUP040009502 (e) Easily-achieved removal or reduction of lead in paint from residential units or public facilities will probably not occur without highly coordinated efforts. HUD has undertaken a number of new actions for detecting and responding to paint - problems in Federally assisted housing, but their effective^ ness remains to be documented and their scope is greatly limited. As the report notes, millions of tons of paint lead still persist as a highly dispersed and accessible hazard. (f) Removal of lead from soils and as dusts parallels removal efforts for paint, in terms of complexity. As the report states, millions of tons of lead are now lingering in soil and as dust. Since soil and dust are pathways of exposure, abate ment effectiveness in these cases is ultimately governed by abatements in paint lead and air lead fallout. 7* Future Directions of Lead as a Public Health Problem With significant downward changes in source-specific amounts of lead that have occurred or will occur, some sources will decline in importance. Simul taneously, other sources such as paint and dust/soil lead will continue to receive more attention and more public calls for action. The "easiest1* parts of lead exposure control have been implemented or are being set in place, namely the use of centralized control mechanisms, such as the phasedown in the amount of lead in the nation's gasoline supply and the levels of lead in a basically centralized food supply. Corrosion control measures for the public drinking water supply are a similar example, since a large segment of the U.S. population derives drinking water from public systems. Definitions of unacceptable lead toxicity risk have been undergoing significant downward revisions in recent years, and further changes downward may occur in the future. The result is that any gains in reducing lead expo sure are offset by the progressive redefining of how much further lead exposure should be reduced. The nation will soon have to face fully the abatement of the most refrac tory and most costly sources of lead exposure and toxicity: paint lead and (dust/soil lead. This will require some hard societal choices. Chief among these choices will be whether remaining and problematic sources will be sys tematically and effectively controlled or whether large numbers of young children and fetuses will bear persistent and unacceptable quantities of lead in their bodies and tissues. 1-50 DUP040009503 (b) The lead toxicity hazard for the U.S, fetal population is multi plied year after'year in the absence of effective lead exposure reductions for the pregnant population. A given fetus is not counted more than once in exposure estimates. Thus, more than 4 million individual fetuses will be at risk for toxic effects over a 10-year period in the absence of effective lead removal or reduction. (c) In utero lead exposure in the United States will continue to increase in importance as a public health issue. 6. Removal or Reduction of Lead in the Child's Environment The. report concludes that a strong case can be made for the necessity of both collective and source-specific efforts to systematically reduce or remove lead from the child's environment. At present, there are millions of young children for whom reduction or removal of environmental lead is the only option for lowering high Pb-B levels. There are, likewise, hundreds of thousands of fetuses in any given year and millions of fetuses over extended time periods who require reduction in lead uptake and concomitant reduction in environmental exposure of the female population of child-bearing age in the United States, A number of important findings in the report are related to environmental lead removal or reduction. Some of the conclusions to be drawn from these findings include: (a) Certain regulatory and other control actions have been reason ably successful in recent years in reducing source-specific lead exposures. Notably, the phasedown of lead in gasoline is producing demonstrable and significant reductions in population Pb-B levels, (b) Reductions of lead in food, particularly for diets of infants and toddlers, have occurred and have had important consequences for the "background" levels of body lead burden. (c) Lead in drinking water is now being attacked on several regula tory fronts by EPA and other relevant agencies. Such actions include bans On the use of lead solder for plumbing, corrosion control measures in public water supplies, and control of lead exposure from lead leaching into water sources in schools, offices, and homes. (d) Control of lead in ambient air by means of air quality standards for lead will continue to have a positive impact on reducing lead emissions from stationary sources. 1-49 DUP040009504 THE NATURE AND EXTENT Of LEAD POISONING IN CHILDREN IN THE UNITED STATES: A REPORT TO CONGRESS PART 3 (CHAPTERS II-XI) THE QUANTITATIVE EXAMINATION OF LEAD EXPOSURE AND TOXICITY IN CHILDREN AND RELATED RISK GROUPS IN THE UNITED STATES: CHARACTERIZATION AND METHODS FOR REDUCTION II--1 DUP0400G9505 11-11 DUP040009506 AMBIENT AiH SOIL SURFACE AND GROUND WATER PLUMBING u DRINKING ^ [ SOFT TISSUE r\ f' , LIVER KIDNEY BONES FECES URINE Figure 11-1. Pathways of load from the environment to man and body disposition of lead. Source: Adapted from EPA (1986a). iI-2 DUP040009507 PART 3 II. INTRODUCTION AND DISCUSSION OF TERMS AND ISSUES A. INTRODUCTION Of the known environmental pollutants, lead has few rivals as a persistent cause of major public health concern. As an element, lead is indivisible and persists indefinitely as a discrete toxic substance. Therefore, lead put into the environment by human activities accumulates, adding to the total amount already there. In the earth's crust, lead is present at only very low background levels. For centuries, however, extensive use has dispersed lead from geologic forma tions into many pathways of contact for human populations. Figure II-l depicts various sources of lead and pathways or routes by which it biologically inter acts with humans. The figure clearly shows that lead is now widely distributed in media that are pathways of intake/uptake for humans. Because of this ubiquitous dispersal, attempts at environmental reduction are difficult. To be fully successful, regulatory controls for lead should consider all pathways simultaneously. One indication of the pervasiveness of lead contamination was provided by Patterson (1965), who calculated that the blood lead level of early, preindustrial humans was 0.5 pg/dl, or about 15 to 30 times lower than the current levels seen in some segments of the U.S, population. Piomelli et al- (1980) measured blood lead levels in a remote population of the Himalayas and found an average Pb~B level of 3.4 pg/dl, which is 3- to 5-fold lower than the levels in parts of the U.S. population. As noted later in this report, lead causes a broad range of adverse health effects in humans and experimental animals because it interferes with the normal functions of cells in general and calcium pathways in particular. These 11*1 DUP040009508 in the 1930s and 1940s, and accelerating through the 1950s and 1960s, the epidemiologic data base describing childhood lead poisoning rapidly expanded. In the 1950s and 1960s, even rudimentary efforts to screen numbers of children showed clear evidence of excessive lead exposure, at alarmingly high prevalence rates, among inner-city children. A better appreciation of the.U.S. lead problem started to emerge in the' late 1960s and early 1970s, when Congress, enacted the 1970 Clean Air Act and the 1971 Lead-Based Paint Poisoning Prevention Act, and the National Institutes of Health (NIH) and other public agencies began to fund significant research on human and experimental animal lead toxicology. The 1971 Lead-Based Paint Poisoning Prevention Act provided assistance to communities for lead screening and treatment programs, particularly the mass screening of children. Screenings began in mid-1971, after which childhood lead poisoning began to be recognized as a widespread public health problem. It came to be seen as a disease that Could affect middle- and upper-class children, children living in rural and suburban areas, and those in low-income, inner-city families. Concurrently, exposure sources were often scrutinized and, as a result, the multimedia nature of the lead problem began to be identified. The 1970 Clean Air Act established the U.S. Environmental Protection Agency (EPA). Through court action in 1975, EPA was required to evaluate atmospheric lead as a "criteria pollutant," in the terminology of the Clean Air Act, Since airborne lead readily enters other .environmental compartments, EPA's assessment of lead as a criteria pollutant also began to define the problem in all segments of the human environment. In the late 1960s, the NIH and other components of the U.S. Public Health Service began to fund comprehensive research on many aspects of the lead problem. Increasingly impressive evidence of the toxicologic potency of lead in humans and experimental animals was produced in the ensuing years. Results have ranged from documented excessive lead body burdens in industrialized countries (Piomelli et al., 1980) to those that show the subcellular mechanisms of lead toxicity (see* e.g., U.S, EPA, 1986a; Silbergeld, 1983a,b; and Sitbergeld et al., 1980, for a comprehensive discussion). To illustrate the U.S. lead problem, consider two categories of potential exposure: lead-based paint and the combustion of leaded gasoline. Pope (1986) estimated that in 1980 about 52% of all occupied residential units contained painted surfaces With lead at op above 0.7 mg lead/cm2, a level judged hazardous to young children (CDC, 1985) and the lowest that can be reliably 11-4 DUP040009509 health effects span the human toxicologic spectrum, from classically known clinical effects in the nervous, red blood cell, and kidney systems, to relac tively subtle biological effects in these and other systems that signal the onset of increasingly severe outcomes. Some of these effects have only recently been discovered with the advent of more sophisticated research techniques. In many cases, however, knowledge of the adverse effects of lead on humans dates back to the Greco-Roman era and beyond (see, e.g., Wedeen, 1934). Given this historical perspective, it is perhaps Surprising that public health concerns did not earlier accelerate efforts to limit the amount of lead entering the U.S. environment or, at a minimum, prompt more debate over the acceptable trade-off between economic utility and adverse health effects. The use of lead increased greatly in the 19th and 20th centuries; it was^ used in new ways and more of it was used in old ways. In at least one case, the commercial advantages of lead may have specifically maximized the probabil ity of an adverse health impact. Paint high in lead content had the advantage pf continuous chalking inside of homes and weathering outside of homes, thereby providing renewed surfaces and a fresh look longer. At the same time, however, dispersion of lead into the environment occurred. The evolution and recognition of childhood lead poisoning as a public health problem in the United States and elsewhere has been described in detail by Lin-Fu (1982a). This problem is understood to encompass in utero lead intoxication as well. In the 18th and 19th centuries, sterility, abortion, stillbirth, and premature delivery were recognized among female 1 ead workers and the wives of lead workers. Hdrtajlity was high in their offspring, as was the incidence of low birth weight, convulsions, failure to thrive, and mental retardation. With progress in industrial hygiene, the number of overtly leadintoxicated workers was significantly reduced and concomitant reductions in the incidence of severe reproductive effects became apparent over time (U.S. EPA, 1986a). The prevalence of direct lead poisoning in children was first examined in Australia in the 1890s (Gibson et at., 1892; Gibson, 1904), and the poisoning was traced to lead-based paint used on exterior railings and walls. In the United States, skepticism among physicians about lead poisoning in children did not lessen until Blackfan (19|L7) reported lead as the source of acute encephalopathy in a number of children. Physicians eventually recognized lead poisoning in children as a clinical entity (McKhann, 1926). II-3 DUP040009510 Regarding the combustion of leaded gasoline in the United States, from 1975 to 1984 a total of 1,087,800 metric tons of lead were consumed (U.S. EPA, 1986a), Virtually all of this lead was dissipated to the atmosphere and other areas of the environment. If lead emissions from earlier periods are included by assuming, in view of its long environmental half-life, that all of the dissipated amount, accumulates, about 4 to 5 million metric tans of lead from' gasoline remain in dust, soil, and sediments (U.S. EPA, 1986a). When examining these figures, one also must consider relative dispersion factors that affect the amount of lead young children take in. The total amount of lead in paint may be roughly similar to that emitted from combusted gasoline, but the relative concentration of lead in media affected by the paint is significantly greater. Consider the amount of lead in paint chips or dust from weathered or chalked paint and the amount in dust and soil from traffic emissions: a lead-paint film contains 10,000 parts per million (ppm) of lead, which is considerably higher than typical levels in dust or soil. This report will document that lead is a pervasive environmental contaminant that causes a wide variety of adverse effects in humans. In short, lead is potentially toxic wherever it is found, and it is found everywhere, B, DISCUSSION OF TERMS AND ISSUES Some of the relevant terms used in Section 118(f) of the Superfund Amend ment and Reauthorization Act (SARA) of 1986 that cover issues and concepts central to the childhood lead problem are defined and discussed in this section. These include: (1) identification of those U.S. child population groups at greatest risk for lead exposure; (2) types of exposure assessments that relate to quantifying lead exposure of individuals and populations; (3) the most relevant meanings of the term ``environmental lead sources," both for their specific identification and for the discussion of interrelationships among exposure pathways; and (4) the nature of adverse health effects , associated with lead exposure in human populations. II-6 DUP040009511 measured by field testing in situ. Even lower levels may be toxic. The above percentage equals about 42 million units, including some 21 million units built before 1940, which have the most leaded paint and are likely to be in the worst state of repair. These older houses are, therefore, the most probable source of lead exposure for young children. Lin-Fu (1982b) estimated that there are,," about 27 million pre-1940 units in the United States. Pope (1986) estimated, based on these and other data for pre-1940 housing, that 99% of all such housing had painted surfaces containing lead. Leaded paint continued to be used in considerable amounts from 1940 until 1959. An estimated 70%, or 16 million housing units built during this interval, have painted surfaces that contain lead at levels above 0.7 mg lead/cm2, based on Pope's best estimates from the survey dfta of Billick and Gray (1978), Lin-Fu (1985a,b), Schier and Hall (1977), the Arizona Department of Health Services (1976), and Gilsinn (1972). For the most recent housing units likely to have sojne leaded paint--those built between 1960 and 1974--Pope estimated on the basis of four surveys, that 20%, about 5 million units, have surfaces with lead levels exceeding 0.7 mg/cm2. Regarding the environmental magnitude of the lead-based paint problem in terms of mass, Clark, of the University of Cincinnati, OH, has estimated the total amount of leaded paint remaining in the 27 million or more housing units built before 1940 and the millions more built since 1940 (communication of J-J. Chisolm, Jr., M.D., to ATSDR, September 4, 1987). Annual U.S. lead use for white paint was identified for each year since 1910, drawing on relevant annual statistics of the Minerals Yearbook, U.S. Bureau of Mines. Since 1910, about 4.2 million short tons (3.9 million metric tons) of lead were used for white paint in the United States. Clark also estimated lead consumption for paint since the 1880s at about 7.0 million short tons (6.4 million metric These figures, as current environmental burdens, overestimate the extent of white paint lead in view of reductions through, for example, the demolition and remodeling of old houses. (5n the other hand, they significantly under estimate total lead paint production, because green, yellow, and black paints also were high in lead content hut are not counted here. Overall, about 3 million tons of lead probably remain in paint accessible to children. This illustrative example takes on further meaning when one examines the millions of young children living in housing units haying this lead burden (see Chapter V). II-5 DUP040009512 Z. Monitoring Lead Exposure in Young Children and Other Risk Populations Health professionals determine the degree of lead exposure of children and other risk populations in three ways. The traditional method is to measure lead in external or environmental media (ambient air, workplace air, food, water, dust, soil, etc.) that are pathways for human exposure. Surveying le^id in these media, termed environmental or ambient monitoring, provides informa tion about the lead exposure sources and the potential risk for persons so exposed to lead. Environmental monitoring does not indicate the actual internal level of lead for any given individual, because individuals may respond differently to an external source of lead exposure. On a group basis, however, one can determine the probable internal exposure level, given knowledge of the concentrations in the external media and the mathematical relationship between the two variables (different levels in the media and different responses in groups of people). In many cases, one must use environ mental monitoring, either because other types of exposure assessment cannot be carried out or because a more direct, systemic measure of exposure is considered unnecessary. Lead exposure is also commonly assessed through biological monitoring and effects monitoring. Biological monitoring is the measurement of the concentra tion of lead in a biological sample, e.g., blood, from an exposed person. Effects monitoring involves measuring some endpoint, e.g., the amount of certain proteins or enzymes associated with lead exposure. For a more compre hensive examination of monitoring exposure to lead, see Elinder et al. (1987). Biological monitoring and effects monitoring have advantages for assessing health effects, giving an integrated picture of a person's uptake of lead from all external sources. To assess lead exposure in children and other risk groups, the level of lead in whole blood (Pb-B) is the most practical biological measure of ongoing lead absorption. This measure is used throughout Chapters IV-VIII as a means of relating lead exposure levels to adverse health effects. A Pb-B lev?! is generally regarded as reflecting relatively recent exposure. However, Pb-B levels also give information on the relative level of exposure at more remote time points. In other words, a child who had the highest Pb-B level at one time will probably have the highest Pb-B level at a future retesting, Pb-B levels do not, however, indicate cumulative past exposure, as do lead levels of mineralizing tissue such as tooth or bone. Such cumulative measures cannot II-B DUP040009513 1, Young Children and Other Groups at Greatest Risk for Lead Exposure and Adverse Health Effects Young children, particularly preschool children, are the subset of the U.S., population most at risk for excessive exposure to lead and its associated adverse health effects. The age interval for children at greatest risk has not been precisely defined. Although infants and toddlers are at particular risk because of their behavior patterns (e.g., hand to mouth activities) and other factors, various effects have been found in children up to 6 to 8 years of age. Since childhood lead exposure actually begins prenatally, i.e., during in utero development, and the effects of such exposure have been reliably measured in terms of both fetal and postnatal developmental impairments, an adequate assessment of the childhood lead problem must encompass the human fetus and its exposure via the pregnant woman. Ypung children are vulnerable to the effects of lead for at least two reasons: their developmental physiology and their contact with parts of their environment contaminated by lead; Children differ from adults both qualita tively and quantitatively in their metabolism of lead. The Centers for Disease Control (1985) and U.S. ERA (1986a) have discussed these differences in detail, and this report provides a comprehensive summary of the physiological distinc tions in Chapter III. The evidence for identifying fetuses as a risk group is described in Chapters III and IV. As noted earlier, the congenital poisoning of children of lead workers in the 19th century was frequently severe and obvious, including often fatal outcomes (U.S. ERA, 1986a). Recent epidemiologic studies show that developmental toxicity also occurs at much lower leVels of fetal lead exposure. These effects include impairments in postnatal neurobehavioral development up to two years of age, reductions in birth weight and gestational age, and possibly other effects at exposure levels that were prevalent and generally considered safe only a few years ago (Davis and Svendsgaard, 1987). Although these effects have been most clearly linked with prenatal lead expo sure indices, the potential role of lead-induced gametotoxic effects on the egg and sperm may also be important (U.S. EPA, 1986a). II-7 DUP040009514 only contribute to direct or proximate exposure but also to indirect exposure via secondary processes. Pathways for human exposure to lead include paint, dust and soil, drinking water, air, and food. Many of these pathways contribute indirectly to exposure via other media. For example, airborne lead fallout contributes to dust and soil lead levels, which are also increased by chalking and weathering of lead paint, both on the interior and exterior of structures. Mobile and stationary sources of lead are referred to in this report. Mobile sources refer to automobiles and other vehicles that burn leaded gaso line;; stationary sources encompass a constellation of lead production, processing, and end-use operations, including primary lead smelters and refineries, secondary lead smelters, and municipal incinerators (U.S. EPA, 1986a). All of these sources emit lead to the atmosphere. Environmental sources of lead differ in their quantitative impact on a given human population, in their geographic distribution, in their relative persistence as a long-term exposure source, and in the types of problems they pose for abatement strategies. For example, sources of high-level lead expo sure for children in older population centers are lead in paint and lead in dust and soil, particularly in areas of deteriorated housing and heavy traffic. In rural areas, remote from,heavy vehicular traffic but near stationary lead operations, children with no leaded paint exposure can still he significantly exposed by inhaling airborne ies<j| particles emitted directly from a facility and by inhaling or ingesting lead in dust inside and outside the house and in contaminated soils (U.S. EPA, 1986a). In some agricultural areas, prior use of lead arsenate as a pesticide may pose a lingering exposure risk, but a risk that is poorly understood. In new housing units, children not otherwise in contact with lead can be exposed to high levels In their drinking water because of the lead in plumbing solder, which is of particular concern where the water is naturally corrosive. Sources are discussed in detail in Chapter VI, which gives estimates of children exposed by source category. Lead is a multimedia pollutant. Therefore, one cannot speak, in biological terms, about lead exposure by isolated sources of contact. The physicochemical and toxicokjnet|c properties of lead produce a net body burden or target organ burden in humans, and it is this net burden that is related to the risk of adverse health effects. In discussing the legislative history of multimedia pollutants, Mushak and Schroeder (1981) pointed out that because of legislative mandates various II-10 DUP04000951S yet be routinely employed in screening programs. The kinetic, toxicological, arid practical aspects of biological monitoring and other approaches to assess ing lead exposure have been extensively discussed by U.S. EPA (1986a). In young children, effects monitoring for lead exposure is primarily based on lead's impact on the heme biosynthetic pathway, as shown by (!) changes in the activity of key enzymes delta-aminolevulinic acid dehydratase (ALA-D) and delta-aminolevulinic acid synthetase (ALA-S), (2) the accumulation of copropor phyrin in urine (CP-U), and (3) the accumulation of protoporphyrin in erythro cytes (EP). For methodological and practical reasons, the EP measure is the effect index most often used in screening children and other population groups. Effects monitoring for exposure in general and lead exposure in particular has drawbacks (Friberg, 1985). Effects monitoring is most useful when the endpoint being measured is specific to lead and sensitive to low levels of lead. Since EP levels can be elevated by iron deficiency, which is common in young children, indexing one relationship requires quantitatively adjusting for the other. An elevated Pb-B level and, consequently, increased lead absorption may exist even when the EP value is within normal limits, now ^35 micrograms (pg) EP/deciliter (dl) of whole blood, We might expect that in high-risk, low socioeconomic status (SES), nutrient (including irpn)-deficient children in urban areas, chronic Pb-B elevation would invariably accompany persistent EP elevation. Analysis of data from the second National Health and Nutrition Examination Survey (NHANES I!) by Mahaffey and Annest (1986) indicates that Pb-B levels in children can be elevated even when EP levels are normal. Of 118 children with Pb-B levels above 30 pg/dl (the CDC criterion level at the time of NHANES II), 47% had EP levels at or below 30 pg/dl, and 58% (Annest and Mahaffey, 1984) had EP levels less than the current EP cutoff value of 35 pg/dl (CDC, 1985). This means that reliance on EP level for initial screening can result in a significant incidence of false negatives or failures to detect toxic Pb-B levels. This finding has important implications for the interpreta tion of screening data, as discussed in Chapter V. 3. Environmental Sources of Lead in the United States with Reference to Young Children and Other Risk Groups As graphically depicted in Figure II-l, several environmental sources of lead exposure pose a risk for young children and fetuses. Many sources not .11-9 DUP040009516 frequency of an effect in a population; (5) the presence of the effect in that population (e.g., young children), most vulnerable to the toxicant; and (6) the cumulative or aggregate impact of various effects within single organ systems on the well-being of the entire organism. Impacts of lead on target organs and systems are evident across a broad exposure range, and effects at low exposures have only more recently been , judged to meet the criterion of health impairment (see, e.g., CDC, 1385). An illustration of this point is the traditional term ,,.anemia,, when applied to lead poisoning. As a measure of lead effect, the tens has come to mean a cluster of adverse effects on heme biosynthesis and erythrocyte stability. These effects are seen at lower levels of lead exposure than have been classically defined as lead anemia. Implicit in accepting these early effects as significant is the notion that preventing such outcomes prevents more serious responses. In other words, preventive medicine has a role in dealing with the effects of exposure to lead. Lead-induced impairments of the body's capacity to offset various stresses from other agents appear to result from reduced hepatic metabolism, even at moderately elevated Pb-B levels (Saenger et al., 1984). As noted by U.S. EPA (1986a), a number of studies show that the body is less able to detoxify foreign substances such as drugs and toxic pollutants because lead reduces hepatic heme, upon which enzyme biosynthesis depends. An important criterion for assessing the significance Of. lead-induced effects is whether an effect is reversible or irreversible, usually meaning a physiological return to normal. In addition, there is the important public health question of whether exposure conditions will be reversible. As noted by EPA (1986a), if removing a subject from lead exposure is highly unlikely for socioeconomic or other reasons, then adverse effects, reversible or not, will persist and operate as de facto irreversible effects. For example, effects of lead on heme biosynthesis in children can technically be reversed by removing lead exposure. When these effects occur in inner-city, low-SES children who remain in a high-risk setting indefinitely, effects persist during the period of their highest vulnerability (see, e.g., CDC, 1985, and EPA, 1986a). The issue of aggregate impact on the overall well-being of humans because of effects on single systems is important in assessing lead toxicity. As discussed In Chapter IV, a disturbance in one system or at one stage of 11-12 DUP040009517 agencies have traditionally carried out their activities on a medium-by-medium basis, with, in many cases, little coordination. Specific laws have called for the assessment and control of the hazards posed by separate media. These laws have created separate standard-setting procedures and criteria,, almost always administered by separate agencies or divisions within agencies. Mushak and Schroeder (1981) also pointed out that the Environmental Law Institute identified 23 statutes affecting toxic agents (such as lead), most of which are found in many environmental media but which have been approached by regimens for a single medium. Lately, however, more coordinated efforts have been used in dealing with multimedia problems. Recent legislation calling for more interagency coordination has bolstered this move. Given the complexity of lead exposure in children, the directive in Section 118(f) to rank children according to exposure source must be inter preted to mean ranking by the major environmental source. Other factors that interact with lead exposure must also be considered. Finally, it should be recognized that even though no single source of exposure may be dominant, the aggregate absorption of lead from many sources may produce unacceptable internal lead levels. These points are discussed further in Chapter VIII. 4. Adverse Health Effects of Lead in Young Children and Other Risk Groups and Their Role in Health Risk Assessment Lead exposure in young children is associated with a broad range of toxi cologic effects, such effects being dose-dependent and inducible at relatively low exposure levels. These adverse health effects are discussed in detail in EPA's Air Quality Criteria for Lead (U.S. EPA, 1986a) and in the CDC's most recent statement on lead poisoning in children (CDC, 1985), Historically, the definition of lead poisoning has progressively expanded in terms of the number of significant effects and the lowest levels of lead exposure associated with these effects. As discussed by U.S, EPA (1986a), exposure to lead produces a continuum of toxic responses. Definitive criteria for judging which lead-related effects are adverse are not easy to state, but some are now accepted as reasonable for judging lead-associated lesions in humans. These include (1) impaired func tioning of a tissue or organ system; (2) reduced reserve capacity of tissues and organs to deal with stresses induced by other toxicants or xenobiotics; (3) the reversibility or irreversibility of the effect; (4) the relative n-ii DUP040009518 development may have far-reaching ramifications for other systems or later stages of development. Such cascading effects have been well described for the multi-organ Impacts of heme reduction (see Figure IV-2). 11-13 DUP040009519 DUP040009520 absorbed, either in situ in the case of the pulmonary compartment or via retroci1iary movement to the buccal cavity and swallowing. In the latter case, absorption can occur from the gastrointestinal tract. In adult humans exposed to lead in ambient air only, the pulmonary deposi tion rate is 30 to SOX (see ILS. EPA, 1986a; Chamberlain, 1983; Morrow et al- , 1980; Chamberlain et al., 1978). Essentially all of this deposited amount is absorbed over a relatively short time (Chamberlain et al., 1978; Morrow et al, -, 1980; and Rabinowitz et al., 1977). The respiratory absorption rate is relatively fixed over a broad range of air lead concentrations that nonoccupational populations are likely to encoun ter, and the rate is generally the same for a number of chemical forms of lead e.g,, chloride and oxide (Morrow et al,, 1980; and Chamberlain et al., 1978). Breathing rate changes and the particle size of lead-containing particulates in air also affect the absorption rate, but the percentages given above refer to typical exposures of general populations. Most of the available quantitative information has been derived from adults, and comparisons'with children under conditions of identical exposure to airborne lead are difficult with respect to relative respiratory dynamics. Young children inhale a proportionately higher daily air volume per unit measure (weight, body area) than do adults (Barltrop, 1972). This is related to higher metabolic demand and therefore higher gas exchange rate. James (1978) has estimated that children have a lung deposition rate of lead that can be up to 2.7-fold higher than in adults on a unit body mass basis. This estimate is supported by anatomical modelling approaches for airway lengths as a function of age and development (Hofmann et al., 1979). The data of Hofmann et al. (1979) indicate that there is a period of maximum childhood intake, specifically at about 6 years of age. 2. Gastrointestinal (GI) Absorption of lead in Human Populations In nonoccupationany exposed populations, the lead absorbed by the GI tract is from the intake of lead in foods and beverages in the case of adults and older children and from the intake of both foods and nonfood items, for example, lead-contaminated dusts and soils, in preschool children. Young children take in nonfood lead via normal mouthing activity and other behaviors associated with oral exploration of the environment. An extreme manifestation 111-2 DUP040009521 Ill, LEAD METABOLISM AND ITS RELATIONSHIP TO LEAD EXPOSURE * AND ADVERSE EFFECTS OF LEAD s Lead "metabolism" (pharmacokinetics, toxicokinetics, biokinetics) refers to the various integrated human body processes that govern the Intake, absorp- '! Lion, distribution, and retention/excretion of lead. These processes may be basically kinetic or they may describe interactive relationships that affect the biokinetic behavior of lead. These elements of in vivo behavior form the - Central link between 'the relatively simple event of external exposure to lead and the ultimate complex manifestation of some lead-associated effect or risk for the effect. It is from this particular perspective that a brief discussion of the topic is provided for the benefit of the general reader. Some points of interest include: (1) those characteristics of lead's metabolic behavior that abet its status as a public health issue; (2) the role of lead metabolism in defining certain subsets of the general population as being at special risk for the adverse effects of lead; and (3) the underlying metabolic characteristics of lead that affect the use of various biological exposure indicators that are widely employed in later chapters of this report. A, LEAD ABSORPTION IN HUMAN POPULATIONS Lead enters the bloodstream from several body compartments, with the rate of absorption (uptake) depending upon the chemical and physical forms of lead and physiological characteristics, for example, nutritional status and age, of the populations exposed to it. 1. Respiratory Absorption of Lead in Human Populations Lead in inhaled air is absorbed eventually in a two-part process: some fraction of the Inhaled air lead is deposited in the pulmonary and higher parts of the respiratory tract, and some amount of this deposited lead burden is III-l DUP040009522 The question of dietary lead bioavailability as a function of such properties as either the chemical or physical form of lead or its matrix (for example, meat or beverages) has been addressed in various studies. In this context, bioavailability refers to the actual quantity being absorbed, rather than the total amount in the gut. Heard and Chamberlain (1982) and Rabinowitz et al. (1980) noted that various chemical forms of lead were equally absorbed and that the dietary matrix imparted a minimal effect. A useful study, albeit.,' one with experimental animals, is that of Oacre and Ter Haar (1977). Results show that lead in soils and road dusts from air lead fallout is absorbed to the same extent in the rodent GI tract as is lead in simple water solutions. This indicates that lead in such material is potentially highly bioavailable when young children ingest it in the course of normal behavior. Within the range of lead levels in food likely to be encountered by even heavily exposed populations, the absorption rate from this route remains the same (Heard and Chamberlain, 1983; Flanagan et al., 1982; and Blake, 1980). Flanagan and co-workers (1982), for example, observed the same absorption rate for a lead dose of 400 pg as for 4 pg. 3. Percutaneous Absorption of Lead in Human Populations The human body absorbs very little lead through the skin, when considering the inorganic ion of lead (the form of interest). Results of one detailed study (Moore et al., 1980) showed that the human skin absorbs an average of about 0.06% of the applied quantity. 4. Transplacental Transfer and Fetal Uptake of Lead in Pregnant Women For the fetus, the route of lead uptake is across the placenta. Lead readily crosses the placental barrier during the entire gestation period, including that critical period when the nervous system is being embryo!ogically formed. Fetal lead uptake is cumulative until birth (Rabinowitz and Needleman, 1982; Alexander and Delves, 1981; and Barltrop, 1969). III-4 f DUP040009523 of this otherwise common behavior is pica, a behavioral trait associated with particularly severe lead poisoning. This topic is addressed in detail else where (U.S. EPA, 1986a; National Research Council> 1976, 1980), In the adult human, the rate of GI lead absorption from typical diets is 10 to 15% of the ingested quantity (Gross, 1981; Rabinowitz eta],, 1980; and Chamberlain et al., 1978). This rate range applies to enteric lead assimilated during usual meal times. Under fasting conditions, such as imbibing leadcontaining beverages between meals, this rate can increase dramatically (Heard and Chamberlain, 1982; Rabinowitz et al., 1980; and Blalce, 1976), The amount can increase to 6ti% or more absorption (Heard and Chamberlain, 1982), A major factor in this increase during fasting is the lower amount of those dietary components that are known to suppress uptake and that are present when meals are ingested. These components are discussed in more detail later in this chapter (Section D), The GI lead absorption rate in Infants and children, about 50%, is consid erably greater than the rate in adults (Ziegler et al., 1978; and Alexander et al,, 1973) indicating a higher relative exposure rate for a given food intake. It is possible that in the Alexander et al. (1973) study, enhanced absorption was influenced by iron deficiency, which is common in that group. However, the Ziegler et al., 1978 study was not complicated by this factor because of the age interval of the children. Related to age-dependent lead absorption from the human GI tract are data from the second National Health and Nutrition Examination Survey (NHANES II) (Mahaffey et al., 1982), which show a moderate peaking in Pb-B at about 18 to 24 months of age. This peak may reflect intrinsic differences in enteric uptake rates at different ages, the highest propensity for ingesting leadcontaminated nonfood items at this age, or both. With regard to the latter factor, estimates of the daily amount of dust or soil young children ingest vary (see Chapters 10 and 11, U.S. EPA, 1986a), but recent empirical studies from a smelter community (Centers for Disease Control, 1986a) yield a range of 121 to 184 mg with one marker technique, and an upper determination of 1,834 mg--about tenfold higher--with another technique. Whatever figure is selected, soil and dust of even moderate lead content clearly can contribute markedly to the oral lead intake. 111-3 DUP040009524 1. Lead Uptake in Soft Tissues In human soft tissue, including the various target organs for toxic action, lead uptake occurs in a complex fashion that reflects the specific tissue kinetics, the external exposure level, the lead level in circulating blood, and other factors. With few exceptions, levels in soft tissue range from about 200 to 500 parts per billion (ppb), and the levels stabi 1 ize in nonaccupationa7ly exposed populations by early adulthood (see, for example, Barry, 1981 and 1975). The 200- to 500-ppb levels of lead for tissues in unexposed populations need not rise very much to indicate toxicity as we index its signs and symptoms today. For example, the lead content in human brain tissue with severe acute or chronic neurotoxic damage is, in many cases, only 1 to 2 ppm or even less, demonstrating that lead can be a potent toxicant at very low levels in tissues. As a second example, Pb-B levels approximating 100 to 150 ppb (10 to 15 pg/dl) are associated with early toxic effects in human tissues now recognized as targets of toxic action. In general, lead does not appear to accumulate in soft tissues with age, and this includes the lung. Such nonaccumulation in the lung is further evidence that lead Is quickly absorbed from the, respiratory tract, as discussed earlier. Some evidence suggests that lead accumulates in human brain tissue with heavy exposure encountered in some occupational settings (Barry, 1975). The question of whether lead accumulates with age in soft tissues is still undecided on statistical grounds, since the usual cross-sectional analysis approach of using pooled autopsy samples from subjects of varying age would -obscure small but toxicological ly important accumulative changes in human populations. This contrasts with lead in mineralizing tissues, where the accumulation rate with age is so huge' that the mode of analysis would not obscure It, The central and peripheral nervous systems of humans, especially key brain regions vulnerable to lead, have no apparent barrier to lead uptake, and this uptake appears to differ among brain regions. Consequently, increased exposure translates to increased entry of lead into the brain across the total exposure range. III-6 DUP040009525 8. DISTRIBUTION OF ABSORBED LEAD IN THE HUMAN BODY Fo p the issues addressed in this report, the in vivo lead is distributed to two types of receiving tissues: soft tissues, including organs considered targets of lead's toxic action, and mineralizing systems, such as teeth and bone. Bone is not only affected toxicologically by lead but also serves as the body's major storage site. Such a tissue as bone accumulates lead at a signif icant rate for much of the human life span and poses a risk as a potential source of mobilizable, endogenous toxicant. With respect to the biokinetics of lead movement and models of systemic behavior, lead in the human body can be viewed as being distributed to at least three compartments (see, e.g., Rabinowitz et al., 1976), Lead in the blood is in its most labile form; lead in soft tissue is somewhat more stable; and lead in bone accumulates steadily in several subcorapartinents, which differ in allowing lead mobility back to blood* Absorbed lead enters the bloodstream, where, under fairly steady exposure conditions, at least 99% becomes bound to the erythrocytes -(DaSilva, 1981; and Everson and Patterson, 1980). With constant exposure, movement of lead from blood to tissues and back to blood establishes a near equilibrium. In short term experimental studies for adults, lead movement from blood has a half-life of about 25 days (Chamberlain et al,, 1978; and Rabinowitz et al., 1976), Pb-B levels will rise or decline, depending on the direction of the exposure change. For adults with abruptly increased exposure, e,g., new lead workers, Pb-B increases to a new "steady-state" level after about 60 days (Griffin et al., 197$; and Tola et al,, 1973), With a marked decrease in exposure, the level to which Pb-B declines and the time required to reach this new level are a complex function of the existing body lead burden, the specific nature of the study design, and the total time of prior exposure (Hryhorczuk et al., 1985; Kang et al., 1983; and O'Flaherty et al-, 1982). When lead workers are removed from exposure in the workplace, Pb-B levels may not fully decline for months or years. Changes in Pb-B of children in the course of development and because of changes in exposure may occur over a slower time frame, Succop et al. (1987) recently reported that the biological half-life of Pb-B of 2-year-old children is about 10 months. HI-S DUP040009526 3 weeks (Chamberlain et al. 1978; Rabinowitz et a1. 1976), which approximates the half-life of lead's movement from blood. Of the fraction of lead moved to bone, about half or ?S3 of the amount originally absorbed will soon be resorbed into blood and then excreted. The rate at which the body eliminates lead depends on age, with young children excreting less of a daily uptake than adults because of greater net ,, movement, of lead to bone. This comparative behavior is depicted in Table 111in which the data of Ziegler et al. (1978) for infants are Compared with data from two adult groups for which information was complete enough for the necessary calculations. TABLE III-l. COMPARATIVE DIETARY LEAD METABOLISM IN INFANTS AND ADULTS3 Variable Infants Adults*3 Group A Group B Dietary intake Fraction absorbed Dietary Pb absorbed Air Pb absorbed Total absorbed Pb Urinary Pb excreted Ratio: urinary/absorbed Pb Endogenous fecal Pb Total excreted Pb Ratio: excreted/absorbed Pb Fraction retained 10.8 0.46 (o.ssr 5.0 (5.9) 0.20 5.5 (6.1) 1.00 0.19 (0.16) 0.5 (1.6) 1.5 (2.6) 0.3 (0.4) 0.34 (0.33) 3.6 0.15 0.54 0.21 0.75 0.47 0,62 0.24 0.71 0.92 0.01 3.9 0.15 0.58 0.11 0.68 0.34 0.50 0.17 0.51 0.75 0.04 aAdapted from U.S. EPA, 1986a, and references cited therein. bMij/kg body weight. cCorrected for endogenous fecal lead when values are in parentheses The body's lead excretion rate as a function of the amount of lead absorbed has not been well studied. Chamberlain (1983) examined a number of clinical and epidemiological studies and produced an aggregate analysis showing that as lead intake and uptake increases, so does the excretion rate. Among retention rates for metal toxicants in humans, that for lead is relatively high, mainly because lead accumulates in bone and teeth. Lead in bone accumulates with age until about 60 years of age, when changes in diet and/or mineral homeostasis lead to a net negative balance; that is, daily loss exceeds the daily intake. However, beyond the years of active accumulation, III-8 DUP040009527 2. lead Uptake in Mineralizing Tissue Many studies, employing both biopsy and autopsy data, have documented that lead primarily localizes in mineral tissue such as bone and teeth and that it continuously accumulates in these sites for most of the human life span (Barry, 1375, 1981; U.S. EPA, 1986a; National Research Council, 1980), Such uptake apparently begins jin utero (Barltrop, 1969) and occurs across all ranges of exposure--that is, there is no threshold for lead uptake in bone. The total body lead content can approximate 200 mg and more in the absence of occupational exposure and can rise to well above this in lead workers. Of the total body content, at least 95% is lodged in mineral tissue (Barry, 1975; Rabinowitz et al ., 1976), Most of the lead in bone had long been considered to be metabolically inert, that is, non^oxic. However, bone now is recognized as a living organ that is sensitive to the toxic effects of lead (Rosen, 1983, 1985); further more, a fraction of its total lead content is more mobile than it is often assumed to be (U.S. EPA, 1986a). This mobile fraction can be resorbed into blood and potentially can exert toxic effects, as discerned frbm kinetic modelling (Rabinowitz et al., 1976), chelation mobilization (Saenger et al,, 1982; PiemeUi et al ., 1984; Araki and Ushio, 1982), and experimental animal studies (e.g,, Hammond, 1973), Lead also accumulates in teeth as a complex function of age (Steenhout and Pourtois, 1981), tooth region, e.g., enamel, secondary dentine, etc. (Needleman and Shapiro, 1974), and tooth type (Delves et al., 1982). Lead accumulates especially in the dentine of childrens' teeth and continues to accumulate until the teeth are shed. Various researchers have used this fact to index cumula tive lead exposure in children (see, e.g,, Needleman et al., 1979). C, LEAD EXCRETION AND RETENTION IN HUMAN POPULATIONS Absorbed lead in the human body that is not retained is eliminated in either urine (about 65%) or bile (35%), The available evidence indicates that about 50% to 60% of daily absorbed lead is rapidly excreted (Chamberlain et al., 1978; and Rabinowitz et al., 1976), with the balance being distributed to bone. This rapidly excreted fraction has a half-life in the body of about III-7 Ziegler et al. {1978),, Experimental data gathered with human volunteers by Heard and Chamberlain (1982) show that lead absorption is significantly sup pressed when lead is administered in diet with calcium and/or phosphorus. Iron deficiency has long been known to be a key factor in the level of systemic lead exposure for young children, especially for those children from poor, inner-city families (Chisolm, 1981; Yip etal., 1981; Watson etal,, 1980). A number of studies (e.g., Chisolm, 1981; Yip et al., 1981; Watson ; 1. . , y* et al., 1980) have established a strong inverse correlation between iron status and Pb-B, the main conclusion to be drawn froin studies of lead-nutrient Interactions is that defects in nutrition will enhance lead absorption/retention and toxici ty risk. This problem is amplified in children where nutrient deficiencies are commonplace and where lead exposure is highest, i.e., 2- to 4-year-old, under developed children* Zinc deficiency can also play a role in enhanced lead absorption and toxicity risk (Markowitz and Rosen, .1981) and can be an interactive factor for children with zinc deficiency because of sickle cell anemia. E. LEAD METABOLISM AND SOME KEY ASPECTS OF LEAD EXPOSURE AND TOXICITY The metabolic behavior of lead in the human body has a major influence on the status of lead as a persisting U.S. public health problem. There are at least three points of connection: (1) lead metabolism as a factor in its behavior as an insidious toxicant even in populations with moderate exposure; (2) differential lead metabolism as a factor in identifying risk populations for both exposure and toxicity; and (3) lead metabolism as it relates to the accuracy and usefulness of biological indicators such as Pb-B in defining the toxicity risk for target tissues, 1. Lead Metabolism and the Nature of Lead Exposure and Toxicity In general, the metabolic behavior of a toxicant is intimately related to toxic responses, which also pertains to lead. With lead, however, some points needing further discussion relate to its propensity to accumulate in the body over time and over a wide range of lead exposures in various intake media with no threshold for the phenomenon in terms of smallest intake rates. III-10 DUP040009529 little total body lead is lost. The half-life of lead in the most dense, mineral portion of bone is about 20 years or more for the active accumulation phase in humans. Lead can be mobilized fro some subcompartment within human bone during various physiological stresses, specifically pregnancy and lactation. Increas es in Pb-B have been documented during pregnancy for a population of smelter region women (Zarie et al., 1987) and during lactation in the careful isotope tracing study of Wanton (1985). Of equal importance, Manton {1985) showed that Pb-Bs at steady state also had sizable inputs from bone lead in two subjects. In young children, the level of lead retention is considerably higher than in adults (Ziegler et al ,, 1978; Alexander et al., 1973), and the location of these higher deposits is unknown. A key factor in lead disposition in children is the metabolic fact that in the first decade of life the skeleton grows exponentially, increasing about 40-fold. Body growth overall and bone uptake of lead result in a huge dilution factor in lead concentration, A more mean ingful measure here is the lead content of bone in children of various ages, which is discussed in detail in U.S. EPA, 1986a. D, METABOLIC INTERACTIONS OF LEAD WITH NUTRIENTS AND OTHER ACTIVE FACTORS IN HUMAN POPULATIONS The interplay of lead metabolism and the physiological status of humans, especially nutritional well-being, figures importantly in the level of lead exposure required to produce effects and manifestations of toxicity. A number of agents interact with lead entering the human body, and the available data consist of both human studies and experimental animal models of such interac tive behavior. A detailed presentation of such interactions has been set forth in U.S. EPA (1986a), and only summary statements are provided here. The major interacting agents of interest, also discussed in Chapter IX as part of exposure prevention strategies, are calcium, iron and, to some extent, phosphorus. Mahaffey and co-worker$ (1976) reported that children with elevated Pb-B had lower intakes of calcium and phosphorus from diet than did a reference population. Similarly, Sorrell and co-workers (1977) found that blood lead was inversely correlated to dietary calcium intake at a high level of statistical significance. Similar results were reported by Johnson and Tenuta (1979) and III-9 DUP040Q09530 2. Lead Metabolism and the Identification of Risk Populations for Lead Those occupationally exposed to lead are an obvious risk population, but one outside of the purpose of this report. At present, we can identify at least two risk populations for lead exposure and toxicity among the nonoccupational'ly exposed general population:. These two risk groups from the general U.S. population are young children and pregnant women, the latter because ofy the exposure of the Vulnerable fetus. Metabolic criteria define these subsets as risk subjects. Young Children as a Risk Group on Metabolic Grounds Young children absorb a greater percentage of ingested lead per unit body measure than do adults. They also take in more lead-containing dietary compo nents per body unit measure because of caloric and energy demands. In addition to haying a greater absorption rate, children retain a greater fraction of lead. This differential is distributed to a rapidly growing skeleton and to soft tissues. Growth dilutes the dose function, but the total lead in the skeleton shows marked net accumulation and can serve as an endogenous source of exposure. Children are most vulnerable to lead effects at the exact time during which they physiologically most need optimal nutritional status. Deficiencies in elements that otherwise suppress lead absorption and toxicity place poorer children at greater risk, since such children are most often poorly nourished. Children are likely to undergo stresses such as chronic diseases that may affect mineral metabolism and lead release from bone. This possibility has not been examined in any detail in children, but we do know that physiological stress such as pregnancy and lactation will mobilize bone lead in women. Furthermore, behavioral traits in young children interact with lead metabolism to define added risks for this group. Normal mouthing activity enhances lead intake and uptake, a subject pursued in more detail in Chapters VI and VIII. Lead bioavailability in nonfood categories (soil, dust, paint chips, etc.) is assumed to be rather high, and these sources contribute to body burden and toxicity risk. 111-12 DUP0400Q9531 When considering information showing that (1) lead can be mobilized from sequestration in bone back to the bloodstream, (2) such stresses as pregnancy and lactation may alter mineral homeostasis enough to effect such mobilization, and (3) low levels of circulating lead are associated with postnatal and .prenatal effects in human populations, we can offer the following conclusions about lead as a unique public health problem: (a) Since lead is a cumulative human toxicant, the usual dose-effect and doseresponse relationships must be applied cautiously to lead in human popula tions (see Chapter IV). For example, when we speak of integrated lead exposure in a target tissue, that Is, toxicity defined as a lead level over some time period, accumulated lead with a slow removal time may be' inherently more toxic than lead moving rapidly in and out of tissues. (b) The accumulation of lead in human body compartments necessitates attention to toxicity risks even if only low levels of lead are being absorbed at a given time. Low intake levels in each of many Intake sources, for exam ple, food and water (see Chapter VIII) further complicate this issue. (c) The above problems of integrative exposure, cumulative dose-effect behav ior, and public health consequences are even further complicated by new prospective studies that document numerous adverse effects in infants that can be traced to In utero exposure, that is, exposure to maternal lead during gestation. There is no metabolic barrier to fetal lead uptake. Furthermore, the amount of lead maternally circulating for fetal uptake may actually be higher than usual if the physiological stress of the pregnancy disrupts the metabolism of minerals in bone and releases lead stored there. (d) The interplay between systemic lead exposure due to ongoing external exposure and that due to accumulated toxicant in bone and elsewhere has been examined. For example, Christoffersson and co-workers (1984) used in vivo measurement of bone lead to show that when human subjects are actively exposed to lead, the blood lead best correlates with the concur rent lead exposure. However, when active exposure stops, blood lead remains troublesomely elevated and is highly correlated statistically with the lead level in the bones of these subjects. These data show that the circulating blood lead is a function of both ongoing and cumulative past exposure (bone lead). The latter contributes via resorption from bone back to blood. III-ll DUP040009532 The Fetus (Pregnant Women) as a Risk Category on Metabolic Grounds As noted* there is no metabolic or anatomical barrier to lead for the fetus, and uptake continues for the entire gestational period, including the embryo!ogical development period for the nervous system and other targets of lead toxicity. The exposure of pregnant women is, therefore, of key impor tance, especially given the evidence of in utero effects at Tow lead levels (see Chapter IV), 3. Lead Metabolism and Biological Exposure Indicators The usefulness of biological or body indicators of internal lead exposure is essentially determined by the metabolic behavior of the toxicant. From the' foregoing discussion in this chapter, lead metabolism tells us that: a. The actual level of lead in blood is a more labile measure and will reflect more recent 'exposure. However, Pb-B can give relative ranking in an exposure group over somewhat extended periods, which may reflect continuing lead washout from accumu lating sites. b. Accumulating tissues, such as bone and teeth, give a cumulative picture of past or ongoing exposure over extended time. c. At present, blood lead is the most useful and practical biologi cal exposure monitor although shortcomings may exist in what it tells about lead behavior in inaccessible tissue sites. As an example of a problem with blood lead, Piomelli et al, (1984) show that if one tests circulating body lead in children by the technique of provoc ative chelation, i.e., a single treatment with a lead binding agent that removes lead and produces lead excretion in urine, this urinary lead amount in a percentage of children with moderately elevated Pb-B levels (25 to 30 pg/dl) is equivalent to levels in those individuals with higher Pb-8 levels and who require hospitalization and treatment. In other words, if only Pb-B levels were relied on, the actual toxicity risk due to toxic, circulating lead might be underestimated. III-13 DUP040Q09533 A, THE EXPOSURE (DOSE) INDEX IN ASSESSMENT OF THE ADVERSE HEALTH EFFECTS OF LEAD IN HUMAN POPULATIONS The concentration of lead in whole blood (Pb-B) has been the most commonly used indicator of exposure in studies relating lead exposure to toxicological and health endpoints. Blood is readily accessible and relatively convenient/tp obtain:. Most other organs and tissues of the body are not as easily sampled. Lead can be accurately, precisely, and reliably measured at quite low concen trations in blood, thus providing an important quantitative index that can be:, related to both external exposure levels and the toxicological or health effects induced by lead. As a link to external exposure, Pb-B levels offer a more direct index of the actual amount of lead that has entered the body. In obtaining quantitative dose-response relationships between lead and biological effects, Pb-B levels have been extremely useful. Indeed, the robustness of these relationships has resulted in the clinical use of Pb-B levels as an indicator of lead-induced injury to organs and tissues (Chisolm and Barltrop, 1979). There are also limitations in Pb-B levels that should be recognized. The relationship between external and internal exposure measures is not linear over the entire range of possible values. For example, Pb-B levels are proportion ately not as elevated at relatively high environmental levels as one would expect from their values at lower environmental levels. The Pb-B levels associated with specific types of biological effects also vary for individuals and populations. Children generally show a much greater vulnerability to toxic effects at a given Pb-B level than adults do at the same level. As an indicator of the total body burden of lead, Pb-B levels may under represent the actual body burden. In a detailed study of children who under went provocative chelation testing, i.e., biochemical removal of lead from the body, Piomelli et al. (1984) found that a sizable number of children who had relatively low Pb-B levels nevertheless had high levels of lead in other compartments of the body. Since lead accumulates over time, indicators of cumulative exposure, such as the amount of lead in teeth or bones, offer certain advantages over Pb-B levels. On the other hand, exposure is not static fn children, and an indicator that responds relatively rapidly to abrupt or intermittent changes in their intake of lead (e.g., through ingestion of lead paint chips) is valuable. IV-2 DUP040009534 IV, ADVERSE HEALTH EFFECTS OF LEAD: RELATIONSHIP TO PUBLIC HEALTH RISK AND SOCIETAL WELL-BEING Section 118(f) of SARA directs that there be an evaluation of the long term adverse consequences of ongoing lead exposure at levels currently being encountered by children in the United States. Both the individual and society as a whole are damaged by adverse health effects associated with lead exposure. Lead-induced reductions in IQ, for instance, not only place the individual at a disadvantage, hut also eventually place the nation at a collective disadvan tage in an increasingly competitive, technical, and cognition-intensive world economy. While the aggregate social cost of lead poisoning in dollar terms is not considered in this report, the reader can refer to a detailed assessment of such costs recently carried out by U.S. EPA (1985). This chapter is organized into four sections. Section A explains why the concentration of lead in blood (Pb-B) is typically used as the measure of expo sure in assessing the health effects of lead. Section B describes the various adverse health effects of lead in children that occur at different levels of lead exposure, with special emphasis on effects that have been found at preva lent levels of population exposure. Section C summarizes current information relating the primary adverse health effects of lead to the lowest exposure levels (in terms of Pb-B concen trations) at which the effects have been reliably observed to occur. Given the progressive decline in the 11 lowest-observed-effeet-levels" throughout the history of lead research, continued work may reveal even lower levels for lead-induced toxicity in the future. Section C also discusses adverse health effects in terms of population risk. Section D discusses the relative persist ence of various effects of lead and considers criteria for defining "persistence of effect." IV-1 DUP040009535 MITOCHONDRION MITOCHONDRIAL MEMBRANE GLYCINE + "$(' Co A ALA SYNTHETASE HEME Pb \FERRO- CHELATASE (INCREASE) IRON+PROTOPORPHYRIN Pb (DIRECTLY OR BY DEREPRESSION) AMINOLEVULINIC ACID (ALA) ALA DEHYDRASE (DECREASE) Pb PORPHOBILINOGEN Pb COPROPORPHYRIN (INCREASE) t IRON Figure iV-1. Effects of lead (Pb) on heme biosynthesis. Source: EPA (1986a). ALA-dehydratase (porphobilinogen synthetase) activity, coproporphyrin utiliza tion, and the insertion of iron into protoporphyrin IX to form the prosthetic group, heme. Companion effects on the uroporphyrins, which are mainly affected at relatively high exposure levels in humans, are also presented. The accumulation of protoporphyrin IX (zinc protoporphyrin, ZPP; proto porphyrin in erythrocytes, EP) is not only an indicator of diminished heme biosynthesis, but also signals general mitochondrial injury, since the'final step in heme biosynthesis, which includes EP, occurs in the mitochondria. Such subcellular injury may impair a variety of processes, including cellular energetics and calcium homeostasis. The various effects of lead within the heme biosynthesis pathway are shown in Table IV-1. Note that these are quali tative in nature. Quantitative relationships are presented in Section C of this chapter. IV-4 DUP040009536 On the whole, Pb-B level remains the scientifically and diagnostically most useful index of internal body exposure to lead. The following sections therefore rely heavily on this important variable in presenting the current understanding of adverse health effects in children, B, MAJOR ADVERSE HEALTH EFFECTS OF LEAD IN CHILDREN There is a wealth of information about the variety and the relative inten sity of adverse effects of lead on different tissues and organ systems of children, including those considered as the critical target organs of lead toxicity. Such effects involve many levels of physiological and anatomical organization within the body, starting with the cel 1ular/subcel1ular level and progressing to higher levels of functional and structural organization. At a sufficient level of lead exposure, virtually all body systems will be injured or have a high risk of injury. The full spectrum of such effects is presented in a comprehensive assessment of this topic in Air Quality Criteria for Lead (13. S, EPA, 1986a). In this chapter the primary focus is on those effects that occur at relatively low or prevalent chronic levels of lead exposure in the United States. 1. Effects of Lead on Heme Biosynthesis. Erythrocyte Physiology and Function, and Erythropoietic Pyrimidine Metabolism Effects on the blood's biochemical functions are interrelated and have variable biological impact. Heme, the iron-containing prosthetic or cofactor group, is critical to the basic function of various heme proteins in cells in many different organ systems. These organs include the blood-forming tissue and the liver, kidney, and brain. In addition to the direct effects of lead on heme biosynthesis, there are potentially significant indirect impacts on the central nervous system, caused by the lead-induced accumulation of deltaami nolevuTinate (ALA), a potential neurotoxicant (discussed in U.S. EPA, 1986a). Figure IV-1 depicts graphically the various steps in the heme biosynthetic pathway that are known to be affected by lead, although the actual mechanisms may not be fully understood in all cases. These steps include the feedback derepression (stimulation) of ALA-synthetase activity, the inhibition of IV-3 DUP040009537 REDUCTION OF HshEB30''POO. / Figure IV-2. Multi-organ impact of reductions on heme body pool by lead. Impairment of heme synthesis by lead results in disruption of a wide variety of important physiological processes in many organs and tissues. Source: EPA (1986a). IV-6 DUP040009538 TABLE IV-1, EFFECTS OF LEAD ON THE HEME BIOSYNTHESIS PATHWAY IN HUMANS Step Affected Results Comments Inhibition of ALA-D activity Accumulation of ALA in the body and excretion. Plasma and urine levels rise; ALA itself may be neurotoxic at higher levels. Feedback derepres sion of activity of ALA-synthetase Accumulation of ALA in the body and excretion. Much less sensitive than ALA-D activity; occurs at Pb-B >40 pg/dl, Inhibited conversion of coproporphyrin Accumulation of copro porphyria in urine. Inhibition of copropor phyrin utilization; indi cates ongoing lead expo sure. Inhibited conversion of protoporphyrin IX (EP) to heme Accumulation of EP in red blood cells. Sensitive measure of lead toxicity; elevation indicates mitochondrial injury. Figure IV-2 graphically depicts lead-associated disturbances of the body heme pool. Most effects are documented, while some are only suggested by avail able experimental data. All of these effects can be summarized as follows: Cl) Hemoglobin effects--Lead can disturb the biosynthesis of hemoglobin, the general oxygen transport substance in mammals, leading* in a dose-dependent manner, to anemia and potential exacerbation of hypoxic responses to other toxic agents. (2!) Neural effects--Lead can reduce the amount of nervous system hemoproteins available for brain cellular energetics and development in neurons, axons, and glia. (3) Renal and endocrine effects--Lead can disturb heme-mediated generation of the important hormonal metabolite of vitamin D, 1,25-(0H)2-vitamin D, This hormone serves a number of metabolic functions in humans, including regulation of calcium metabolism and function. (A) Hepatic effects--Lead can impair the ability of heme-dependent liver enzyme systems to adequately detoxify foreign substances. IV-5 DUP0400Q9539 The history of research on lead has shown a progressive decline in the lowest exposure levels at which neurotoxic and other effects can be detected. Consequently, the attention of the medical and research community has largely shifted to the effects of chronic, low-level lead exposure (although cases of severe poisoning still occur). Epidemiologic studies have been the primary means of identifying the effects of prevalent lead exposure levels on popula tions of children. These studies have been of two general types: (1) crosssectional or retrospective studies, which examine variables at a particular time point in the present or reconstructed past, and (2) longitudinal or prospective studies, which measure variables over an extended period of time into the future* Longitudinal or prospective designs have a number of advantages for the study of environmental pollutants. In the case of lead, a key advantage of prospective studies is that one can evaluate each subject's pattern of lead exposure with more accuracy and precision than one can with cross-sectional or retrospective studies. Information on the history of exposure is obviously important in assessing the effects of a cumulative toxicant on endpoints such as neurobehavioral functions, which may reflect alterations induced during critical periods of earlier neurological development. In the subsections that follow, important recent findings from a group of prospective studies are discussed first, followed by a summary of findings from cross-sectional and other investigations of childhood lead neurotoxicity. a. Prospective Studies of Lead Neurotoxicity Findings from a group of well-conducted studies now indicate that distur bances in early neurobehavioral development occur at levels well below those considered "safe" or even "normal" in recent years. The most clearly ident ified effect thus far has been lower scores on the Mental Development Index of the Bayley Scales of Infant Development, a well-standardized test of infant intelligence. Other developmental endpoints, such as shorter gestational age and lower birth weight, have also been associated with prenatal load exposure in many of these studies, but are discussed separately below in Section 3 ("Other Adverse Health Effects"), A recent interpretive review of these studies (Davis and Svendsgaard, 1987) has assessed in greater detail the features of the studies and their implications for public health. IV-8 OUP040009540 in addition to its effects on heme biosynthesis, lead has related effects on the cellular health and function of the red blood cell, inducing deleterious changes,, such as enhanced fragility and higher rates of lysis. Such cell destruction can result in enough hemolytic loss of hemoglobin to significantly augment the lead-induced anemia that occurs through other routes. Lead-induced disturbances in red blood cell formation and maturatipft also occur by way of alterations in pyrimidine metabolism. Inhibition pf the enzyme pyrimidine-5*nuc'feotidase . (Py-5'-N) impairs the degradation of large nucleic acid biomoleculles and interferes with normal cellular energetics involved Irt the formation of the mature erythrocyte. 2. Neurotoxic Effects of Lead in Children Although'lead has diverse health effects, its neurotbxic effects in children are particularly notable because of the sensitivity of the developing nervous system. Indeed, the central nervous system is the primary target organ for lead toxicity in children. In the earlier part of this century, childhood lead neurotoxicity was primarily recognized as the result of acute, high-level lead exposure resulting, for example, from the ingestion of leaded paint chips. Prior to the introduction of chelation therapy, which biochemically removes a portion of lead from the body, severe lead poisoning with encephalopathy had a mortality rate of 65% (NAS, 1972), Since the advent of chelation treatment, mortality rates have declined significantly. In the United States, the use and refinement of chelation therapy in lead poisoning owes much to the work of Chisolm and colleagues in Baltimore (NAS, 1972). The Pb-B levels associated with such severe poisoning were quite high, but were also quite variable, reflecting individual differences in vulnerability and varying times between the exposure episode and clinical intervention. Children surviving acute poisoning episodes, with or without manifest encepha lopathy, were often found to have severe neurological sequelae, traced to permanent damage to the central nervous system. Observations by Byers and Lord (1943) and other clinicians showed that children manifested mental retardation, seizures, optic atrophy, sensory-motor deficits, and behavioral dysfunctions long after their acute poisoning experiences. Perlstein and Attala (1966) reported such sequelae in 37% of children who suffered lead poisoning without evidence of encephalopathy. IV-7 DUP040009541 OT-AI n er 9 X8 CO 0 e 10 rt O *4 v C' rt -- 9 H .0 n fl 3 -- ID CD it ( </> ui oo 4f f g r* fit o A < A o 3 I .S 3 ft ** ? & a x- CT S** V* * M O fli > m a*c 9 O <Q > C >H 9 Ck -* H U> :0^!N KB -H Of Ol 3 Of Q.*9 > * ft) 1 '9rO --x < n-- - a rt rt op i,3 . rr: 3A C 5w 9 in* a. 9, . 9 rt !.'ft n Of 9: 9 ft ID Q 0.1 .0 9 f* .3* A O 9 a 9 -0 ft Jfli' 9l -* - 3 O '9 ID Or .<: . 1 .ID OB 0, 33 fi. X yt% W ID ftO e it car -* .0 9 a. *8 C * 9 O Oi ,-^.rt .O (Q >4 h ID ft .0 9 i'"-? ;VI < 1 19 !* .ft 3 v .(S* i'3 !: V 9 ft ID -9 i1JBP8* ID ! 9 9 ft n ;-.3 id Oft 0 91 9 3 9 at ft 9 3 9 ft ID 9 9 .at --* v 3 ft) ft <? M ft* fl p >9 CD ft VI v 9 CD 3 O (A ft 3 9 ft Of ISO '4b 9 0 3 n 9 9 ft ,3 *< n 9 Ml A VI 9 ft IP x 9 O W 9? <t (A X* 9 (fl OB -9 ft ar n 9 9 d S3 1H 00 --9 * ft ft (a an (SO M JO M 4* 9 p M ,4b O r s All p X -9 2 a9e 's.ig -* Q. A 9 r-^ft *t) CP O " 3 99 -O ' .O IA .ft 3 9. ft 9mt* f9 : OI 9J O _-H :XA 9- 9A VI e0 9 ** S fa .A cr .3 8 (t <BB w 3 M n N ,4D' .9 O m -3 a. 0is m* -3 ft IS) 0 ft (A . 1 5 e .3 ft .0 9 (3 A 9 O Mb ft W '.cr 30 "H 3 t3ip n ft 0 9 ID A O 9 9* _* cb T Of 9 Q. j-i s 1 .*4 ID aB). <a 9 0 c *0 VI -M .3 9 V* ft VI rt at (A ID .<* O * n 0 09 O fD .3 <A < n ft 9O 3 -3 Of 3 30 A rt O Ml* -. <1 9 ft 0 X3 c A flu 'W' m 19 0e (A 9 ft ft O ..3* *0 wmim 9 X * 3 A 0 3 c AA 9 ft >' Cb S9 rt 9 9 Ml 9 rmC 90 3 .3T 9 0) . 9A ft ft ft) 9 ft M- fll W^s M AOv^ CD cn 0 ** *- to as ai 0 OB 8 A 09 A A .w X -* ft VO-- 9 * 3 Q9* 01.3 O 3 A ' H 9 W9 9 (O ft A OB A ft >1 ft 9 at 9 w9 *. Ml tV S 00 <71 M 13 00 tsl -X to 00 >4 cr .w fS H* u> 00 4b H <p s < rf* 9 8 .9 3 *** A ft 9 fS 1-4 S u* M SO 00 >4 N-* 99 A -^1 A 9 A .3 n A or 9 DUP0400G9542 A number of prospective studies are currently Underway in various parts of the world, but those conducted in Boston, Cincinnati, and Cleveland, in the United States, and Port Pirie, South Australia, have progressed far enough to provide published results that can be critically assessed and interpreted* As noted by Davis and Svendsgaard (1987), these four studies collectively provide evidence that is much stronger and more compelling than any single study or past studies in general could provide. Among the strengths of these studies are the fact that, although indepen dently conducted, they have benefited from the exchange of information and ideas among the principal investigators concerning the design and analysis of their work (Bornschein and Rabinowitz, 1985). Also, as a group, these studies are much more sophisticated methodologically than most previous work. For example, they consider and employ appropriate Controls for many more covariates and possible confounders, and with study populations numbering in the hundreds, they have greater statistical power to detect subtle effects than most earlier studies had. their analytic methods for measuring blood lead levels are quite accurate and reliable. Moreover, by consistently using the Bayley Scales and certain other Outcome measures, they have assessed developmental effects in a manner that permits a direct comparison of their results. Thus, more confi dence may be placed i:n the conclusions and weight of evidence provided by this body of work. Table IV-2 summarizes some of the key features of the four prospective studies reviewed below. It may be useful to note that the Bayley Scales of Infant Development comprise three indexes of mental, motor, and emotional development. Of particular importance here is the Mental Development Index (MBI)which was designed to assess; "sensory-perceptual acuities, discrimi nations, and the ability to respond to these; the early acquisition of `object consteincy` and memory, learning, and problem-solving ability; vocalizations and the beginnings of verbal communication; And early evidence of the ability to jnrm generalizations and classifications, which is the basis of abstract thinking" (Bayley, 1969, p.3). The scales have a mean of 100 and a standard deviation of 16. The first prospective study to report effects Of prenatal lead exposure on later postnatal development was conducted in Boston by Bellinger et al. (1984). Blood lead levels were measured for 249 umbilical cords of infants born to IV-9 DUP040009543 Cincinnati study. It is important to note that the statistical significance and the magnitude of the effects described here were already adjusted for various factors such as maternal alcohol and tobacco usage, home environment, and SES. More recent analyses of 12-month data for this same cohort have indi cated that deficits in the MDI and other effects persist at least through the first year of life (Dietrich et al,, 1987c), which, again, is consistent- / ' with findings from the Boston study. Reports from Ernhart et al. (1985a, 1986, 1987a) have also addressed the issue of prenatal lead exposure and postnatal neurobehayioral function as examined in a prospective study in Cleveland, Ohio, Maternal and cord blood samples were obtained at the time of delivery from 185 mothers (X = 6,5 pg/dl) and 162 infants (X = 5.8 pg/dl). Of these, only 132 samples were actual motherinfant pairs. The infants were evaluated on the Brazelton and the GrahamRosenblith neonatal behavioral assessment scales* which showed three signifi cant effects (out of 17 outcomes examined) related to blood lead: abnormal reflexes, neurological soft signs, and muscle tonus. Using the restricted data set of 13R mother-infant pairs, only neurological soft signs were significantly related to cord blood lead. A brief report (Wolf et al., 1985) on later outcomes in this same cohort mentioned a statistically significant relationsnip between the neurological soft signs measure and the Bayley MDI scores at 12 mohths. Thus, despite ttjie comparatively small number of subjects in this study, it appears, as noted by bavis and Svendsgaard (1987), that neurobehavioral effects of quite low prenatal lead exposure were detected at birth and that, indirectly, 12-month Bayley MDI scores may have declined as a result. Another major prospective study is under way in Port Pirie, South Australia. Preliminary results of testing 592 children on the Bayley MDI and PDl scales at 24 months of age have been reported by Vimpani et al. (1985) and Baghurst et al, (1987). Multiple regression analyses indicated that lead exposure was significantly related to reduced MDI scores. For every 10-pg/dl increase in blood lead, scores on the 24-month MDI dropped an average of about 2 points, which is notably consistent with findings from the Boston and Cincinnati studies. However, unlike the latter studies, the strongest rela tionship in Port Pirie was found using postnatal blood lead. Blood lead levels rose sharply in the Port Pirie cohort from about 14 pg/dl at 6 months of age to approximately 21 pg/dl at 15 months. Davis and Svendsgaard (1987) suggest that earlier testing on the Bayley Scales (e.g., IV-12 DUP040009544 middle- to upper-middle class parents. The use of higher socioeconomic-status ($$) subjects Complements the focus on lower SES subjects -jn most other lead studies. Multivariate regression analyses for 216 subjects showed an associa tion between cord blood lead levels and performance on ihe Bayley MDI at six months of age. The covariate-adjusted difference between low (X = 1,8 pg/dl) and high (X = 14.6 pg/dl) lead exposure groups was nearly 6 points on the MDI. Continued follow-up of these subjects has shown that a 4-8 point deficit in MDI scores persisted at 12, 18, and 24 months of age (Bellinger et at., 1985, 1986, 1987a), No effect was evident using postnatal blood lead levels. More recently, Bellinger et al. (1987b) have reported that the Boston cohort of children also show cognitive deficits on the McCarthy Scales of Chil dren's Abilities et about 5 years of age. Although initial analyses do not indicate that these deficits cap be attributed to prenatal lead exposure (after v adjusting for the influence of potentially confounding factors), they do show a significant relationship to earlier blood lead levels (at 24 months) rather than concurrent levels. Dietrich et al. (1986, 1987a,b) enrolled 305 pregnant women from the inner city of Cincinnati and measured their blood lead levels at the first prenatal clinic visit (X = 8.0 pg/dl for 245 subjects). Blood lead concentrations of the newborn infants were determined at postnatal day 10 (X = 4.5 pg/dl for 280 subjects). Regression analyses (including a statistical technique known as structural equation modeling) indicated that prenatal lead exposure was in versely related to male infants' scores on the 6-month Bayley MOI as well as the IPsychomotor Development Index (PDI). These effects were both direct and indirect; that is, prenatal lead levels were not only directly related to impaired performance on the Bayley Scales, but were also related to reduced gestational age and reduced birth weight, whicih in turn were associated with lower MDI and PDI scores. The total direct and indirect effects of prenatal lead exposure on MDI scores amounted to approximately 8 points deficit for every 10-pg/dI increase in blood lead level (Dietrich et al., 1987b). A similar association was found between MDI scores and neonatal blood lead, but preliminary analyses using postnatal blood lead measurements at 3 and 6 months indicated no significant relationships (Dietrich et al., 1986b). Thus, as in the Boston study, prenatal rather than postnatal lead exposure had the predominant influence on postnatal neurobehavioral perfor mance. Interestingly, however, these effects were confined to the males in the IV-11 DUP040009545 lit various populations of children with known exposure to lead (e.g., residents of snelter communities or inner-city children identified through lead screening programs). By today's frame of reference, exposure levels for these subjects were quite high, with mean levels well above 50 pg/dl in many instances. For example, de la Burde and Choate (1972) found various neurobehavioral dysfunc tions and IQ deficits in children whose Pb-B levels averaged 58 pg/dl at the^ ' time of assessment. Later follow-up (de la Burde and Choate, 1975) indicated that the dysfunctions and deficits persisted* A variety of similar neuro behavioral impairments were also evident in both post-encephalopathic children (Rummo, 1974; Rummo et al., 1979) and "asymptomatic" children (Kotok et al., 1977). The difficulties in drawing conclusions about the likelihood of causal relationships from these early studies are illustrated by the work of Perino and Ernhart (1974), who found an association between lower IQ scores and Pb-B levels in children identified through the New York City lead screening program. Follow-up investigation of these children, with control for parental education, led Ernhart et al. (1981) to conclude that the effect they had first reported was probably not due to lead or represented at best only a minimal effect on intelligence. Furthermore, after resnalysis of their earlier data, Ernhart et al. (1985b) concluded that their results provided no indication of an effect of lead on intelligence in the children they had examined* Despite the limitations of the early epidemiologic investigations, their findings pointed the way for later studies at lower exposure levels. An important pioneering study of a general population of children without known elevated lead exposure was conducted by Needleman et al. (1979). The deciduous teeth of subjects were analyzed for lead content, which served as an indicator of cumulative lead exposure for the more than 2,000 children enrolled in the study. Based on classroom teacher ratings of the behavior of these children, an apparent dose-response relationship was found. More detailed analyses, taking into account various confounding variables, showed significant differ ences in IQ and certain other neurobehavioral measures for 58 high-lead child ren versus 100 low-lead children. Later analyses of the data from this study extended the findings and their implications. For example, Needleman et al. (1982) noted that a difference of 4 points in mean verbal IQs for the bighand low-lead groups meant that children in the high-lead group were three times as likely to have a verbal IQ below SO, and no high-lead children scored IV-14 DUP040009546 at 6 months) might have revealed a stronger effect of prenatal exposure than could be detected later, after blood lead levels had Increased so much between 6 and 15 months. More recent, but still preliminary, analyses incorporating controls for maternal intelligence and quality of the home environment indi cated that the blood lead-MDI relationship was "markedly attenuated" when home environment measures were included in the multivariate regressions (Vimpani et al., 1987). Nevertheless, the association between 6-month blood lead levels and 24-month MDI scores remained statistically significant. Other prospective studies are being conducted by McBride et al. (1987) in Sydney, Australia, by Rothenberg et al. (1987) in Mexico City, Mexico, by Grazianc et al, (1987) in Titova Mitrovica, Yugoslavia, and by Moore et al. (1987) in Glasgow, Scotland. The results from these studies are still prelim inary or have not yet been reported in sufficient detail to allow critical evaluation. In sum, the studies for which adequate information is available are remarkably consistent in identifying a link between low-level lead exposure during early development and later neurobehavioral performance as reflected in deficits on the Bayley Mental Development index. Moreover, the studies generally point to the prenatal period of exposure as the most critical, although postnatal exposure may still be important and even override the effect of prenatal exposure under some conditions. Blood lead levels of 10 to 15 Mg/di, and possibly lower, constitute a level of concern for these effects (Davis and Svendsgaard, 1987; U.S. EPA, 1986a), The public health implications of a 2- to 8-point decline in Bayley MDI scores have been examined by Davis and Syendsgaard (1987) and Grant and Davis (1987), They noted that, although a change of a few points in the MDI for an individual child may not be clinically significant, a 4-point downward shift in a normal distribution of MDI scores for a population of children would result in 50% more children scoring below 80. b. Cross-$ectional and Other Studies of Lead Neurotoxicity A great deal of important and useful information on the neurotoxic effects of lead in children has been provided by other epidemiological studies. A detailed and comprehensive evaluation of this body of work may be found in U.S. EPA (1986a), Starting in the early 1970s, several studies were devoted to assessing the relationship between variables such as IQ and blood lead levels IV-13 DUP040009547 little of no effect on IQ as measured in the British studies. But it is also quite possible that IQ tests or other aspects of the design and analysis of these studies are inadequate to detect lead-induced neurological impairments at the relatively low exposure levels involved (Smith, 1985). Other recent studies provide more suggestive evidence that lead exposure at such relatively low levels may in fact be significantly associated with deficits in IQ* For example, Schroeder and Hawk (1987), in replicating earlier work (Schroeder et al., 1985), found a highly significant linear relationship between IQ and blood lead level over a range of 6 to 47 pg/dl in a group of 75 black children. Since these children were all of low socioeconomic status, SIIS was not a confounder in this study+ Studies by Fulton et al. (1987) in Edinburgh, Scotland, and by Hatzakis et al. (1987) in Lavrion, Greece also provide strong evidence of IQ deficits related to children's lead exposure at blood lead levels below 25 pg/dl. Considered .singly* none of the above studies can provide definitive evi dence that low-level lead exposure is linked to reduced cognitive performance in children. However, Needleman (1987) recently reported the results of a meta-analysis of 13 such studies and noted that the joint probability of obtaining the reported results was less than 3 in a billion. Thus, the overall pattern of findings supports the conclusion that low-level lead exposure is related to neurobehavioral dysfunction in children. In addition to the above assessments of the relationship of lead to cognition and behavior, other aspects of lead-associated neurotoxicity have been examined. Burchfiel et al. (1980) examined components of the EEG profiles 'for a subset of children studied by Needleman et al. (1979) and found signif icant differences in EEG activity in the higher dentine-lead group. Otto and his co-workers (Otto et al., 1981; Benignus et al., 1981; Otto et al., 1982, 1985) have also evaluated neurophysiological function in relation to blood lead levels in children. Using various test paradigms, they have found disturbances in features of the EEG that correlate with Pb-B levels. In some cases, these effects appeared to persist for 2 to 5 years. These invest!gators have also reported eiectrophysiological alterations measured throogh auditory brainstem evoked potentials (e.g., Robinson et al., 1985, 1987). In addition, evidence of lead-related reduced hearing acuity has been reported by Robinson et al. (1985), supported by an analysis of audiometric data from NHAHES II for children aged 4 to 19 years (Schwartz and Otto, 1987). The IV-16 DUP040009548 in the superior IQ range (>125). Follow-up investigation of the same children's school performance indicated that, four years later, high-lead children were significantly more likely to have been retained in grade (Bellinger et al.. 1984b). Smith et al. (1983) investigated the relationship between lead levels in teeth and measures of behavior and intelligence in oyer 400 British children, but found that, after correcting for social class, home quality, and other confounding factors, the association between lead and IQ or academic perfor mance was not statistically significant. Tooth-lead levels in these children were significantly below those reported in other industrialized countries. Similar findings were reported by Harvey et al. (1984) for almost 200 British children with low Pb-B levels (mean: 1$, 5 jig/dl): after adjusting for confounding variables such as social class, the association between blood lead and IQ was no longer significant. Social class may have also confounded the positive results of Yule and his colleagues in their studies of British child ren, In their first study, IQ was reduced as a function of increasing blood lead level (Yule et al., 1981), but a better controlled replication study (Lansdown at al., 1986) showed no significant effect of lead on IQ, Other work by Yule add lansdown (1983) and Hunter et al. (1985) showed no significant effect on IQ but did shpw significant effects on reaction time, consistent with findings by Needleman et al. (1979), Similarly, teacher ratings of high-lead children (Pb-B levels: 12 to 26 pg/dl) indicated behavioral impairments in line with the earlier findings of Need!eman et al, (1979). A series of studies in Germany by Winneke et al, (1982, 1983, 1984) par allel the British findings in several respects. Social variables appeared to play an important role in the associations between neurobehavioral function and lead exposure. With mean blood lead levels below 15 pg/dl, IQ scores were not significantly reduced, but reaction time performance and certain other neurobehavioral functions did show significant impairments (Winneke et al.. 1984). Although the British and German studies show few if any significant associations between low-level lead exposure and cognitive function after controlling for social class, the findings are consistent in the direction of their effect and compatible with an overall dose-response relationship, with these studies falling at the low end of the lead-IQ relationship (U.S. EPA, 1986a). It may be, as Pocock et al, (1987) have concluded, that lead has IV-15 DUP040009549 et al., 1982). The geometric mean blood lead level for the mothers was approximately 14 pg/dl and for the Infants was approximately 12 pg/dl. The clearest evidence concerning an effect of lead on birth weight and growth comes from the Cincinnati study. Preliminary analyses by Bprhschein et al. (1987a,c) have indicated that, for approximately every 10-pg/dl incre ment in blood lead, the decrease in birth weight ranged from 58 to 601 grams, depending on the age of the mother. Birth length also appeared to be signifi cantly related to maternal blood lead (-2,5 cm per log unit blood lead), although the effect was evident only in white infants. Other prospective studies are suggestive but less definitive regarding birth weight and fetal growth, Bellinger et a!. (1984) reported data showing an exposure-re1ated trend in the percentage of small-for-gestational age infants in the Boston study, but the differences fell just short of statistical significance at p = 0.05. In Port Pirie, the proportion of low-birth-weight deliveries was more than double that outside Port Pirie (respective maternal blood lead levels: 10.4 vs. 5,5 pg/dl). Yet within both groups, low-birthweight pregnancies were (nonsignificantly) associated with 1ower blood lead levels. Also, regression analyses indicated no evidence of intrauterine growth retardation using "small-for-dates" data. To complicate matters further, head circumference was significantly inversely related tp maternal blood lead, but crown-heel length showed no association with lead exposure. Other findings from the Port Pirie study are pertinent here. Of the 23 miscarriages in this study, all but One occurred fn the more highly exposed Port Pirie mothers. Also, 10 of 11 stillbirths occurred to Port Pirie women. Specifically, the proportion of stillbirths was 17.5/1000 live births in Port Pirie versus 5.8/1000 outside Port Pirie and 8-0/1000 for all of South Australia. Nevertheless, the average maternal blood lead level at delivery was significantly lower for stillbirths (7.9 pg/dl) than for live births (10.4 pg/dl). As noted by Davis and Svendsgaard (1987), these anomalous findings for birth weight and stillbirths in the Port Pirie study suggest the possibility that the fetus and/or placenta was acting as a "sink" for the mother's body burden in such cases. Congenital malformations were also considered in the Port Pirie study, but no significant relationship to lead exposure was found. Unfortunately, too little information was presented on this aspect of the Port Pirie study by McMichael et al, (1986) to judge the strength of their conclusions. Although Ernhart et al. (1986, 1987b) also reported no significant relationship between IV-18 DU P040009550 relationship between Pb-B level and hearing threshold was highly significant (p <0.0001) for the large dataset from NHANES II. As noted by the authors, such impairment of hearing could contribute to other reports of neurobehavioral deficits such as learning disabilities and poor classroom behavior. 3, Other Adverse Effects of Lead on the Health of Young Children Even a cursory review of the myriad effects of lead on children is beyond the scope of this report. For a more comprehensive evaluation, the reader is referred to the Air Quality Criteria Document for Lead (U.S. EPA, 1986a). How ever,, certain recent findings related to child growth and development are summarized here because of their statistical and public health significance. In addition to neurobehayioral endpoints, the prospective studies described above have examined Various outcomes related to fetal and postnatal growth and maturation. In the Port Pirie study, McMichael et al, (1986) enrolled 831 pregnant women and followed 774 of the pregnancies to completion. Multivariate analysis showed that pre-term deliveries (before the 37th week of pregnancy) were significantly related to maternal blood lead at delivery. If late fetal deaths were excluded, the association was even stronger: the relative risk of pre-term delivery at exposure levels of 14 pg/dl or greater was 8.7 times the risk at levels up to 8 pg/dl. The Cincinnati prospective study has also noted an effect of prenatal lead exposure on the duration of gestation. As mentioned above, Dietrich et al. (1986, 1987a,b) found that declines in Bayley scores were mediated in part by reduced gestational age associated with lead exposure. The effect amounted to about a half-week's reduction in gestation for about every 10-pg/dl increment tn blood lead. Note that this effect was detected despite the fact that infants of less than 35 weeks gestational age were excluded from the Cincinnati study. Similarly, the Boston Study (Bellinger et al., 1984) excluded Infants of less than 34 weeks gestational age. As noted by Davis and Svendsgaard (1987) in their review of these findings, such criteria would make it more difficult to detect an effect on duration of gestation. Gestational age was also shown to be significantly reduced as a function of increasing cord or maternal blood lead levels in a well-conducted crosssectional study of 236 mothers and their infants in Glasgow, Scotland (Moore IV-17 DUP040009551 C. D0SE-EFFECT/DOSE-RESPOKSE RELATIONSHIPS FOR PEDIATRIC LEAD EXPOSURE In this section, information from the two previous subsections is inte grated to give a quantitative picture of the relationship between adverse outcomes and Pb-B levels in children. Outcomes are measured as either cate gorical variables or continuous variables, conventionally termed responses and effects, respectively. Thus, one may refer to either dose-t'esponse or doseeffect relationships, depending on whether the outcome is discrete or continuous. Table IV-3 summarizes lowest observed effect levels (LOELs) for a variety of important adverse health effects in children, based on e critical evaluation and interpretation of these findings by U.S. EPA (1986a), with updating. As shown in the table, the severity of effects increases as lead exposure levels increase. However, a constellation of effects, including alterations in neurobehavioral development and electrophysiological function, disturbances in heme biosynthesis, and deficits in growth and maturation, both prenatally and later in childhood, is evident at blood lead levels of 10 to 15 pg/dl, and possibly lower {U.S, EPA, 1986a). Some recent work also suggests that auditory acuity is reduced at these levels as well. At levels still belpw 20 pg/dl, erythrocyte protoporphyrin is elevated, and disturbances in l,25-(QH)2-vitarain D and early signs of impaired erythro poietic pyrimidine metabolism are evident. Cross-sectional studies reveal IQ deficitis at Pb-B levels starting below 25 pg/dl and at progressively higher levels as well, A detailed dose-response relationship in a population of children has been described only for EP elevation. Using probit techniques, Plomelli et al, (1582) have reported the EP dose-response relationship depicted in Figure IV-3. Thisi plot represents response at both 1 and 2 standard deviations as Pb-B rise!s. The impression to be gained from Table IV-3 is that the Pb-B threshold level of 15 to 25 pg/dl is already associated with the onset of a number of early biological changes. This report provides population estimations in various chapters in terms of three Pb-B ceilings: 25 pg/dl (based on CDC, 1985), 20 pg/dl (based on WHO, 1986), and 15 pg/dl (based on U.S. EPA, 1986a). Selecting these particular values for the purposes of this report does not imply that lower levels are safe. IV-20 lead exposure and congenital malformations for the Cleveland study, that study had a comparatively small number of subjects and a limited range of blood lead values, which would have made it difficult to detect an effect of lead if one existed. However, a retrospective study by Needleman et al. (1984) did report an association between cord blood lead and the occurrence of minor malforma tions in 4,354 infants born in Boston. The effect was significant only for minor malformations (e.g., hemangiomas/lymphangiomas, hydroceles, skin tags, papillae* undescended testicles) taken as a whole, not for any single malfor mation. Also, unexpected significant reductions in first trimester bleeding, premature labor, and neonatal respiratory distress were found to be associated with higher prenatal lead exposure* Although no definitive judgment can be reached at this point regarding the possible teratogenic effects of low-level lead exposure as far as congenital malformations are concerned, other effects of lead on fetal development seem more clearcut. As concluded by Davis and Svendsgaard (1987), the weight of available evidence suggests that the duration of gestation is affected by exposure to lead during pregnancy and that such effects can occur at blood lead levels below 15 pg/dl. In addition, birth weight and possibly other aspects of fetal growth appear to be reduced by prenatal lead exposure levels of less than 15 pg/dl. Recent analyses also suggest that delays in developmental milestones (e.g., age of first sitting up, walking, or speaking) are related to PbHJ levels in children (Schwartz pnd Ottg, 1987). Later growth also appears to be affected by lead exposure postnatally. Schwartz et al. (1986) have recently reported that an analysis of the NHANES II dataset revealed significant relationships between Pb-B levels and height (p <0,0001), weight (p <0,001), and chest circumference (p <0.026) in young children (<7 years old). These growth milestones were inversely related to Pb-fi levels over the range of 5 to 35 pg/dl. Work in Belgium by Lauwers et al. (1986) also points to a relationship between children's lead exposure and dis turbances in physical growth up to about 8 years of age. Although a number of potentially confounding variables were considered in these studies, a more definitive epidemiologic design would be a prospective study. Preliminary analyses of data for 260 infants from the Cincinnati prospective lead study (Shukla et al., 1987) in fact indicate that covariate-adjusted growth rates are significantly related to postnatal increases in blood lead levels. This relationship was only evident in infants whose mothers had Pb-B levels of ~8 pg/dl or higher. IV-19 D UP040009553 Figure IV-3. Dose-response for evaluation of EP as a function of blood lead level using probit analysis. Geometric mean plus 1 S.D. 33 jug/di; geometric mean plus 2 S.D, 53 Mfl/dl. Source: Piomelii at al. (1982). (3) If lead-associated effects Induced in childhood resolve themselves beyond childhood, what evidence remains that there are no deficits in overall development associated with these effects? For example, even if IQ decre ments are present only in early childhood, what other more permanent deficits may be acquired in terms of emotional development, social inter* actions, and other facets of human development? (4) Might one have to reconcile de facto meanings for the inherent reversibil ity or irreversibility of certain effects? As noted earlier, even in the face of biological reversibility there may be socioeconomic irrevers ibility of lead exposure and hence potential adverse health effects. In addition, there may be persistence of internal lead exposure well beyond early childhood in Individuals burdened by bone lead accumulations that are later released into other compartments of the body. IV-22 DUP040009554 TABLE IV-3, LOWEST OBSERVABLE EFFECT LEVEL (Pb-B) FOR EFFECTS IN CHILDREN Lowest Effect Pb-B (pg/dl) 10-15 (prenatal & postnatal) Neurological Effects Deficits in neurobehavioral develop ment (Bayley and McCarthy Scales); electrophysiological changes Heme Synthesis Effects ALA-D inhibition Other Effects Reduced gesta tional age and weight at birth; reduced size up to age 7-8 years 15-20 EP elevation Impaired vitamin D metabolism; Py-5-N inhibi tion <25 Lower IQ, slower reaction time (studied crosssectional ly) 30 Slowed nerve conduc tion velocity 40 Reduced hemo globin; elevated CP and ALA-U 70 Peripheral neuro Frank anemia pathies 80-100 Encephalopathy Colic, other GI effects; kidney effects aA<Japt@d from U.5. EPA (1986a), with updating. D. PERSISTENCE OF ADVERSE HEALTH EFFECTS FROM LEAD EXPOSURE IN YOUNG CHILDREN For this topic, these questions should he considered: (1) What is the time frame to be defined under the term persistent? Does it include only childhood or the entire life span? (2) Are the persistent effects to be compared with societal or clinical values and judgments that encompass optimal psychological and physical well-being, or simply the absence of overt disease? IV-21 DUP040009555 & Io 3 > 1 >i to m 9*0 to"J2 W we 9 IV .9 *r w * 9< . 6 44 44 9 to 9 S-g ill X> V **- < * to 9 gX * > 4* t t- & . fc-oSg. toSgV OV ft. 4^ s M fit.,t4o4 VI 44 ft4- lux ft n CVV .O ft44 is a i- 4* oS Oft 961 gvi --ma -c 9 i&i at *il* i5 v M .<*- IV 1 9 + ** +* *4 I E 9 !> - 6 -* * 9 -p- *. S & '9 44 .44 9 4 M il M, II U*f8>t. |&- 5 i2Sfftt.f13f!t gSe >>U to I9 51|aS41i :o * tT B fr >9 *o 9 9 4ft- x5 ft. v 22 0*1* e si * EV v- > IV ** ft*4 C VI U 9 ftJg * gE VI 9 II > *4 . 44 * >*- u i e 1 ft. o. ft. o :v>k o .e ft. t. a. _ S*O *fOt.. 4L- f*t.- c 4* en^c e isi o *!**'.' (I B . 0 44.il 52 09 30 p. .9 44 i-- t". . ;.0i. O U >p<- u c<M'i o4- v>i 44 ftn. oft. Wtn ML >VI VcI fIVt oftrtf) *o w fc. IV 9^ WO9 .? ft lftfi.3 g *-- 44 i- j|| IA ,9 0 O fc5 _ : B i*r O 9 ft. I o fSetl*t' .XS * to . 44 e8 5i # * n 9 TJ S' Og si mo. ssssai^s 41ft. to.44 44=4 44 *4 ft.*;-- v> in M ft "to > ** 9 * 9 9 ft- x: X 3 go X 5oS 9 0 +4 I O^.ftot 9 44 ft. ftf.i STS g S o ->*9 & M-C V M -- IV '9 SI L -U to * *. sV;I *:tQ tt44ss a..."g-oixf 9 to -- 4 4* .B mm +> V) o si c e ES5ft P- I 44 to . AUk 2t * ft XO .9' 9 VI . ft >*9 9 s .S1 C*9i 9 .9 V .ft us " Scf ft. o*c ScJ 1- -- 44 95 V 9O 9 tf> >k 4 B 9O 99 Z&2 9 M .fOt X 9 S. X9 * 5 *EH j z 444" ^-S *g .44 Ulft y' -ft v 99 ft -C ui 9 BO O Ui 9 a v I 1 4 >| p u in X-*4 & .** oM 9 .4* sfB 2 $ St44 ft. O & I ?8 e.M p--1 IV ** M.9 & K 44 M 4 IV t**b 9 5 esc i o5 o-X 9 * IV-24 ? p r* (A f DUP040009556 It is generally considered that lead-induced lesions of the central nervous system are largely irreversible (American Academy of Pediatrics, 1987), table IV-4 tabulates various lead-induced effects due to prenatal or postnatal exposure, with comments about the persistence of such effects. These assess ments spring from both cross-sectional and prospective epidemiologic studies, and provide multiple indications of persisting, long-term health effects in children. However, firm conclusions about the persistence and ultimate impact Of such effects are difficult to state at present because of the limited time Spans over which children have thus far been studied. A more definitive assessment of the persistence issue will require the continuing examination of children in prospective studies. As noted by Grant and Davis (1987), ontogeny is characterized both by its plasticity and by its sequential dependency. Developing organisms may be able to compensate for certain deficiencies, if they occur early enough in the maturation of the individual. For example, children often show catch-up growth spurts. Thus, it is possible that early developmental lags, particularly those that are somewhat subtle, could "disappear" at later ages. But it is also important tp note that, even if a lead-induced lag in cognitive or physical development were no longer detectable liter (which depends very much on the sensitivity of available measurement methods), this would not necessarily imply that the earlier impairment was without consequence. Research in developmental and physiological psychology has clearly shown that the actualization of beha vioral capabilities requires appropriate periods of functional neural activity for proper development. Thus, even transient or, in themselves, reversible deficits during parly development may hake potentially serious and long-lasting sequelae. Moreover, secondary effects of early developmental perturbations need not be strictly sequential. Given the complex interactions that figure into the psychosocial development of children, attempts to compensate for lead-induced deficits in one area of a child's development may affect other areas of development. Of particular relevance to the question of persisting effects of lead on neurobeihavioral function is a large body of experimental animal research that demonstrates deficits in various aspects of behavior for several years after experimentally controlled lead exposure has been terminated. These effects have been reliably and consistently found in nonhuman primates as well as other species. Discussion of these studies is beyond the scope of this report; IV-23 DUP040009557 This hierarchical array of types of exposure assessment is illustrated in Table Vt-X for lead in drinking water. In Section F of this chapter, estimates are given forj (1) number of children in an environment likely to have poten tial exposure to elevated levels of lead in water; (2) number of children who will have some degree of actual exposure due to elevated lead levels in waiter, but exposures not necessarily high enough to produce lead poisoning. Finally, (3) number of children who have varying elevated lead exposures (Pb-B elevations) to lead levels in water above the proposed maximum contaminant level (MCL) of 20 pg/dl. 2. Relationships of External to Internal Lead Exposure on a Total Population Before applying any biological indicator for lead (such as Pb-B) to population surveys or to categorize risk, its quantitative dimensions-- especially the distribution of Pb-B levels among that population--must be understood. Populations show a range of responses, including a range of Pb-B levels, rather than a single uniform response to lead exposure. This vari ability of responses occurs because individuals within a population react in different ways to the same exposure* because of host factors. Also, the Inherent nature of toxicant distribution, as affected by toxic cellular or organ responses, can internally increase toxicant levels enough to affect their distribution, which is called dose-dependent distribution. In humans, Pb-B values are distributed in a log-normal rather than a normal manner. A log-normal distribution, unlike a normal distribution, is skewed and not symmetrically bell-shaped. One consequence of this skewing, which i$ crucial to public health* is that the segment with highest blood lead levels, the upper tail of this distribution, includes a larger fraction of the entire population than it would in a normal distribution. The actual fraction of these Individuals in a given population can be defined by the geometric standard deviation (GSD) and the geometric mean (GM). Risk assessors or risk managers consider this segment when defining some desirable cut-off value in a cumulative frequency to protect a risk population at some selected exposure level, such as some specified Pb-B level. From the GSD, percentages of populations at risk can be calculated as well as the mean or median population lead burden, which is required for the VI-3 DUP040009560 Source Category Lead in drink ing water 6. Lead in food TABLE VI-1, (continued) Level of Precision Method of Exposure Measurement Actual exposure Summation of corresponding actual exposure numbers from first three actual exposure categories, or use of multimedia regres sion equations (not possible with present data) Potential exposure Numbers of young chiIdren in homes with either old lead plumbing or with lead solder in new home Actual exposure that is measurable but not highest toxicity risk Numbers of young children in homes with lead levels in drinking water above 20 pg/1 Actual exposure at or near toxic levels Number of children esti mated from NHANES II prevalences of projected toxic Pb-B levels Potential exposure at or near toxic levels Number of U.S. children within selected age group Actual exposure Fraction of those poten tially exposed children whose food lead intake may raise Pb-B high enough to cause concern next step in establishing regulations. The maximum amount of lead that regulators permit in a lead Source without exceeding these mean or median values can also be computed. These regulated levels usually correspond to the amount of anthropogenic activity, such as emissions from industry and auto exhaust. If, by using these calculations, it is determined that, for example, 9956 of the U.S, population lies below a specific Pb-B ceiling level, about 2.4 million individuals would still be considered to have an unacceptable level of toxicity risk. These observations are relevant for lead sources that are ubiquitous in the United States, but which show "moderate" concentrations when given as the VI-S DUP0400095S8 average Pb-B resulting from a specific source. The propensity to assess the extent of the lead problem with these averages can be misleading. Because lower averages apparently would suggest a lower public health risk, they can result in misleading interpretations when studying inherently serious effects or when there are tens to hundreds of millions in the population being discussed. The reasons for why this is so follow from the discussion below. Figure VI-1 illustrates a hypothetical blood lead distribution for a human population. The quantitative usefulness of such a figure can be seen in the 1986 Draft Report of the World Health Organization for air quality guideline recommendations in the European community (WHO, 1936). In developing guide- , lines for lead levels in air for Europe, the WHO Working Group for lead took several approaches; one approach determined the following parameters. (1) Based on available evidence at the time (September 1984), the group determined that a Pb-B level of 20 pg/dl was the exposure level of action (WHO, 1986). (2) The group also determined that this Pb-B 20 pg/dl value was to be prevented in 98% of the European community populations. (3) Because only data on adults were available, the requisite GH and GSD data were employed to determine that a 98% cumulative frequency for a 20 pg/dl Pb-B level required a median Pb-8 value ct 10,5 pg/dl in adult popula tions. In other words, for the Pb-B level in 98% of an adult population to remain below 20 pg/dl, that population requires a median Pb-B level of 10.5 pg/dl. These three parameters are depicted in Figure VI-1, The shaded area represents subjects in the remaining 2% of the distribution above the level of 20 pg/dl. If we were to apply this approach to the U.S. population, we would first determine--using the lowest of the three projection formulae of the U.S, Census Bureau--that the 1985 projected adult population is 175 million. If we also allow 98% to have levels below 20 pg/dl, with a 10.5 pg/dl median, the remain ing 2% still gives 3.5 million individuals at some risk of lead toxicity. If we expand the protection (cumulative frequency) band to 99,5% and/or reduce the acceptable Pb-B level to 15 pg/dl or less, then this median will be considerably below 10.5 pg/dl. VI-6 DUP040009559 TABLE VI-1. CATEGORIES QF ESTIMATION METHODS FDR CHILDREN EXPOSED TO LEAD BY SOURCE Source Category Level of Precision Method of Exposure Measurement 1. Lead in paint Potential exposure Determination of numbers of children in housing / with highest likely leadpaint burdens; complements Chapter V data Potential exposure with a better indica tion of actual expo sure risk Number of children esti- mated to be in deteri orated housing with leaded paint: peeling paint, broken plaster, other damage ;s Likely actual exposure Use of a specifically determined prevalence fpr an NHANES II stratum matching such children; other, regional survey data 2. Lead in gasoline Potent1al exposure (Pb-B changes) in a subset of U.S. urban child population Total number of young children in the 100 largest U.S. cities Actual exposures based Logistic regression on leaded gasoline analysis to estimate combustion numbers of children below selected Pb-B \ criterion values 3. Lead from sta tionary sources Potential exposure Total of young children in communities near lead operations Actual exposure Prevalence of indicated Pb-B levels, at or above some criterion level in actual field studies of . stationary sources 4. Lead in dusts and soils Potential exposure Summation of potential exposure numbers from the above three categories (continued on following page) VI-4 DUP040009561 VI. EXAMINATION OF NUMBERS OF LEAD-EXPOSED U.S. CHILDREN BY LEAD SOURCE A. GENERAL ISSUES Three general points need to be discussed before source-specific chi1dhood lead exposure can be addressed. First, "exposure" must be defined according to the available data and the intent of the Congressional directive. Second, a relationship must be established between the lead source and the exposure population to assess the biological diversity of human population response. Third, behavioral characteristics and other covariates influencing the degree to which exposure to lead in the external environment results in internal (systemic) exposure must be studied. 1, The Level of Exposure Risk in Human Populations Characterized and Quantified by Lead Source Source-specific exposures are difficult to delineate because of multimedia exposures to lead. When exposures come from several sources, how should they be ranked? For example, children exposed to lead in paint (by either direct chewing or swallowing paint chips) often simultaneously contact dust from chalked or weathered paint. Therefore, one source of lead may be the dominant but not the sole source. For rural or suburban adults, food or water can be a major source of lead. It is difficult to quantify exposure once the important sources have been determined. Section 118(f) places no statutory restraints on defining exposure and estimating the number of children exposed. As noted in Chapter II, human exposure can be indexed either by external or internal means--that is, environmental or biological monitoring. General environmental monitoring can estimate external exposure in the population. However, these estimates are very broad because they estimate the number of subjects at the lead source, regardless of the level of Contact with VI-1 DUP040009562 the source. Although these estimates produce the largest numbers, they are the least accurate when associating exposure with the actual risk of toxicity. For example, when leaded paint exposure is estimated in this way,, houses containing lead paint are counted and the number of children from the U.S. Census count is distributed proportionally among them. A more accurate exposure assessment can be achieved if individuals are exposed only to a source containing lead levels exceeding that needed to-' elevate Pb-B levels. This estimate is determined by some empirical relation ship* usually through use of regression equations. Lead levels in all old leaded paint are high enough for this estimate; so are lead levels in some dust and soil contaminated from lead fallout in air or weathering paint (U.S. EPA, 1986a). Blood lead from water and food can also be assessed using this method. The most accurate way to assess exposure for source-specific lead is to study elevations in a biological indicator. For example, determining if elevated Pb-B levels can be traced to the intake or uptake of source-specific lead. Reliable information is needed when using biological monitoring to esti mate lead-exposed populations by source. This reliable information requires som means of apportioning a given Pb-B level among input sources. When available, this information would be invaluable in reporting the true scope of source-based lead poisoning in the United States. In view of this, we need to discuss the relationship Of Pb-B level to sources In more detail. The levels of precision in assessing population exposures by lead source are given in Table VI-1. This table summarizes the type of exposure analysis needed for each level of precision within a given source category. From the table, one can determine the approximate exposure level associated with each type of estimation. Those children estimated to be exposed internally (in vivo, systemically) at unacceptable levels of Pb-B are of greatest concern. Those children estimated to have a measurable increase in systemic exposure, i.e,, elevated Pb-B levels, but who have not been characterized by risk level for adverse effects achieved by the increase are of second greatest concern. Finally, those children estimated to be in an external lead environment and who risk internal contact with thetoxicant, although no data indicating systemic uptake exist, are the third concern. Children with potential exposure are at higher risk than children ip environments with no lead. VI-2 DUP040009563 have an impact on Pb-B levels and their prevalences in the general child popula tion, and this point is established in Chapter VI. At present, the third national survey of its type, NHANES III, is in the planning stage, and eventually results of this survey (expected in the mid1990s) will produce more precise numbers for prevalences of Pb-B levels in strata used in NHANES II and in this report. In the interim, the 1990 U.S. Census will also be conducted. For the present* however, the estimates and U.S. Census counts of children in Chapter V are the best that can be done with the available data. y-51 DUP040009564 Equally, we do not know the consequences of such paint removals in terms of increasing the raw lead content of the sites' dusts and soils within reach of these young children. Another factor to consider when examining the significance of housing age is the presence of lead in plumbing and the potential contamination of the drinking water. Older housing stay contain leadplumbing, and the most recent stock may contain lead in the solder used for copper piping. In either case, lead may leach into the drinking Water, which is discussed more fully in Chapter VI. The environment in which young children are housed, which depends on the income of young families at the start of the family phase of the life cycle as well as the availability of housing units of different ages, exposes a Targe proportion of young children regard ess of family income to the older housing stock that in turn is likely to contain the paint with the highest lead content. The ubiquity of Pb-B leve S representing health risks found by the NHANES II survey is supported by th s finding that young children frequently live in the type of housing most lik ely to contain sources of lead: in paint. drinking water, and dust/soil. Finally, one significant but qften unrecognized point about childhood exposure! sources such as leaded paint deserves emphasis. Until leaded paint and contaminated dust and soil are removed from young children's environment, the number of young children at risk for adverse health effects will accumulate over time and continue to present a serious public health problem since each new cohort of children will in turn be exposed tp lead in the environment. In other words, the cumulative tally of exposed children becomes much larger as time passes than the specific county given at one point in time. This is due to both the high mobility within the high leaded paint zones in which the high-risk families live and the sociological fact that poof families may be "locked*1 into such housing for many years. 5, Conclusions and Overview This report represents the first systematic effort to quantify the extent of the U.S. child lead-poisoning problem and to place such numbers in some context of distribution of the children, the lead sources, the adverse health responses, and strategies for lead reduction or removal. This chapter is a key V-49 DUP040009565 component of this effort and is important both for the numbers provided and for helping answer the obvious questions "Which children have the problem?" and "What can we start to do about it?" From the key findings of Chapter V, we conclude that the total number of U.S. children exposed to lead at unacceptable levels (Pb-B >15 pg/dl), 2.4 million SMSA children or 17% of the SMSA child total, arise from many different socioeconomic and demographic strata. It was to be expected that the "traditional* high-risk groups, e.g,, poor, inner-city black children, would have figured prominently in the estimation outcomes, and they do. These high-risk groups are usually defined a$ such jin terns of high prevalence rates of elevated Pb-B levels. Less well understood, perhaps, is the fact that the totals for exposed strata in this chapter are derived from both a prevalence for a given Pb-B and the base population by which the prevalence fraction is multiplied to give a stratum final total. The consequences of an estimating exercise, across strata, for exposure totals is singly that large numbers in a stratum's base population can have quite low prevalences for certain Pb-B levels and still yield numbers that are comparable to those obtained from high-risk strata that have smaller base populations of children but quite high prevalences of elevated Pb-B levels. In Chapter V, a variety of estimating strategies were employed, and provide quite different numbers for exposure estimates. These differences were explained earlier in the summary. Furthermore, some of the totals complement each other, providing different views of the same total population of U.S. children* For example, examining the very detailed U.S. Census Bureau counts {not estimates) of children in the 318 SMSAs reported in terms of housing age and family income (Section it) produces the unexpected finding that more children in older housing (high paint-lead levels) were also in noncentralcity, nonpoverty families than were children associated with the typical risk groups. This observation corresponds to this report's projected Pb-B distribu tions in the nation's children. These distributions in high-risk housing might account for why certain Pb-B prevalences in the otherwise lower-risk strata of U.S. SMSA children are as high as they are* In other words, distribution of the nation's children into high lead-exposure risk bousing is uniform enough that all strata of such children, when examined by means of a national composite survey such as NHANES II, will produce significant prevalences. Clearly, however, other sources also i V-50 DUP040009566 and other surveys. Screenings are not always intensive, for example, houseto-house; in most cases, they are conducted in clinics. Any factor that affects the characteristics of clinic visits also affects Pb-B prevalences. For example, the mothers who bring children to clinics may be more concerned, informed, and motivated than those who do not bring their children. Finally, communities with the highest prevalences may not have unique situations. Their approach to the problem simply may be more systematic than in other communities, and therefore, they report the highest rates. The more appropriate question may well be why all communities do not have higher rates rather than why certain communities have high rates. This type of question,' cannot be answered unless the screening programs are again centrally administered. 4. Children With Potential Exposure to Leaded Paint in the SMSAs This section summarizes an attempt to identify potential lead exposure by each $MSA and by a specific source, leaded paint. It therefore combines approaches dealing with source-specific exposure described earlier in Chapter V and those in Chapter VI. The number of children living in pre-1950 housing was obtained from the actual 1980 Census enumeration. Table V-20 and Appendix D present the ranking of SHSAs by the number of children in pre-1950 housing and show that young children are least often found in the newest housing, built in 1970-1980, This is probably due to the fact that young families are least able to afford newer housing and particularly newer units inside central cities. While children in families with the lowest incomes were found disproportionately in the older housing, large proportions of children in the highest income families were also found living in the oldest housing stock. Furthermore, the children with family Incomes above the poverty levels frequently constituted the largest proportion in the oldest housing. While there is no perfect correlation between the age of the housing and the presence of a leaded paint hazard* note that weathering and chalking occur even when there is no dilapidation or deterioration of the housing. We do not know how many pre-1950 housing units have been renovated or had high leadcontent paint removed, but we can say with some confidence that the fraction is quite low, given data for Massachusetts cities described in Chapter IX. V-48 DUP040009568 exposure cases was .1.5%. In terms of numbers, more children appear to be screened at present, although statistical comparisons with the older CDC framework would be difficult. Toxicity responses for 1985-1986 ranged from 0.3% for four programs to 11.0% for the City of St. Louis program. The five highest prevalences are 11.0% (St. Louis), 9.0% (Augusta and Savannah, GA), 4.9% (Harrisburg, PA), 3.5% (Washington, DC) and 3.5% (Merrimac Valley, MA, a program within a MCH pro ject). Most of the rates for confirmed toxicity cases were below 2%. Prevalences reported for earlier years include those from state agencies, as summarized by the Public Health Foundation. For FY 1983, reporting agencies screened 675,571 children and recorded a prevalence of 1.5%. Similarly, the CDC data for FY 1981 indicated that 535,730 children were screened, with 21,897 meeting the toxicity risk criteria then in use--a prevalence of about 4%. For the reasons noted above, we cannot closely compare these three sets of results. Trends in prevalences over time, at least in the years under CDC control, suggest a moderate decline in toxicity risk from 1973 on. Data from two programs for 1973 to 1985, and data from the St. Louis, M0, program show downward shifts, even with changes in risk classifications. With the 1985 change in the CDC toxicity risk classifications, we might expect the number of toxicity risk positive results to increase, and the New York City screening program results show such an increase. In future years, then, the prevalences will reflect this change in classification, but they will also reflect the impact of reduced levels of lead in gasoline and food. 3, Comparison of Prevalences Found in NHANES II Updated Prevalences and U.S. Screening Programs Because the NHANES II prevalences, and therefore the updated adjusted rates, are based on Pb-B determinations for the subjects, there is consequently no intervening problem of first determining EPs. These rates are not subject to systematic underreporting due to false negative results found when EP deter minations are used to classify the initial population group being evaluated and identify who will then be tested for Pb-B levels. Screening programs, however, test for EP first. Other factors in screening programs probably produce lower prevalences com pared with those that can be predicted on the basis of results from NHANES II V-47 DUP040009567 economic recession occurred in the intervening years, and poverty is associated with higher prevalence of higher Pb-B levels. Applying prevalences at indicated Pb-B criterion values involved using the relevant original NHANES II data base in tandem with a projection process to establish prevalences for 1984. The projections use the original data set, which consists of actual measurements obtained during 1976-1980, the field phase,' of the survey. Projections were made via logistic regression analysis and were employed to update prevalences for Pb-B levels of 15, 20, and 25:pg/dl. The reasons for selecting these Pb-B values are discussed in Chapter IV and the pro- " _ 14 bleiD of over- and underestimates was discussed in the first section of Chapter V. : Projection of the NHANES II prevalences to 1984 is tlie principal phase of the process that includes the element of uncertainty always associated with any estimation process. Given the universally recognized high quality of the design and execution of the NHANES II survey and the relatively good reliabil ity of logistic regression analyses, the results presented in Section A of this chapter are reasonable. We employed U.S. Census data base populations within strata and the pro jected Pb-B prevalences to estimate the number of children with Pb-B above selected levels at various levels of geographic differentiation. Early efforts were made to estimate the number of exposed children in each of the 318 SMSAs. Such an approach subsequently was judged to contain too much uncertainty and was abandoned. Next, an attempt was made to derive projected prevalences for each of the four major U.S. regions identified and employed in the NHANES II survey, and to combine the rates with the stratified SMSA populations in each of the four regions. Generating satisfactory projections at the regional level was not possible for several reasons. We therefore calculated the numbers of white and black children as a function of Pb-B levels and the nationwide total population of the SMSAs. These Stratified exposure estimates appear in Tables V-4, V-5, V-6, V-7, and V-8. The estimates presented in Tables V-4 through V-8 show that criterion Pb-B levels representing health risks are found in all child population segments, not only in the target populations usually defined by the screening programs as being at risk. These target populations constitute a large component of the population at risk, but they do not, by any means, constitute that entire population. V-45 DUP040009569 The large projected numbers of children at risk among those with suburban and other "Not Inside Central City" residences are shown in Table V-5 and V-S, The prevalences for these children are lower than those for "Inside Central City" children, but this is countered by the finding that more children live in the suburbs in most, though not all, SHSAs. Hence, the estimates reflect both of these key factors* Table V-8 shows the overall dimensions of the problem among the SMSAxhild population, as well as the distribution by "Inside Central City" and other residence when available. About 13,840,000 young black and white children lived in all SMSAs in 1984, and 2,381,000, or about 17% were estimated to h|ve Pb-B levels above 15 pg/d, reasonable estimates for white and black children living in SHSAs in 1984. Furthermore, when balancing the specific factors leading to overestimations and undjarestimatipns discussed before, these esti mates for white and black children ift SHSAs should be considered as the best estimates that can be made based on available scientific data. 2. Numbers of Lead-Exposed Children Detected by Screening Programs Over the years, lead-exposure screening efforts and the factors related to them have varied considerably. These factors include defining the risk of toxicity, administrative organization, and amount of funding. When CDG administered the screening programs, there were more than 60 active programs with an established and fairly rigid reporting protocol. At present, there are about 40-45; but the exact number is difficult to identify since only states report and reporting is voluntary. Programs now are sup ported by state-based block grants controlled by state agencies, and Only states submit screening results rather than each program as was done under CPC admin istration. The state agencies should be commended for these efforts, but the numbers being reported may be less representative of the exposure problem than were obtained under central CDC control and with uniform criteria. These changes have made it difficult to estimate time trends, determine prevalences, and compare current prevalences with those obtained under prior, CDC-administered programs. for the mpst recent level of screening activity, the results of ATSDR's December 1986 survey of existing programs show that for 1985, 785,285 children were screened in 40 or more programs and that the overall rate of elevated V-46 DUP040009570 TABLE y-21, CINCINNATI, OHIO-RENWCKY SMSA 19BD CENSUS COUNTT)F CHILDREN OF ALL RACES 0.5-5 YEARS OLD BYFAMILY INCOME, URBAN STATUS, AND AGE OF HOUSING <0 P o h- o CO 05 H 1 o rv ov rH o> p VO ii- tz cr> : J H uu 1 o ;-01 in 1i r*H O m 05 H 4i1 SQ. P's. fO O ^ CM CM -<* O O O H H CO lO co fn* CO H *#* O O O H CM 05 05 tn f*. 10 CO CM CO O O O |H %CO 05 10* H *? eo csj -- m O O O rH NCOH fv 05 CO H f>. 0 0 0 H J*. CM H 5 * r-l CO 0 0 0H r>. co CD r-r<t- tu>s O O O rl co de* CO CM 05 com P O O H O 05 H .* a mom H CM m 0 0 0rH VO CM CM HN O O O H 05 CO 05 in co m H H VO O1 O ! O ;j H1 P8 .* cb m rH CM m O O O H "<5 ; P. o H- O CO o ; ' i o K c 05 a) H u ~a r* 8 05 i lO CJ 05 rH H-- 1 l QO m s- 05 rH jO ' j 3E 2O m 05 HI .4S ]! A. 000 000 co m co 05 co m rH .O O VD CO CO OOO OOO CO co .0 H 0 0 rH CM OOO OOO co ^ m 0" co XT t O O CM CM H OOO OOO CM*C.O*CO* *< O H O O co 05 H 000 000 0 vo co r*s K m H VD O O 9* H 05 000 000 05 rs vo H -o* vo CM O O CM CO m OOO OOO 05 05 Hf c m < in CM 0 0 CM m CO OOO OOO CM,*0CO CM 00 ^S* H O O O m CM OOO 000 CO*1 rH* VO.* vb VO CM H CSJ CO 0; 0, 0 in .CM 1 H' OOO OOO NOW CMmt^ CM O O CO t m CO OOO OOO CM CO 05 H CO 05 CM 0. -O9* ; ms1 -*r OOO OOO *t CO H m cMm H CM 0I 0 CO *# 1 >J P P *r" r- O O -r-- <0 t1,0 05 05 t. r-- .p 05 05 r-- P 05 ' P <0 -C 05 to 05 <0 1 C P OX > P C *P OJ O O0 rH O f- -' C* HO O VO ' rH O HP 1 Ol O 4> O l O 1/5 OIO ,<tt OOO T3 O OO 000 P TO 00 r OO * OO r <0 r- **0 in iA 0 in <0 *0 m s.. in ID >rl P c V* VO ** P3 VO -H ^ UD * P VO *H O. ** 8 q v* 1 in 1 V HA- AB O V AH H V ** AS V-43 DUP040009571 Tables showing the relationship of family income and housing age for the children showed, first of all and not surprisingly, that children in the highest income group constitute the majority of the children in the SMSAs. Consequently, these children frequently are a large portion of residents in each of the three ages of housing categories (Table V-21, Complete sets in Appendices A, B, and C). Exceptions are SMSAs of more recent growth where such children tend to live in the suburban areas and are found relatively infrequently in recently constructed housing in the central city. In the other SMSAs, children tend to be distributed more in relation to their proportions in the child population. Table V-21 is a detailed illustrative compilation for housing age and family income in the SMSA for Cincinnati, OH-KY. The tables in Appendices A, B, and C show the distribution of the three income levels in the column "Percent-Total" and the rows labeled "Total SMSA" for the larger SMSAs and the single set of rows for the smaller SMSAs. We found that while the children from the highest income population lived dispro portionately more frequently in the newest and newer housing, they still represent a significant portion of the residents in the oldest housing as well. D. SUMMARY AND OVERVIEW Discussion of Sections A, B, and C and a summary are presented here. Given the diverse topics, each section is first discussed separately. 1. Lead-Exposed Children in SMSAs Every effort was made to establish accurate numbers for the population bases used to project the numbers of children exposed to lead levels described in Chapter V, Section A. The number of children in each SMSA constituting the base populations, for which the strata were isolated and to which the prevalences were applied, consist of actual U.S. Census counts and counts based on legal documents, i.e., birth and infant death certificates. In these enumerations, the only sources of variation for our purposes were the rounding off to the nearest hundred and applying population strata distributions four years earlier than 1984. These two factors would have minimal impact on the accuracy of Compiling the base population. The time discrepancy results in a conservative outcome since an V-44 DUP040009572 TABLE V-20, (continued) Rank SMSA Children 0.5-5 Years Number in Percent pre-1950 of total housing in SMSA Total Number in SMSA 240 Texarkana, TX-Texarkana, AR 241 Asheville, NC 242 Longview-Marshal1, TX 243 Fayetteville, NC 244 Lafayette, LA 245 Lafayette-West Lafayette, IN 246 Lynchburg, VA 247 Wilmington, NC 248 Daytona Beach, FL 245) West Palm Beach- Boca Raton, FL 250 Medford, OR 251 Fayettevi11e-Springdale, AR 252 R:ichi and-Kennewi ck-Pasco, WA 253 Burlington, VT 254 Yuba City, CA 2515 Florence, AL 255 Rock Hill, SC 257 Hickory, NC 258 Monroe, LA 253 Chico, CA 260 Bradenton, Ft 261 Petersburg-Colonial Heights- Hopewell, VA .262 Athens, GA 263 Newport News-Hampton, VA 264 Las Vegas, NV 265 Tallahassee, FL 266 Melbourne-Titusvi11e- Cocoa, FL 267 Albany, GA 268 Tuscaloosa, AL 269 Reno, NV 270 Ocala, FL 271 Olympia, WA 272 Anchorage, AK 273 Redding, CA 274 Gainesville, FL 275 Fort Collins, CO 276 Clarksvi11e-Hopkinsvi lie, TN-KY 277 Odessa, TX 278 Florence, SC 279 Jacksonville, NC 2,400 2,400 2,400 2,400 2,300 2,200 2,200 2,200 2,200 2,200 2,100 2,100 2,100 2,000 2,000 2,000 1,900 1,900 1,900 1,800 1,700 1,700 1,700 1,700 1,700 1,600 1,600 1,500 1,500 1,500 1,400 1,400 1,400 1,300 1,300 1,300 1,300 1,200 1,000 1,000 21.8 20.0 15.7 8.5 14.0 24.4 20.8 17.3 13.8 6.5 16.4 13.5 12.7 20.8 18.5 16.9 24.7 18.6 14.6 17.3 17.9 15.7 15,6 9.8 4.3 11.0 9.2 12.7 11.4 11.3 16.9 13.0 7.0 12.4 11.1 9.5 9.1 9.9 9.7 8.5 11,000 12,000 15,300 28,30f 16,400 9,000 10,600 12,700 15,900 35,600 , 12,800 15,500 16,500 9,600 10,800 11,800 7,700 10,200 13,400 10,400 9,500 10,800 10,900 17,400 40,000 14,500 17,300 11,80.0 13,000 13,300 8,3.00 10,800 20,100 10,500 11,700 13,700 14,300 12,100 10,300 11,800 (continued on following page) V-41 DUP040009573 TABLE V-20. (continued) Rank SMSA Children 0.5-5 Years Number in Percent pre-1950 of total housing in SMSA Total Number in SMSA 280 Chariottesvilie, VA 281 Fort Myers-Cape Coral, FL 282 Columbia, MO 283 Sarasota, FL 284 Pascagouia-Moss Point, MS 900 13.8 6,500 800 5.7 i4,ior 600 6.7 8,900 400 4.3 9,300 400 3.1 12,900 COMBINED SMSAs 285 El Paso, TX A Las Cruces, NM 286 Greensboro-Winston-Salem- High Point A Burlington, NC 10,300 7,400 287 Fitchburg-Leominster A Pittsfield, MA 288 Bangor A Lewiston-Auburn, ME 289 Bristol & Meriden, CT 290 Bismarck, NO A Grand Forks, MN 291 Dubuque & Iowa City, IA 292 Lawton & Enid, OK 293 Laredo & Victoria, TX 294 La Crosse, VII A Rochester, MN 295 Little Rock A Pine Bluff, AR 296 Bloomington, IN A Owensboro, KY 297 Casper, WY A Great Falls, MT 298 Midland A San Angelo, TX 299 Topeka A Lawrence, KS 300 Bryan-Coliege Station A Sherman-Denison, TX 301 Ft. Walton Beach A Panama City, FL 6,400 6,300 5,400 5,100 5,000 4,600 4,000 3,900 3,700 3,700 3,500 2,900 2,800 2,400 2,000 TOTAL 4,374,600 15.4 19.7 49.6 54.3 46.2 25.6 36.0 25.1 18.6 25.3 25.2 23.6 20.5 18.2 20.3 17.1 9.6 30.6 66,800 37,500 12,900 11,600 11,700 19,900 13,900 18,300 21,500 15,400 14,700 15,700 17,100 15,900 13,800 14,000 20,800 14,278,900 Thirty-three SMSAs and one paired SMSA showed 50% or more of all children living in pre-1950 housing units, with Jersey City, NJ, showing 72.6%. Among the 122 SMSAs for which we could separate "Inside Central City/Outside Central City" status, we found 14 SMSAs where 70% or more of the inner-city children lived in pre-1950 housing. In Buffalo, NY, 84.8% of inner-city children lived in the oldest housing. V-42 DUP040009574 TABLE V-20. (continued) Rank SMSA 157 Salihas-SeasideMonterey, CA 150 Raleigh-Durhatn, NO 159 Baton Rouge, LA 1(50 Vallejo-Fairfield-Napa, CA 1(51 Benton Harbor, Ml 1(52 Provo-Orem, UT 163 Orlando, FL 164 Altoona, PA 165 Green Bay, WI isfi Ann Arbor, MI 167 Jackson, MS 1658 Sioux City, IA-NB 169, Galveston-Texas City, TX 170 Santa Cruz, CA 171 Parkersburg-Marietta, WV-OH 172 Lincoln, NB 173 Madison, WI 174 Oxnard-S i mi Vailey- Ventura, CA 175 Waterloo-Cedar Falls, IA 176 Montgomery, AL 177 Brownsvi He-Karl i ngen- San Benito, TX 178 Waco, TX 179 St. Cloud, MN 180 Springfield, MO 181 Newark, OH 18:2 VinelandrMiT1vi11e- Bridgeton, NJ 183 Brockton, MA 184 Cedar Rapids, IA 185 Santa Barbara-Santa Maria- Lompoc, CA 18)5 Bloomington-Normal, IL 187 Wausau, WI 188 Fort Smith, AR-OK 189 Cumberland, MD-WV 190 St. Joseph, MO 191 Muncie, IN 192 Albuquerque, NM 193 York, PA 194 Eau Claire, WI 195 Atlantic City, NJ Children 0,5-5 Years Number in Percent Total pre-1950 of total Number housing in SMSA in SMSA 5,300 18.9 28,000 5,300 5,300 5,200 5,100 5,100 5,100 5,000 5,000 5,000 5,000 4,900 4,900 4,800 4,800 4,800 4,8Q0 4,800 18.9 10.8 16.8 32.9 13.4 9.3 44.6 30.5 21.8 16.3 43.8 28.7 32.4 30.6 28.6 20.6 9.8 28,100 49,100- 30,900 15,300 38,100 54,600 11,200 16,400 22,900 30,700 11,800 17,100 14,800 15,700 16,800 23,300 48,900 4,700 4.700 4,700 34.8 38.3 17.7 13,500 24,000 24,000 4.500 4,600 4,600 4,500 4,400 30.1 26.9 26.1 44.1 38.6 15,300 17,100 17,600 10,200 11,400 4.400 4,400 4,400 36.4 30.6 30.6 12,100 14,400 14,400 4,300 4,300 4,300 4,200 4,200 4,200 4,200 4,100 4,100 4,100 45.7 40.6 23.9 57.5 55.3 38.2 10.5 59.4 38,7 29,5 9,400 10,600 18,000 7,300 7,600 11,000 40,000 6,900 10,600 13,900 (continued on following page) V-39 DUP040009575 TABLE V-20. (continued) Rank SMSA Children 0.5-5 Years Number in Percent pre-1950 of total housing in SMSA Total Number in SMSA 196 Lake Charles, LA 197 Eugene-Springfield, OR 198 Mansfield, OH 199 Amarillo, TX 200 Columbia, SC 201 Kokomo, IN 202: Norwalk, CT 203 Fargo-Moorhead, ND-MN 204 Alexandria, LA 205 New Britain, CT 206 Kankakee, IL 207 Wichita Falls, TX 208 Roanoke, VA ate Lakeland-Winter Haven, FL 210 Augusta, GA-SC 211 Bellingham, WA 2112 Abilene, TX 213 Pueblo, CO 214 Columbus, GA-AL 2.15 Macon, GA 216 Anniston, AL 217 Biloxi-Gulfport, MS 218 Pensacola, FL 219 Huntsville, AL 220 State College, PA 221 Danville, VA 222 Greeley, CO 223 Fort Lauderdale-Hollywood, FL 224 Danbury, CT 2.25 Lubbock, TX 226 Hagerstown, MD 227 Anderson, SC 25^ Gadsden, AL 229 Bay City, MI 230 Billings, MT 20: Champaign-Urbana-Rantoul, IL 20 Colorado Springs, CO 233 Tucson, AZ 22.4 Tyler, TX 235 Bremerton, WA 236 Sioux Falls, SO 237 Boise City, ID 238 Killeen-Temple, TX 2,# Nashua, NH 4,100 4,000 3,900 3,900 3,900 3,800 3,700 3,700 3,700 3,600 3,600 3,400 3,400 3,400 3,300 3,200 3,200 3,200 3,200 3,200 3,100 3,100 3,100 3,100 3,000 3,000 3,000 3,000 2,900 2,900 2,800 2,800 .2,700 2,700 2,700 2,700 2,700 2,700 2,600 2,600 2,500 2,500 2,500 2,400 24.3 17.6 38.2 21.7 11.6 36.5 50.0 28.5 21.0 42.4 34.0 30.4 19.1 15.0 11.0 38.1 29.9 28.1 14.5 12.6 30.4 17,1 12.5 11.7 41.7 28.3 23.8 4.9 25.4 14.1 37.8 26.9 28.1 25.5 25.0 20.9 9.2 8.3 2111 18.8 26.0 15.2 10.6 25.5 16,900 22,700 , 10,200' 18,000 33,500 10,400 7,400 13,000 : 17,600 8,500 10,600 11,200 17,800 22,700 30,000 8,400 10,700 11,400 22,000 25,400 10,200 18,100 24,800 26,500 7,200 . 10,600 12,600 61,300 11,400 20,600 7,400 10,400 9,600 10,600 10,800 12,900 29,500 46,100 12,300 13,800 9,600 16,400 23.600 9,400 (continued on following page) V-40 DUP040009576 TABLE V-20. (continued) Rank SMSA Children 0.5-5 Years Number in Percent pre-1950 of total housing in SMSA Total Number in SMSA 78 Tulsa, OK 79 Hunti ngton- Ashland, WV-KY-OH 80 Trenton, NJ SI Jacksonville, FL 82 Binghamton, NY-PA S3 San Jose, CA 84 Newburgh-Middletown, NY 85 Erie, PA 86 Corpus Ghristi, TX 87 New Brunswick-Perth Amboy- Sayreville, NO 83 Lexington-Fayette, KY 89 Bakersfield, CA 90 'Lima, OH SI Long Branch-Asbury Park, NJ 92 Terre Haute, IN 93 Spokane, WA 94 Beaumont-Port Arthur, TX 95 Honolulu, HI 96 Chariotte-Gastonia, NC 97 Evansville, IN-KY 98 Richmond, VA 99 Reading, PA 100 Knoxville, TN 101 Saginaw, MI 102 Kalamazoo-Portage, MI 103 Rockford* IL 104 Waterbury,. CT IDS Johnson City-Kingsport- Bristol, TN-VA 106 Appleton-Qshkosh, W1 107 Fall River, MA-Rl 103 Racine, WI 109 Lorain-Elyria* OH no Greenvi11 e-Spartanburg, SC in New Bedford, MA 112 Battle Creek, MI 113 Poughkeepsie, NY 114 Shreveport, LA 115 New London-Norwich, CT-RI 110 Oes Moines, IA 117 Stockton, CA 118 Hami1ton-Middletown, OH 11,900 11,400 11,400 11,000 10,900 10,800 10,200 10,000 9,900 9,800 9,700 9,700 9,500 9,500 9,400 9,400 9,200 9,200 9,000 8,700 8,700 8,600 8,500 8,400 8,400 8,300 8,200 8,200 8,100 8,000 7,900 7,900 7,800 7,700 7,600 7,600 7,600 7,500 7,500 7,500 7,300 18.0 40.4 52.8 15.5 53.7 10.0 46.6 44.1 27.7 22.9 32.4 20.1 48.2 25.0 28.5 28.5 13.3 13.3 16.5 34.3 18.6 62.8 24.4 38.2 34.0 31.4 42.9 23.1 29.5 58.8 45.9 32.1 16.3 57.5 45.8 36.7 19.9 36,0 26.6 21.4 31,1 66,100 / 28,500 . 21,600 70,900 20,300 108,500 21,900 ' 22,700 35,700 42,800 29,900 48,200 13,700 38,000 33,000 33,000 69,400 69,400 54,400 25,400 46,800 13,700 34,900 22,000 24,700 26,400 19,100 35,500 27,500 13,600 17,200 24,600 47,800 13,400 16,600 20,700 38,200 21,400 27,200 35,000 23,500 (continued on following page) V-37 DUP040009577 TABLE V-20. (continued) Rank SMSA Children 0.5-5 Years Number in Percent pre-1950 of total housing in SMSA Total Number in SMSA IIS Wheeling, WV-OH 120. Springfield, OH 121 Stamford, CT 122 Lowell, MA-NH 123 Springfield, IL 124 Mobile, AL 1215 Portland, ME 12(5 Joplin, MO 127 Jackson, MI 128 Manchester, NH 120 Mus kegon-Nortpn Shores- Muskegon Heights, MI 130 Charleston, WV 131 Charleston-North Charleston, SC 132 Anderson* IN 133 Yakima, WA 134 McAl1en-Pharr- Edinburg, TX ii5 Austin, TX 136 SteubenvilleWeirton, QH-WV 137 Chattanooga, TN-6A 138 Santa Rosa, CA 139 Visalia-Tuiare- Porterville, CA 140 Portsmouth-Dover- Rochester, NH-ME 141 Salem, OR 142 Williamsport, PA 14.3 Janesville-Beloit, WI 144 Harrisburg, PA 145 Kenosha, WI 146 Decatur, IL 147 Modesto, CA 143 Glens Falls, NY 149 Elkhart, IN 150 Salisbury-Concord, NC 151 Sheboygan, WI 152 Johnstown, PA 153 Lancaster, PA 154 Savannah, GA 15S Sharon, PA 156 Elmira, NY 7,200 7,100 7,100 6,900 6,900 6,900 6,800 6,500 6,400 6,400 6,400 6,400 6,400 6,200 6,200 6,200 6,200 6,100 6,100 6,000 6,000 5,900 5,900 .5,700 5,700 5,600 5,600 5,600 5,600 5,500 5,500 5,500 5,400 5,400 5,400 5,400 5,300 5,300 51.1 49.3 47.0 43.1 42.6 15.5 48.2 59.6 48.5 47.8 40.5 . 30.3 15.8 47.3 37.3 17.5 13.6 42.4 . 22.1 22.8 20.4 52.5 24.2 58.2 45.2 54.9 43.8 47.1 22.3 58.5 41.0 37.2 61.4 56.8 53.5 22.6 47.3 40. a 14,100 14,400 15,100 16,000 16,200 44,600 14,100 10,900 13,200 13,400 15,800 21,100 40,600 13,100 16,600 35,500 45,500 14,400 27,600 26.300 29,400 11,300 24,400 9,80.0 12,600 10,200 10,400 11,900 25,100 9,400 13,400 14,800 8,8.(10 9,500 10,100 24,0:00 11 ,i200 13,0.00 (continued on following page) V-38 DUP040009578 TABLE V-2Q. RANKING Of 1980 CENSUS SMSAs BY NUMBER OF CHILDREN 0,5-5 YEARS OLD LIVING IN PRE-1950 HOUSING, AND TOTAL NUMBER OF YOUNG CHILDREN IN SMSA Rank SMSA Children 0,5-5 Years Number in Percent pre-1950 of total ` housing in SMSA Total Number in SMSA 1 New York, NY-NJ 2 Chicago, IL 3 Los Angeles-Long Beach, CA 4 Philadelphia, PA 5 Detroit, MI 6 Boston, MA 7 Newark, NJ 8 Cleveland, OH 9 San Francisco-Oakland, CA 10 Pittsburgh, PA 11 St. Louis, MO-IL 12 Minneapolis-St, Paul, MN-WI 13 Baltimore, MD 14 Milwaukee, WI 15 Nassau-Suffolk, NY 16 Washington, DC-MD-VA 17 Buffalo, NY 18 Cincinnati, OH-KY-IN 19 Dallas-Fort Worth, TX 20 Houston, TX 2i Rochester, NY 22 Jersey City, NJ .23 Albany-Schenectady-Troy, NY 24 Providence-Warwick- Pawtucket, RI-MA 25 Portland, OR 26 Toledo, OH-MI 27 Columbus, OH 28 Kansas City, MO-KA 29 New Orleans, LA 30 Seattle-Everett, WA 31 Indianapolis, IN 32 Riverside-San Bernardino- Ontario, CA 33 Denver-Boulder, CO 34 Syracuse, NY 3:5 Northeast Pennsylvania 36 Gary-Hammbnd-East Chicago, IN 37 San Diego, CA 38 San Antonio, TX 39 Akron, OH 422,800 271,500 225,700 172,500 141,900 110,400 80,300 75,100 74,800 71,300 69,200 60,000 56,700 53,100 51,100 48,900 46,800 44,300 40,900 36,400 35,900 34,200 34,000 33,300 32,900 32,100 31,500 31,500 28,600 28,600 27,700 25,900 25,300 24,700 24,400 24,400 23,900 23,000 22,900 60.1 43.2 33.5 46.4 37.8 62.7 53.1 49.1 32.3 47.4 34.0 32.2 34.2 43.5 26.5 20.9 51.3 35.4 15.3 12.4 45.4 72.6 54.3 53.3 45.0 45.0 30.4 28,0 24.2 23.3 27.6 16.5 17.7 45.7 53.0 37.3 15.4 20.7 40,2 703,500 628,800 628,800 371,800 375,800 176,100 151,200 153,000 231,500 150,500 203,600 186,600 165,700 122,100 192,500 234,400 91,300 125,000 267,400 293,400 79,000 47,100 62,600 62,500 71,300 71,300 103,600 112,300 118,000 122,600 100,400 156,600 142,900 54,000 46,000 65,500 154,800 111,200 56,900 (continued on following page) V-35 DUP040009579 TABLE V-20. (conti nued) Rank SMSA Children 0.5-5 Years Number in Percent pre-1950 of total housing in SMSA Total Number in SMSA 40 Dayton, OH 41 Hartford, CT 42 Atlanta, GA . 43 AT T entown-Bethl ehem- Easton, PA-NJ 44 Grand Rapids, MI m Patarson-GIifton- Passaic, NJ 46 Salt Lake City-Ogden, UT 47 Louisville, KY-IN 41 NorfoT k-VA Beach- Portsmouth, VA-NC 49 Flint, MI 50 Birmingham, AL 51 Youngstown-Warren, OH 52 SpringfieTd-ChicopeeHolyoke, MA-CT 53 Lansing-East Lansing, MI 54 Fort Wayne, IN 55 Davenport-Rock Island- Moline, IA-IL 56 New Haven-West Haven, CT 57 Bridgeport, CT 58 Canton, OH 59 Sacramento, CA 60 Memphis, TN-AR-MS 61 Miami, FL 62 Wichita, KS 63 Anahein-Santa AnaGarden Grove, CA 64 Worcester, MA 65 Tacoma, WA 66 Omaha, NB-IA 67 Oklahoma City, OK 68 Teunpa-St. Petersburg, FL 69 Duluth-Superior, MN-WI 70 South Bend, IN 71 Nsshvi11e-Davidson, TN 72 Peoria, IL 73 Fresno, CA 74 Wilmington, DE-NO-MD 75 Utica-Rome, NY 76 Phoenix, AZ 77 Lawrence-Haverhi11, MA-NH 22,800 21,900 21,900 21,600 21,000 ,20*600 20,600 19,800 19,100 19,000 18,600 18,000 17,500 17,500 16,500 15,800 15,600 14,800 14,400 14,100 14,100 13,800 13,700 13,500 13,400 13,200 13,100 13,100 12,800 12,600 12,600 12,600 12,500 12,500 12,200 12,000 12,000 11,900 32.9 12.4 12.4 50.6 37.0 59.4 14.7 24.7 25.5 36.1 25.5 40.1 47,9 39.3 43.8 39.9 47.6 53.0 51.3 16.4 16.4 11,9 32; 9 8.5 51.0 27,5 26.3 17.0 13.0 50.4 45.8 17.4 34.7 25,8 29.5 46.7 9.4 54.3 69,400 176,400 176,400 42,700 56,800 37,400 140,500 80,100 72,900 52,600 72,900 44,900 36,500 44,500 37,700 39,600 32,800 27,900 34,700 86,100 86,100 116,100 41,700 159,600 26,300 48,000 49,800 76,900 98,800 25,000 27,500 72,500 36,000 48,500 41,300 25,700 127,900 21,900 (continued on following page) V-36 DUP0400Q9580 C. RANKING OF (CHILDREN WITH POTENTIAL EXPOSURE TO PAINT LEAD IN HOUSING In the previous sections, estimates were given for the number of young white end black children in all SMSAs predicted to have Pb-B levels above .selected criterion values as well as the findings from local screening pro grams? In these estimates, specific sources of lead were not considered. Since the age of housing indicates the degree of exposure to lead in paint, we analyzed the distribution of children living in SMSAs by the age of their housing units. This discussion represents a combination of both area-based exposure and source-specific exposure, as presented in Chapter VI. 1. Strategies and Methods As discussed in Chapter VI, age of housing in the U.S. may indicate general levels of exposure from leaded paint, e.g., the oldest housing has the highest lead concentration in its paint and the highest frequency (percentage) of leaded paint per age category. In U.S, Census enumerations, as noted earlier, the larger SMSAs separated children living in central cities from those not in central cities. In addi tion, the data permitted grouping of the housing units into three categories: pre-1950, 1950-1969, and 1970-1980. The pfe-1950 housing includes that portion of the housing stock that has the highest concentrations of lead in any leaded paint applied, i-e., 20 to 50% lead by weight. However, the paint supply used on pre-1940 housing, which had the very highest lead concentration, most likely carried over into the 1940s, During 1950-1969, lead concentrations were decreased, and post-1970 lead content was regulated and paint supplies with higher concentrations became exhausted. The data for age of the housing units were available for all young children regardless of race/ethnic origin, and we were able to report this information for the total child populations, not just for white and black children. We have tabulated the census counts of children residing in old housing units for each SMSA, the percentage they represent, and have ranked the SMSAs by the number of children in pre-1950 housing in Table V-20. When several SMSAs were found to have the same number of children in pre-1950 housing, the percentage these chil dren represented was used as a second ranking criterion and the SMSAs ordered from highest to lowest percentage (see #35 and #36 in Table V-20), V-33 DUPO4OO09581 'We also prepared detailed tabulations for each SMSA showing the same ranking of the SMSAs and including the numbers of children residing in the other two housing age groups, as well as the distributions for children "Inside Central City" and those "Outside Central City" when available- Appendix 0 contains this table. The paired SMSAs are shown separately at the end of the tables, since the pairs of SMSAs are reported as units and a similar distribu tion of age of housing had to be assumed for each of the pair. The relationship of the children's distribution by the age of their housing and their economic status is of Interest. According to popular wisdom and the definition of target populations for 1ead-screening programs, the poorest children are found in older housing. However, the findings shown in Tables V--20 and Appendix 0 located large numbers of children in old housing more than would be accounted for by the population segment in poverty. Conse quently, we further examined the relationship of income levels and residence by age of housing unit. Table V-21, an example of the resulting tabulations for each SMSA, shows an SMSA of over 1 million population. Appendices A, B, and C contain the tables for individual SMSAs in the three population size groups. 2. Bespits Table V-20 summarizes all SMSAs ranked by the number of young children in pre-1950 housing. This ranking does not automatically correlate with the size of the SMSA populations nor does it correlate with the total SMSA population of young children. For example, Phoenix, AZ, was ranked 76th, and San Jose, CA, was ranked 85th, even though both are in the group of 38 SMSAs with total popu lations of over 1 million; nationally* phoenix ranks 26th and San Jose ranks 30th in terms of total populations. It is not unexpected that the older popula tion centers contain large proportions of children living in older housing. The chronology of urban and suburban growth varied enormously among SMSAs, as Appendix Table D shows. Some SMSAs grew most rapidly between 1950 and 1969, and others between 1970 and 1980. In general, for the older SMSAs, the children living in housing built from 1970-1980 represented a small percentage of those living in the central city. However, this finding is not true of SMSAs that have achieved maximum growth since the 1950s, as is apparent, for example, when comparing Buffalo, NY, and Houston, TX, ranked 17th and 20th, respectively. V-34 DUP040009582 TABLE V-18. RATE OF FIRST HOSPITALIZATION AND ASSOCIATED MEAN Pb-B (pg/dl) IN "ASYMPTOMATIC" CHILDREN OF NEWARK, NJ, BY YEAR OF FIRST ADMISSION3 Year of Admission Number of Children First Hospitalized Rateb Mean Pb-B (pg/dl) 1972 1973 1974 1975 1976 1977 1978 1979 1980 89 81 42 40 23 28 (29); 32 (35)c 42 71 (72)' ' 19.1 18.0 9.7 9.6 5.7 7.5 9.5 11.9 21.4 74.9 76.6 71.8 69.6 63.0 62.3 66.1 63.7 64.7 aAdapted from Schneider and Lavenhar (1986). bPer 10,000 Newark children. cNumber of children in the rate estimate. decreased, the screening van and the public education program were eliminated and lead laboratory services were reduced. The Newark, NJ, experience is fur ther discussed in the section on imperatives and strategies for abating lead poisoning and exposure (Chapter IX). Are the results of state and local high-risk screening efforts duplicated in the nation in terms of present status and trends? We can answer this by examining results of the national NHANES II (1976-1980) study described earlier. 2, The NHANES II Study Using the NHANES II statistical design and blood specimen collection pro gram, analysis of EP and Pb-B values could be performed on a national level, thus adding new dimensions to the interpretation of results from screening programs. As Mahaffey et si- (1982) reported, the prevalence of Pb-B levels above 30 pg/dl (the action level for toxicity risk at the time of the NHANES II survey) in young children sampled by NHANES II was higher than predicted from screening data. When black children in low SES families in the central city were examined, very high prevalence rates were estimated. However, these rates seem to be reflected only in results of screening programs that target very V-31 DUP040009583 similar pediatric populations, such as St. Louis and New York City, in Table V-19, NHANES II data for young children are summarized by race and age. The summary Includes means, medians, and the Pb-B distribution at four levels. Within race, the two childhood age categories are not distinguishable as to means, medians, and distributions; but across race, higher levels observed in black children are statistically significant. Overall, urbanization and income are directly associated with lead exposure, especially among black children. ^ TABLE V-19. BLOOD LEAD LEVELS (pg/dl) IN U.S. CHILDREN BY RACE AND AGE, 1976-1980* Race and Age Mean Pb-B Median Pb-B Prevalences of Pb-B at pg/dl ________Levels of: <20 20-29 30-39 &40 WHITE 0.5-2 yr 3-5 yr 15.0 14.9 14.0 14.0 80.2 17.3 2.2 0,3 82.7 15.4 1.6 0.3 BLACK 0.5-2 yr 3-5 yr 20.9 20.8 19.0 20.0 50.5 46.3 34.2 43.3 13,0 8.5 2.3 1.9 aAdapted from Mahaffey et al , (1982) and based on NHANES II data. As noted earlier, the NHANES II data collected over the survey years showed a significant decline In Pb-B levels in children, which was strongly associated with the phasedown of lead in gasoline. A detailed discussion of this relationship is presented in the next chapter. Overall, the rate of the decTine and related data suggested lower mean Pb-B levels for children in the 1980s. Results of the 1983 survey df Hispanic children, the "Hispanic NHANES," as yet available only as preliminary unpublished information, appear to agree with this suggested trend. Children in the highest risk categories--for example, inner-city black children in low SES families-- have more complex exposures, such as leaded paint and leaded paint weathering and chalking, than U.S. children as a whole. For this group, Pb-B levels may not be declining In the same way and at the same rate as for U.S. children as a whole. V-32- DUP040009584 TABLE V-16. TEMPORAL VARIATION OF LEAD TOXICITY CASES IN SELECTED LEAD POISONING SCREENING PROGRAMS, 1973-l985a'b Year Pb Toxicity Cases (% Of Screened) National New York Cityc St. Louis 1973 1974 1975 1976 1977. 1978 1979 1980 1981 1982 1983 1984 . 1985" 19,059 (6.4) 24,443 (5 4) 30,343 (7.2) 33,043 (8.1) 28,072 (7.4) 26,734 (6.5) 32,362 (6.8) 25,293 (5.0) 18,272 (3.6) 10,114 (2.0) 9,317 (1.6) 5,035 (1.1) 11,739 (1.5) 761 (0.6) 494 (0.4) 1,559 (1.4) 984 (1.0) 652 (0.7) 802 (0.7) 931 (0.8) 976 (0.7) 1,538 (1.2) 1,259 (0.9) 1,201 (0.8) 979 (0.6) 1,337 (0.6) 2,396 (32.3) 1,577 (27.0) 2,530 (22.9) 3,709 (28,0) 3,519 (24.0) 2,080 (15.2) 1,560 (12.5) 1,422 (11.4) 1,422 (12.4) 1,278 (10.9) 869 (7.6) 1,066 (8.2) 1,356 (11.0) National screening figures given by CDC, 1973-1981 (CDC, 1982), by ASTHO for FYs 1982-1984, (Public Health Foundation, 1986) and by ATSDR survey for 1985 results. bNew York and St. Louis figures as provided to ATSDR by respondents. 'CPositive cases refer to children hospitalized and given chelation therapy. The number is considerably less than total positive screens, above 40 pg/dl or all tlasses in 1978 classification scheme. See Table V-12 for total positive screening cases in New York City for FY 1981 (N = 5,010, 4.3%). ^Year in which CDC criteria for toxicity changed. We also compared changes in exposure or toxicity evaluated in case studies with changes detailed in the usual screening program summaries. Chisolm et al. (1985) have pointed out that average Pb-B values in Baltimore may not be declin ing significantly among subjects at highest risk. For example, in 1956, the mean Pb~B level for a sizable group of children (N = 330) at highest risk was 43 pg/d'l. In 1975, 19 years later, the mean Pb-B level for 155 children at highest risk was 38 pg/dl. These two means are both high and virtually indistinguishable. A related question concerns whether the distribution of lead-intoxicated children among the three CDC risk categories changes over time independent of changes in the CDC classification schemes. EPA, in its initial cost-benefit analysis of reducing lead in gasoline, examined quarterly data from CDC screening programs for the percentage of chil dren with lead toxicity who were in Classes III and IV for the years 1977-1981 V-29 and found no change in the 20 quarters for these nationwide data (U.S. EPA, 1984). The experience of the targe Chicago Health Department program also suggests little change* Table V-17 shows the city's screening results for 1981 through 1985. Table V-17 shows little change over this time in the number of Chicago children in the highest and next-to-highest risk categories, (Classes IV and III, respectively). In Chicago, therefore, the distribution apparently is not shifting toward lower degrees of risk--that is, the percentages of children in' Classes III and IV are not decreasing. TABLE V-17. LEAD-SCREENING STATISTICS FOR THE CHICAGO DEPARTMENT OF HEALTH, 1981 TO 1985,a BY CDC CLASSIFICATION 11, III, OR iyb Year Number First Screens Initial Positive (IP) II(% IP) III(% IP) m% IP) 1981 1982 1983 1984 1985 35,352 34,499 35,185 35,961 37,409 797 466 (58) 275 (35) 56 (7) 875 563 (64) 324 (37) 51 (6) 843 545 (65) 252 (30) 46 (5) 837 549 (66) 238 (28) 50 (6) 693 410 (59) 238 (34) 45 (6) aAclapted from 1985 Report, Chicago Department of Health: Lead-Screening Statistics. k$ee Table V-9 for description of classification scheme. Finally, the numbers of reportedly "asymptomatic" children with high Pb-B levels entering the health care system for the first time should be examined. In particular, we need to assess the rates of these child admissions over the years and examine the corresponding! mean Pb-B values in the groups of children admitted. Such relationships have been djescribed by Schneider and Lavenhar (1986), who examined the medical records of Newark, NO, inner-city children hospitalized for treatment of lead toxicity. Table V-18 shows some of their results, includ ing the rate of first hospital admissions pier 10,000 urban children and the group mean Pb-B levels from 1972 through 1980* In Newark, NJ, the rate of child admissions for chelation therapy declined from 1972 until 1976, after which it increased significantly through I960. This rise does not appear to be due to changes in chelation treatment criteria, and no movement downward in the Pb-B index signaled such a change. The rise in rate does coincide with declines in funding starting in 1976 and continuing through 1980. Because funds were V-30 DUP040Q09586 In Table V-15, for the Oetober-Oecettiber quarter of 1985, the number of New York City lead toxicity cases using the previous classification of COC is compared with the number found using the new classification (Bureau of bead Poisoning Control, Department of Health, City of New York* 1985)/ The numbers are only for the fourth quarter of 1985 because the new classifications were not. used until October 1, 1985. When the previous classifications are used to compare the numbers for the fourth quarter of 1984 and 1985, the numbers of x positives do not materially differ statistically. But when the new classifica tion was used, the number of cases for the fourth quarter of 1985 increased 61.4% over the number for the fourth quarter of 1984 (502 cases compared with 311). Furthermore, the increase (the difference between 292 cases with the previous levels and 502 with the new--or 210 cases) Is 42% of the cases for the fourth quarter of 1985. TABLE V-15. IMPACT OF NEW GDC LEAD EXPOSURE SCREENING GUIDELINES ON THE NUMBER OF LEAD TOXICITY CASES IN NEW YORK CITY' 1984 Cases 1985 Cases Previous CDC Guidelines (% Change)*5 New CDC Guidelines (% Change)*5 October November December 132 99 70 119 (-9.8) 95 (-4.0) 78 (+11.3) 191 (+45.0) 176 (+77.8) 135 (+92.9) TOTAL 311 292 (-6,0) 502 (+61,4) aFrom: 1985 Annual Report, NYCDH, Bureau of Lead Poisoning Control. L "Relative to same quarter in 1984. With the new CDC classification scheme, the number of lead toxicity cases should increase in communities having screening programs.. The 1985 guidelines include reducing Pb-B, for the lowest classification, to a level near that pre vailing in a significant.fraction of urban children, 25 pg/dl. Changes in the New York City program (Table V-15) may or may not be typical of the impact, but programs with a large number of children with excessive lead exposure due to leaded paint and contaminated dust and soil are expected to increase. When CDC redefined lead toxicity risk, the number of children potentially in the positive category significantly increased. Having a lower cutoff level V-27 DUP040009587 may offset, to soma extent, the decreases in Pb-B levels associated with reduce tiions in some lead sources, such as gasoline and food, as noted earlier in this chapter. From a broader perspective, do the various screening programs offer conclusive information about the extent of lead poisoning over the years? Clearly, the screening results given in the previous tables show markedly reduced numbers of cases of acute and subacute lead poisoning found in U.S. cities when compared to numbers, commonly due to leaded paint ingestion, fduntif in the 1930s through the 1960s. Reducing the lead content of gasoline has helped lower the degree of chronic poisoning. In the past, sniffing leaded gasoline was an occasional source of subacute lead exposure, but as leaded gasoline is phased out (U.S. EPA, 1986a), the number of these cases should decrease. The rate of chronic lead poisoning in young U.S. children appears to be decreasing moderately, but the absolute numbers of toxicity and the percentages of screenings that show toxicity still indicate a continuing problem. Table V-16 shows lead screening program results nationally and for two loca tions. The national figures for 1973 through 1981 are from CDC; for FY 1982 through FY 1984 from ASTHO (Public Health Foundation, 1986); and for 1985, from the December 1986 ATSDR surveys. Please note that the New York City rates of toxicity in tables V-14 and V-16 refer to medically managed children and not total Class II-IV positives (see Table V-12 for such FY 1981 totals). National screening results suggest a moderate decline in cases of lead tox icity over time. This is true even when complicating factors are consideredsuch as changes in protocols for laboratory quality assurance, new lead toxicity criteria, differences in levels of adherence to target populati|jn criteria, and the moderate decline in toxicity cases caused by reducing the lead content of gasoline. However, this table clearly shows that many children still suffer from lead toxicity. In St. Louis, for example, the number of lead toxicity cases has declined from the early 1970s, but the percentage of screening tests that are positive for toxicity is still unacceptable, and this percentage has not essentially changed for the past 6 to 7 years. For FY 1981, CDC figures of total positives (Table V-12) for New York City give a rate of 4.3%, The St. Louis program illustrates the difficulty In eliminating the prevalence of lead poisoning by communitywide intervention, even though the overall program efforts were effective over an extended time. V-28 DUP0400Q9588 Agency program Massachusetts - Statewide TABLE V-14; <continued) , Number of Children Screened (Year) 142,000 (FY 85) 166,900 (FY 86) Cases of Confirmed Pb Toxicity (%) 1,531 1,011 (1.0) (0.6) Maternal and Child Health Projects Boston 29,925 (FY 85) 29,356 (FY 86) Holyoke 1,547 (FY 86) Merrimac Valley 5,050 (FY 85) 3,619 (FY 86) North Shore 4,038 (FY 86) Southeastern Massachusetts 4,745 (FY 85) University 3,775 (FY 86) 507 (1.7) 337 (1.2) 23 (1.5) 177 (3.5) 42 (1.2) 46 (1.2) 54 (1.1) 35 (0.9) Springfield 1,735 (FY 85) 352 (FY 86) 34 (2.0) 3 (0.9) New Hampshire 5,021 (FY 85/July-June) 6,483 (FY 86/July-June) 24 (0.5) 46 (0.7) New Jersey 58,080 (CY 85) 1,690 (2.9) New York - New York CityT Bronx Brooklyn Manhattan Queens Richmond (Unknown) 206,467 (FY 85) 44,501 72,314 47,456 38,604 3,256 (356) 1,337 288 720 154 154 24 (0.7) (0.7) (1.0) (0.3) (0.4) (0.7) North Carolina 15,567 (FY 85/Oct-Sept) 66 (0.4) Pennsylvania Philadelphia N,E. Philadelphia Allegheny Co. Harrisburg Erie Co, 22,894 (FY 85) 15,133 983 2,092 2,026 1,080 631 (0.3) 357 (2.3) 8 (0.8) 32 (1.6) 101 (4.9) 9 (0,8) Rhode Island 14,640 (CY 85) 280 (2.0) South Carolina 64,993 (FY 86) 920 (1.2) (continued on following page) V-25 DUP040009589 Agency program Texas Dallas City ' Vermont TOTAL TABLE V-14. (continued) Number of Children Screened (Year) 35,000 (Average for several years) 402 (Jan.-Aug. 1985) 785,285 Cases of Confirmed Pb Toxicity (%) 350-7008 (1-2)91 1 (0.3) 11,739 (1.5)h aFY 85 programs mainly using CDC 1978 statement classification scheme. Calendar Year 1985 (CY 85) programs use 1985 scheme in some cases. bFY 88 and CY 86 summaries mainly use 1985 CDC scheme. cSum of the two cities, dFfrst screens only, e19&5 CDC scheme starting July 1985. f 1985 CDC scheme starting October 1985; confirmed cases refer to actually medica11y managed, not Class II-IV pos1tives, ^Estimated, ^Includes upper estimates of cases for Dallas, TX: 700. patterns in young children. The summary report of Mahaffey et al, (1982) shows that between 1975-1980 about 10% of black children 3 to 5 years old had a Pb-B level of 30 pg/dl or above, whereas the corresponding figure for the 20-29 pg/dl Pb-8 fraction of the distribution was 43.3%. The mean and median Pb-B values for this particular part of the population were 20.8 and 20.0 pg/dl, respec tively, As discussed extensively by U.S. EPA (1985, 1986a), this distribution has shifted downward in children as a group and will continue to do so for some time. The magnitude of the shift in inner-city children, one of the target groups in screening, however, would probably be smaller than for U.S. children as a whole, which can be attributed to the disproportionately higher concen trations of lead in paint and related dusts in the environment of these children, , The changes in prevalence, which resulted from lowering the Pb-B and P levels used for screening (CDC.., 1985), can theoretically be seen in a program with stable protocols and targeting criteria. Fortunately, changes in lead toxicity rates were assessed in New York City for the last quarter of 1985 relative to the last quarter of 1984. V-26 DUP040D09590 TABLE -13. LEAD POISONING SCREENING OF CHILDREN REPORTED BY 27 STATE AND LOCAL AGENCIES, FY 1983' State or Other Agency Number of Children Screened Cases of Confirmed Pb Toxicity (%) Arkansas Connecticut Delaware Washington, DC Idaho Illinois Indiana Iowa Kansas Kentucky Louisiana Maryland Mas sachusetts Michigan Minnesota Mi ssouri Nebraska Nev? Jersey New York North Carolina lif Pennsylvania -Rhode Island South Carolina Virginia West Virginia Wisconsin 4,787 22,533 5,187 15,750 380 25,340 1,265 2,478 2,642 7,416 51,804, 45,000 130,000 14,700 1,816 11,778 2,090 35,534 160,960 14,000 19,543 19,994 10,364 23,832 8,401 449. 4,322 70b (1.5) - 145 (2.8) 132 (0.8) 8 (2.1) 136. (0.5) lb (0.1) 30 (1.2) 29 (1.1) 105 (1.4) 269. (0.5). 348b (0.8) 1,000 (0.8) 434 (3.0) 18 (1.0) 1,278 (10.9) 39 (1.9) -(1,930 evaluated) 4,205 (2.6) 80 (0.6) -(416 eval uated)4* 450 (2.3). 180 (1.7) 88 (0.4) 84 (1.0) aS* (0.2). (4.3/ TOTAL 676,571 9,317 (1.6) aPubli.c Health Foundation (1986). bEstimated by respondent. c0n"ly totals evaluated; actual number of positives were not provided. The responses ATSDR received indicate that the results are derived mainly from the old CDC classification scheme if FY 1985 was employed. Other programs, reporting for a calendar year of screening, sent tabulations reflecting the change over to the new 1985 CDC classification scheme during 1985, This latter case is typified by the programs of St, Louis and NewJforR City, When using lower Pb-B and EP levels to classify toxicity, we might expect the numbers of positive lead toxicity cases to rise. Such a prediction, nationwide, can be made using the NHANES II data to predict Pb-B distribution V-23 DUP040009591 TABLE: V-14. CURRENT (1985-1986) LEAD SCREENING ACTIVITIES REPORTED BY STATE AND LOCAL PROGRAMS TO ATSORa'b Agency program Delaware Washington, DC Georgia Augusta Savannah Illinois Chicago Indiana Iowa 12 counties Scott County Kansas Wyandotte Worcester Michigan Detroit Minnesota Hennepin Co. (Minneapolis) St. Paul Mississippi Ml ssouri St. Louis City Number of Children Screened (Year) 5,818 (FY 85/July-June) 17,000 (FY 85/0ct-Sept) 2,960 (FY 85/0ct-Sept) 5,684 (FY 85/0ct-$ept) 37,409 (CY 85) 3,770 (FY 85) 2,143 (CY 85) 897 (Jan-Nov 86) 5,098 (CY 85) 8,161 (FY 85) 9,658 (FY 86) 20,248 (CY 85) 13,132 (Jan-Aug 86) 3,563 (Jan 85-June 86) 8,555 (CY 85) 8,553 (Jan-Nov, 86) 3,628 (FY 86, Oct-Sept) 12,308 (CY 85)' 9,758 (Jan-Oct 86) Cases of Conf1rmed Pb Toxicity (%) 130 (2.2) 595 (3.6) 808/8,644 (9.OF 693 17 28 9 16 71 72 371 392 26 64 41 29 1,356 1,653 (1- 8)' (0.5) (1.3) (1-0) (0*3) (0.9) (0.8) (1.8) (3.0) (0.7) (0.8) (0.5) (0.8) (11.0) (16.0) Nebraska Douglas Co. Maryland Baltimore Remainder of state 3,167 (FY 86/Oct-Sept) 29 (0.8) 30,583 (CY 85) 18,132 (CY 85) 504 (1.7) 46 (0.3) (continued on following page) V-24 DUP040009592 TABLE V-12. RESULTS OF SCREENING IN U.S..CHILDHOOD LEAD POISONING PROJECTS, FY 1981 Program Number Screened Numbers of Children With Pb Toxicitv Total Class II Classes III & IV United States 535,730 21,897 14,446 7,451 DHHS' Region I Bridgeport, CT Waterbury, CT Augusta, ME Boston, MA Lawrence, MA Worcester, MA Rhode island 51,282 4,619 2,855 3,546 20,250 6,552 6,026 7,433 1,622 142 64 20 615 404 110 267 1,042 84 41 10 408 300 75 124 580 58 23 10 207 104 35 143 DHHS Region II Atlantic City, NJ Camden, NJ East Orange, NJ Elizabeth, NJ Jersey City, NJ Long Branch, NJ Newark, NJ Paterson, NJ Plainfield, NJ New Jersy (other programs) Erie Co., NY Monroe Co., NY New York City Onondaga Co, NY Westchester Co., NY 171,723 1,151 3,657 3,401 284 3,880 1,117 8,500 4,305 3,334 615 7,134 5,735. 115,864 7,305 5,446 8,786 lU 134 132 17 437 31 1,201 385 121 146 330 349. 5,010 217 135 6,013 49 74 84 11 284 25 882 282 89 75 249 278 3,382 151 98 2,773 62 60 48 6 153 6 319 103 32 71 81 101 1,628 66 37 DHHS Region III Delaware Washington, DC Baltimore, MO A'l 1 entowri-Bethl ehem. PA Chester, PA Philadelphia, PA Wilkes-Barre, PA Lynchburg, VA Newport News, VA Norfolk, VA Portsmouth, VA Richmond, VA 84,195 4,876 12,183 21,840 1,456 2,126 22,126 2,091 1,352 2,968 4,075 2,462 5,800 3,722 136 205 576 12 42 2,399 SO 30 57 65 55 75 2,422 98 141 381 9 29 1,541 36 20 31 43 35 42 1,301 38 64 195 3 13 858 14 10 26 22 20 33 DHHS Region IV Augusta, GA Savannah-Cbatbam Co. , GA 47,631 2,793 3,555 614 412 45 32 129 S3 202 13 46 . (continued on following page) V-21 DUP040009593 TABLE V-12. (continued) Program Number Screened Numbers of Children With Pb Toxicitv Total Class II Classes III & IV Louisville, KY Cabarrus Co., NC South Carolina Memphis, TN 10,147 982 27,667 2,487 178 124 13 9 231 155 18 9 54 4 76 9 OHMS Reqion V Chicago, IL Kankakee, IL Madison County, IL Rockford, IL Wciukegan-Lake Co., IL Illinois (other programs) Ft. Wayne, IN Detroit, MI Grand Rapids, MI Wayne Co., MI St. Paul, MN Akron, OH Cincinnati, OH Cleveland, OH Beloit, WI Milwaukee, WI 108,430 32,861 2,468 2,288 2,341 3,570 5,184 532 19,281 688 1,818 2,107 4,637 9,085 14,151 779 6,640 5,087 2,070 56 105 30 35 145 19 926 19 75 15 149 191 921 15 316 3,255 1,159 40 66 18 22 84 11 652 15 55 5. 144 119 668 11 192 1,832 917 16 39 12 13 61 8 274 4 20 10 5 72 253 4 124 OHHS Realon VI Arkansas Louisiana Hew Orleans, LA Houston, TX 48,944 12,976 18,022 12,858 5,088 571 366 177 106 41 25 291 199 62 36 205 71 16 92 26 OHHS Reaion VII Cedar Rapids/Linn Co. , IA Oavenport/Scott Co,, IA St. Louis, MO Springfield, HO Omaha, NE 19,487 3,115 2,005 11,231 484 2,552 1,486 42 34 1,323 18 69 935 29 19 829 8 50 551 13 15 494 10 19 OHHS Reqion IX Alameda Co., CA Los Angeles, CA 4,033 529 3,504 92 -- 92 7 7 aU<ing CDC classification scheme of 1978 C0C statement (QC, 1978). Tabular data from CDC*s Mortality and Morbidity Weekly Report, October, 1982 (CDC, 1982). In the 1978 classification, toxicity risk begins with Pb-B $30 pg/dl and EP $50 pg/dl whole blood. u Estimated figures. V-22 , 1 DUP040009594 TABLE V-10. COC LEAD SCREENING CLASSIFICATION SCHEME AS OF JANUARY 1985, USING THE HEMATOFLUOROMETER3 Blood Lead (pg/dl) Not Done Erythrocyte Protoporphyrin (pg/dl Whole Blood)*5 <35 - ' 35-74 75-174 SI75 I ' '_c ' " _c ....._c S24 25-49 50-69 S70 I JV . Ia Ib II _d III _d ,,d III III IV EPP6 III IV IV instrument for field measurement of EP, see CDC (1985) statement. K eZine protoporphyrin measured with hematof1uorometer and free EP with chemical method. 1 Requires a Pb-B measurement, ^Not usually observed. ^Erythropoietic protoporphyria (EPP), a genetic disease, is a possibility. TABLE V-ll. Blood Lead (pg/dl) Not Done <24 25-49 50-69 ^70 CDG LEAD SCREENING CLASSIFICATION SCHEME AS OF JANUARY 1985, USING CHEMICAL ANALYSIS OF EPa ...-............... ....... .......... ........ .......... 8 ...........m, .. Erythrocyte Protoporphyrin (ua/dl Whole Blood) <35 35-109 110-249 250 I _c _c I Ia ia EPP6 Ifa II in III ,d III in IV _d IV IV aSee CDC (1985) statement for more details. ^"Free" erythrocyte protoporphyrin measured by chemical method, eRequires a Pb-B measurement. dNot usually observed, eEr.ythropoietic protoporphyria (EPP), a genetic disease, is a possibility. V-19 DUP040G09595 Screening programs are now conducted with methods that tend to under* report the true screening prevalences of PbrB levels. Since an EP level is the first step in assessing lead exposure in young children, children who have a "normal" EP level but an elevated Pb-8 level will not be counted as a subject risking toxicity. The rate of these "false negatives" was reported to be con siderable (see earlier quantitative discussion in Chapter II). Furthermore,/ the true rate may be even higher than when the prevalence of lead exposure is determined mainly at the time of clinic visits or the equivalent, compared with, for example, intensive, door-to-door canvassing. Tables V-9, V-10, and V-ll show, changes in risk classifications that consist of lowering the Pb-B level for the lowest category by 5 pg (from 30 to 25 pg/dl) and lowering the EP level in, whole blood by 15 units (from 50 to 35). As rioted elsewhere, these changes represent a trade-off between the lead levels the pediatric health community sees as harmful and the logistics of screening and the technical limits of the EP measuring methods routinely used- In other words, Pb-B levels below the CDC level of 25 pg/dl for whole blood should not necessarily be viewed as "safe." In Table V-12, we have presented groups of children screened in the CDC program for FY 1981 and have given the number of children positive for lead toxicity based on the older action levels of 30 pg/dl Pb-B and 50 pg/dl EP. The numbers of responses currently defined, as positive are Separated further into two risk groups. Class II and combined Classes III and IV. Data in Table V-12 are as reported in the Morbidity and Mortality Weekly Report (CDC, 1982). Table V-13 shows a summary of the more recent screening results that ASTHO collected from state health agencies. Twenty-seven state agencies provided numbers of young children screened for lead toxicity, but only 24 provided data on confirmed cases of toxicity (Public Health Foundation, 1986). To determine the current scope and outcomes for various lead screening programs, ATSDR asked all state and known county or city screening units for information on the numbers screened, the numbers of confirmed lead toxicity cases, and the relevant time periods. Data from this ATSDR survey are in Table V-14. The survey period covers the time during which CDC distributed its January 1985 lead statement. Data in this table therefore represent numbers from some combination of the former and present screening classification schemes (For schemes see Tables V-9 through V~U.) V-20 DUP040009596 Services (DHHS), Part of CDC's overall efforts included establishing a labora tory proficiency testing service for Pb-8 and EP measurements in screening and other child medicine services. This was under the aegis of the Center for Environmental Health, In FY 1982, screening and other grant programs were incorporated into the Maternal and Child Health (MCH) Block Grant Program and administered by the / Maternal and Child Health Division, Bureau of Health Care and Delivery Assis tance,. Health Resources and Services Administration, DHHS, 'Although Farfel (1985) proposes that this change was attended by funding reductions, it is not possible to identify an actual reduction figure. As noted by lin-Fu (1987), each state receiving the block grant portion of money determined its own priorities within the MCH programs, including lead screening. Furthermore, in many cases lead-screening costs are included in budgets for comprehensive pediatric services (Lin-Fu, 1987). At present, the Association of State and Territorial Health Officials' (ASTHQ's) administrative unit, the Public Health Foundation, is collecting data on childhood lead-poisoning prevention efforts from the various states; however, participation is voluntary, A number of states and constituent programs within the states have attempted to maintain the same level of effort that prevailed under CDC administration of the programs, in general, this is the case for the major programs in New York City, Chicago, Baltimore, and Massachusetts. In FYs 1982 and 1983, the numbers of reporting states were 26 and 33, respectively. Has the number of programs decreased? This question cannot be answered very well without detailed canvassing. During the present administra tive period, each state agency reports their results, and a given state may have more than one program unit as defined under the former CDC system. In December 1986, ATSOR canvassed reporting states and other jurisdictions; 41 program units responded with usable data. For all responding programs, the county was over 45 units. This tally included the MCH projects in Massachusetts and counted the rest of the state as one screening unit. Screening data for different geographic areas have been tabulated. For several reasons, including continuity across time and differences in program characteristics, shown are: (1) data for the final year of the original program administered by CDC, FY 1981; (2) screening results from the programs under the V-17 DUP040009597 'Maternal, and Child Health Block Grant as reported under the ASTHQ program (FY 1983); and (3) survey results gathered by ATSDR in December 1986. The ATSDR survey include results from agencies reporting by fiscal and calendar years, reported within 1985 or 1986 or both, and from independent programs within the various states. Within each program period and between program periods, several factors , have influenced, and continue to influence, screening results. (1) The screen ing risk classifications have changed since the results set forth in the following tables were gathered. These various classification schemes, are shown in Tables V-9, V-10, and V-ll. (2) Targeting high-risk populations has proba-f; biy changed over the years. From FY 1972 to 1981, the strategies for screening populations, under CDC guidance, were uniform. The main goal was to screen groups of children in the community .judged at high risk and having high preva lence rates for elevated Pb-B levels and for lead poisoning serious enough to warrant medical or public health action. Although this screening may give the number of children exposed in high-risk areas, it does not necessarily reflect the nationwide status of the lead problem. This screening was appropriate for the original purpose, that is, to concentrate attention on those children Who most urgently need screening. TABLE V-9. CDC LEAD SCREENING CLASSIFICATION SCHEME, 1978-198$* Blood Lead (pg/dl) Erythrocyte Protoporphyrin Cuo/dl Whole 81ood) 50-109 11Q-249 >250 30-49 II III III 50-69 III III IV m b IV IV aC1ass1ficatiori numbers increase with increased 11 toxicity" risk and need for diagnostic evaluation. A given class, e.g., Class III, can represent a com bination of Pb-B/EP results. See CDC (1978) statement for more details. u Not commonly encountered in screened populations. V-18 DUP040009598 realized that birthrates in these race/ethnic groups are relatively high and consequently, these children will constitute an ever increasing proportion of the total child population in the future. Fourth, children residing in SMSAs account for about B03S of the total child population. According to available data, children not residing in SMSAS exhibit lower prevalences than SMSA-based rates. However, the data base is not ade-> ' qiuate for calculating meaningful stratification. In summary, it is impossible to define precisely the various elements of overestimations and underestimations. Therefore, the estimates presented should be characterized conservatively as best estimates that cah be based on available scientific data. The findings summarized iin Table V-8 indicate the extent of the problem, but they obscure insights into demographic/socioeConomic characteristics that have been associated with varying prevalences. These can be observed for one Pb-B level (15 pg/dl) as indicated in Table V-7. The tables showing the esti mates of prevalences for the strata (Tables V-l, V-2, and V-3) show the expected negative association of socioeconomic status and Pb-B level. A positive associ ation is found for density of population. Residence in the central cities and race also are associated with the variations in prevalence. The most important finding, however, is that no strata of these children are totally exempt from risk of Pb-B levels high enough to represent a poten tially adverse health impact. A numerically very large stratum of children, characterized by family income above the poverty level and predominantly white, is found to be of suburban residential status (Not in Central City), Although the estimated prevalences in these children are relatively low, estimates of those at risk should not be ignored when planning screening and case finding programs because such a large number of children are in the stratum. White children in the highest income group, living "Outside Inner City" and estimated to have Pb-B levels above 15 pg/dl totaled about 350,000 nationwide* (For the small SMSAs, we added half the estimated numbers of white high-income children with that Pb-B level.) Table V-7 summarizes the distribution of children predicted to show Pb-B levels above 15 pg/dl by the strata for all SMSAs. The residential distribu tion of children is reflected in this table: black children are overrepre sented in the poverty and low income strata as well as in the inner city areas V-15 DUP040G09599 of the SMSAs. But the ubiquity of the exposure to lead at >35 pg/dl is the striking finding. There are no strata of children totally free of this poten tial health risk, which holds true for higher Pb-B levels as well. 11. NUMBERS OF LEAD-EXPOSED CHILDREN BY COMMUNITY-BASED SCREENING PROGRAMS In the previous section, the number of lead-exposed children was identic fiied and categorized by socioeconomic-demographic variables and prevalence of selected Pb-B leyels. In this section, we will discuss U,$. communities that have screening programs for identifying young children at risk. Elevated Pb-B level Plus elevated erythrocyte protoporphyrin (EP) in blood is the measure used for assessing this risk- Because these screening programs are defined geographically as to city, county, or states these programs and their locales come within the general meaning of the directives of Section 3.3.8(f)(1)(A) of SARA- In general, children living in these screening sites are considered to be at highest risk for lead exposure/toxicity, as we presently understand it. This section briefly discusses the Second National Health and Nutrition Examination Survey (NHANES IX;) to compare with the lead screening efforts used over the years, 3.. Lead-Screening Programs Before examining in detail the results of the various lead exposure screening programs operating in U.S. communities it is useful to consider how the screening programs developed and their current status for interpreting the results of these programs. An additional overview of the U.S. screening process is also presented later, in the chapter dealing with exposure abatement and related Issues, A comprehensive history of the public health aspects and operational characteristics was presented by Lin-fu (1985a,b). Screening activities were first mandated and supported by the 1971 LeadBased Paint Poisoning Prevention Act, and the actual project started in fiscal Year (FY) 1972. Shortly thereafter, the U.S, Centers for Disease Control (CDC) was given administrative responsibilities for these activities. By FY 1981, under CDC's guidance, screening in the United States had expanded to more than 60 programs and represented eight regions of the Department of Health and Human V-16 DUP040009600 TABLE V-7, ESTIMATED NUMBERS GF CHILDREN, G.E-5 YEARS OLD. WHO ARE PROJECTED TO EXCEED 15 a/dl BY FAMILY INCOME AND RACE IN ALL SMSAs, 19B4 4>->> cn <0 P O H* ooo o CM o CO o'* o> in Q3 csf CM PH 8 * o oVO a o CO;* o pH fs CM P) r> O o o .* ro>k . ' * *r--: CJ 2 #* fs CO in - CO f*. rH S- CO* Afi <*/ Pc .J'3' CM a> 0o CL. s- oo .E c 1. V) r-- <c (0 El . O o ooo f* VO co .< cn in tino to rH H o COA O o o>k . |S* f-v fH t- P O o o o c * k CM* CM o r* O CO r r-- . CO to iw ,H * r"" 10 >s *P r- Z O pH Ail <0 iPc 0) o !0 0 , `r* SE in SC H .'rrH V . tip O z p H<* r-i !>- O . Ajmf. r>CM iO j-i -2h 5- P |5 rH AH 'i'*--I` . <0 v)-;5P" C lvo' T' 0Z :JPPf"- iH. mv t'lC im o * C0 * CO CO c o (* p0 10 (A p-- (0 3 CQ -Q. O n. o o CO fk rH 0 so U e *~4 0 >% a (0 r-.OS s *0 u. 0) o kp r* x: 3 wv] Oo .# p* ** in rH rH O CO CM k CM rH : O o CO k CO CM CM CO Qo * %n CM is. rHI rH O to m CO rs CO fs pH U JZ r" u <0 r<--9 >P o m F- CM pH O O ^1* o to rH rH O is.*k to It o CO t k CM * rH 1 0) <p f Jc 3: HO* O o CO r-> pH O O m#k cy It pH * O o k * r>* pH CM OO Oo pH k COk fs o rH O cO in nt CO o r*r o fQ Tp<D0 >P o H* o& ta c sz op O O CMk ,k ; P 01 a ; (0 Sr o O u G rH m rH 3 B CM o co :: a. o 10 Q. to >s pi JO. ta -C rr (0 p u p o . . p -C >s . s _rH inM r j= p k rH rH i, .r' >- rH r>- CO 3z rH </> k TO <P |W < JZ 1--' -p (0 SC. o 4- Sp <4- w T3 3- C 0 O o O : CO t X3 Oo 3- .k- .k CO to k in P O rH rH in c CM Pv rH ta rH rH CM Vz TO P p 3 iC a. O o 0) U JT> u r-- X o OO O <u x: ;frr COM CO rH 1 c= .o pH fs. rH rH r 3 in < CO O P CO .3 ^0 as r-- jC 3 . P a. c o o r> to CM r-- (0 : va P *D 0) c <0 V) o oo os l- k 00 r>* : fc- .rr p - I1 o rr>' V) O t- CO p H ' i *r r~ 0 P a fs O* P e *> COm CO (0 P rH O 13 c c 0 iu rH o. C *0 t -O #0 a. k c *r p 0 x: i r-- r u <0 tn <P U :r-- , !' pO (O r o <u T3 o 10 P a CO <0 O x: x: i--. P P r x>a> in O oW H-> r x: :rH 3= MAM u r~ U <0 d -p o p- ; '3 3 <0 c ! .vft VA o !< < r i -P i i'Z S <0 te 0 tn *0 :3 <0 fr PU OC h- rH U0 V-13 DUP040009601 TABLE V-8. SUMMARY OF ESTIMATED NUMBERS OF CHILDREN 0.5-5 YEARS OLD IN ALL SMSAs, WHO ARE PROJECTED TO EXCEED SELECTED LEVELS OF BLOOD LEAD, BY URBAN STATUS, 1984 Characteristic Population Base Blood Lead Level Cua/dl) >15 >20 >25 In SMSAs >1,000,000 7,251,000 1,493,400 459,500 128,200 In Central .City 2,886,200 Not Ih Central City 4,364,800 901,800 591,600 301,700 157,800 86,200 42^000 In SMSAs <1,000,000 3,536,400 483,000 142,400 40,300 In Central City 1,504,800 Mot In Central City 2,031,600 301,100 181,900 93,800 48,600 27,500 12,800 In Small SMSAs 3,052,600a 404,200 113,600 31,200 National Total 13,840,000 2,380,600 715,500 200,700 aTotal Includes 6,800 children who could not be stratified by income and were not included in estimates for three Pb-B levels. result from four sources. First, different numbers of children in each cell of the original NHANES II data base introduce different levels of precision into the prevalences. Second, the logistic regression analysis only accounted for the reduction of lead from a single source, leaded gasoline. Any reduction due to lowered levels in foods was not accounted for. The reduced amount of lead in food among the 30 strata of children cannot be calculated with available 'data; therefore, it is impossible to factor this reduction for the strata into the logistic regression analysis. Third, the total number of all U.S. lead-exposed children has been under estimated due to the exclusion of sizable national population segments. The calculations made did not include children of Hispanic and "All Other Races" origins who live in SMSAs. They were excluded since no reliable prevalences could be calculated for them;. In a considerable number of SMSAs, particularly in the West and Southwest regions of the country, these children account for larger totals than black children. Although no complete data sets are avail able for children of Hispanic origin, nor for any other significantly large race/ethnic origin groups, it is reasonable to assume that the association between high Pb-B levels and poverty would hold for such groups. Cultural and other differences are still undefined in terms of Pb-B. Finally, it should be V-14 DUP040009602  .J it 1>U <COn III rH MU64j6:a3** 6g 4 mSZ W i- C o ixn LU CO 114 OZ 3< >-t LU CO CD LU I-- -* CD - LU O O J LU < "D C CD feg SC CL. LCUD LU Cg LU *C CD CD CO :c z u ID rH ZL All 00 C00 413: a. oo s0- JD E 3 Z. : o o on o in St' cm o rH CM rH o St OO o rH fr* rH 0* IX St rH rH oo o VO CM o00 P CO CO uo t*. CO CM to o o <0 m O CSI to O *t o CM rH o in * rH CD O mJ Z CD CD LCOg ZH <C > LU PH > -J O CM to A CM Lf) LU Cf CD X 13 fig !l|. rVH -Gwm* O ''pZ*j h nr to so A LzeUg <c M. ,bw-4j:,xi! '1 S<CinO. X^i ::lil'zf-H: [ rH .LU D- ] A CD Le0g -UJ-i <Xc LU ZCxDO L8 M. >03 *- Z <V CLUD r03- &3E h- "s Z' r3-Cui :x : * st fN. CM O 4k CO rH ICL--iOJ U0 UC.cJC3DJ', ! 2|[> -0LJJ3J CD C0J3D' ! <t i J-H 1: !1 XSi :aaCB --< >i p-Gm CortDj eg U> , ;:! l oO 4pU*3-C= vn- v O O to CM st o -ovw oo ->y ; CO rH Oo Oo k CMk SrHt CM OO COm O,4k CM CO H D.(1Dg0 O <0 00 O (- o o st CO * CM rH 4k St o o <CC6MMM St OrH1 O V0M* 3.e: ** o oo 03 in O Oo . !> <h pH St o Oo St r*> rH O O co * . *t rH co rH o t*. rH rH oosv oo CrHO o o 4k CM,4k frHs st o S0,4*k M41 CM CSOt MpU10> eo O-pu 4to4 foi- Oo o o on r-< .p C0 tn c m *t X AH 0 u. o E . u oO o o -. f** r* c o pH in , rH 44 r- p" O P- CMft* st rH St CM i 0 pH o O L. . 0k * 1; +4 <*- co rH i V o CD -C to :.0. 0 -*r *f* 4CDO <A p t O o : .3 CL S.t0k 0k O CM * 1 s Q. .'i a) r>- CM CM st i J !'1; T3 P p<--0 CM CM P0 V) +4 CM CO Cc7> o o CO 0* .00 0 <VI tfl CM CO CM X rH C 00 o 4*r4- IGD <0 0 o owk o trHo PO OOrH* -St 8kM rH O .4* oo w CO st : i r3-- i: <Qaw.. :: t0u* i 4co0S04r~ rrs X wrvH c *or'rp*rS rH ' SpHt OO sot* fx4k oo tfro. to0k pH o :rH .40r4 3L AN Dg PU0" m r* oroH St to4k H a 4to4 o rH poHo 4k rH took CM ur404 }--o p0> OC 40r4" .Z 1 f0l | 8I11 | i *IU|811 fl 1 Va0). 44 !-St pH z4.0C4 ! 063. 0 pMt0op s404 trA- ;-44 jrpc- V) <iXn rr4003C*CaO*4pL.. f+m04m 4O4 J44t fot*- 4004 0o -3pp 0 < 43X e *40or4 E 3t0o .44 O C 0k c 44r "O0 4DDs to 4<40 O u v-ii DUP040009603 TABLE V-6, ESTIMATED HUMBER OF CHILDREN 0.5-5 YEARS OLD, WHO ARE PROJECTED TO EXCEED THREE LEVELS OF BLOOD LEAD (pg/dT) BY FAMILY INCOME AND RACE IN SMALL SMSAs, 1984 Family Income/ Race Number Pb-B ua/dl >15 >20 >25 <$5,000 White 249,700 59,700 17,200 4,500 Black Total** 100,200 349,900 56,600 116,300 23,000 40,200 7,400 11,900 $6,000-14.999 White 741,000 97,800 25,200 6,700 Black Total^ 141,100 882,100 56,900 154,700 19,200 44,400 5,600 12,300 6$15.000 White 1,670,800 96,900 20,000 5,000 Black Totalb 143,000 1,813,800 36,300 133,200 9,000 29,000 2,000 7,000 Unstratified Total 6,800 * ** National Total* 3,052,600 404,200 113,600 31,200 aSM$As with less than 1 million population except Nassau-Suffolk, NY, which has more than 1 million but no Central City. ^Totals by addition, not estimation. *No estimates possible. In Table V-8, the overall findings show a 1984 child population of about 13,840,000 living in SMSAs. Of these, 2,381,000 are expected to have Pb-B levels above 15 pg/dl, indicating that about 17% of the target population is at risk for adverse health impacts from lead exposure. About 5% of the children would be expected to have Pb-B levels above 20 pg/dl and about 1.5% would have Pb-B levels above 25 pg/dl. Before discussing these findings, their limitations as "national totals11 must be emphasized. These limitations include both underestimates and overes timates due to the methodologies employed. These estimation uncertainties may V-12 DUP040009604 TABLE V-3. PROJECTED PERCENTAGES OF CHILDREN 0.5-5 YEARS OLD ESTIMATED TO EXCEED SELECTED Pb-B CRITERION VALUES BY FAMILY INCOME AND RACE WHO LIVE IN SMALL SMSAs, 1984 Family Income/ Race >15 pg/dl >20 pg/dl >25 pg/dl <$6,000 Whi ter 23.9 6.9 1.8 Black 56.5 22.9 7.4 $6.000-14,999 White 13.2 3.4 0.9 Black 40.3 13,6 4.0 2$15,000 White 5.8 1.2 0.3 Black 25.4 6.3 1.4 aSMSAs with less than 1 million population. In a second attempt to geographically specify lead exposure, projected prevalence estimates were calculated for the four major regions used in the original NHANES II survey: Northeast, Midwest, West, and South. However, statistical projection data could not be established for these regions, this was due in part to the small numbers of children with higher Pb-B/levels in some regions, such as the West. If these small numbers had been used to calcu late prevalences in the region, some prevalences would have had unacceptable margins of estimating error. Consequently, in this report, we provide the updated Pb-B prevalence calculations for selected pb-B levels and the nation's urbanized childhood lead-exposure status for each of the 30 socioeconomic/ demographic strata described earlier. Tables V-4, V-5, and V-6 present the results of applying the estimated prevalences of the 30 strata of children in all SMSAs. Table V-4 depicts chiTdren living inside central cities for the SMSAs where such division was possible, and Table V-5 shows the children outside central cities in these SMSAs. Table V-6 shows the findings for smaller and paired SMSA child popula tions. A partial summary of these three tables for children with Pb-B levels above 15 pg/dl is presented in Table V-7. Table V-8 presents overall summary data. V-9 OX"A a b n -H .cn a O 3 :Q cP CA ft 0da1d: >' (A fit w --h 3 01 C-d+a -d* o -* *< CP 3' 00 o 3 01d a* 3 : Q. c p CO --! CL O S*1 O c p (A cP L--Cd+p AaLid -d* : 0i o3 a3* "O' o cP T3 3C 3-d* O mM< 01 n 0> M ID CM*l* cp CD , cn (A r *j*i 3 0 o 3 . dad ID --3ad | ID TT:' 5 o ,4b . 00 O cip w tfi ID , 'PSli'l! !.! o O 3' fP 3-It * 3* c p 01 3" (A to ID o M T3 01 .M* 3--1 -3 01 ' H* O --4 tod: -cdp* o dt o o. 3'. : 3' o /-\ ">; j to .A M "O idCO O ' ;0D S3ad* *3 c--ad.1 : o 0 0 3 CL .e-d+a 0 CO 3 ro z CO **. > 0 (J1 (0 (A -d: ' o o $--1. CadLt <"p 3 ' 3 (Q rOl rp -pdt n CD p 01 *w ai o CO -d!*4 00 o o ro o 4b dai . CO amd 01 0 3T M O! .a* o o 4a dM 00 o M dO >4 fO 4b o o v H* str tn 3-d o o 09 cr> .VCO CJi o o -> O! o o o ,tC* O o o ro o O <* HH o 3' fSJ d -d t~J < rP (A 0* a--fo CD CO 4b 4a -CO o 4b .Cl CO ro Ol (0 X3 *!S Oo ro o H* O CO o CO o o c o o o o C <+ <A U ,-d .r-a** CL 0 o O 0 3 ID O ;idM ro scan d Mcn .tMit M ro .>4 b rP 00 01 o ci "J o o o \f-* 01 o o 9 o 3' -Oii i dii ft b ID 3 <A . CJ o M i|id ilii^J 9 -jit CO -fb <ron ! , ** M . .ro o-5 !!! i o Oo oo 3-o3 <9 MV M WZ 05 cn l-.olso <HC Oi tO O -9 * >o0 o vcn oroo 0 .0-a9d rP :01d n n n* cn sC o ar o ,^p oi M 4a to CO to 4a M ro ro CO 00 c n CO . dS4 ro to CO o O- o o o - M O cn -9 .an 00 M 9o 9o 4a CO ^4 o CO M i- .at*o cn Oo o9 M M cn o 9 m00 cn CO \o >4 ro ooo 9oo 00 CO 4a CO 00 4cnb CO CO CO .9 CO ooo oO9 ro M i> .00 M w 4k .t* --CO 9 to o oOo ooo CO Oi CO 00 1* t0* 0 do >4 - o oo O O o 9 ro *4 ta doro -- o00 o 4ooa -4b oO -4 0 JmQm9U f+ ta 0j n 7? n A -VP 9 *- m 39 o H* o 0 nn 01 a -as 0i --dj>*i o SC ID t-A 3 O 0 3 0 Ss ' -H CD r* rti 09 < r* 4a o a ro H* M 4a CO wCO ro dO - AO o o ooo M CO --ro w wo Cli to 9 ooO o9 4a CO .ro -ar* o u 4a oo o AO to o M CO O ro 9 to Vj 9oo Ooo . Z !; C 3 ID 'J r* m > rn cn 3 --1 | OH :3 3> 3H <q m S C3 a. " :w G '3 08 09 -< m IPO m to 3> 3O V nrid-* "n . cr -< o z MH T9 ifi 3 I cr> V T-.O3(A ro tS_` o0 A Sal-* CL - 3 z roa O aa Zm :ai;m.dz 3> ZO 9 cn ya > cin .""9 m -< m 1:---:r*1 > V < (A rcon z o 9 r* o 9 ocn CO 4a 9 rcon to d CO 4b 4a o o oO9 * OJ ro ro CO to d 4a .CO CO to 4a o oo 9oo M L-* ccon o --.9 rs> dto -n J v4 o oo O O o 9 - 4 d4 CO 9 dSI ocn 9 N4 O O CooO z c 3 3 m n V Mcn "O (A 3i 3cn 3> V ro t: iv o0 M a3 V rcon z h-4 SC oo m > O 73 mm liaS1 ' -3H0 "3O0 >O r* Cd m oo i-i --i -4 rn L-4 O m o H- zm X CA O Zm ca m >9 'f.ilfitA 0JCC 38 iiiF'iili rn J'to r- oo 4a m< 9m* CA m9 DUP040009606 Analysis (J. Schwartz and H. Pitcher) performed a statistical procedure called logistic regression analysis to update estimates of prevalences to 1984 and produce prevalences at the selected criterion values of >15, >20, and >25 pg/dl for SMSA populations of children in the required strata. A detailed discussion of this logistic regression/projection methodology is presented in the second, part of Appendix G. ^ 2. Results Tables V-l and V-2 give estimated prevalences of Pb-B levels in children above three selected levels; 15, 20, and 25 pg/dl within the strata. Tables V-l and V-2, respectively, show these rates for "Inside Central City" and "Outside Central City" categories. Shown are three family income levels to indicate relative poverty, and each income category has two classifications by race. Each of these 6 strata is further divided into "SMSA with population 1 million" and "SMSA with population <1 million." In 122 SMSAs, we had 12 strata available to us, and each strata gave us three prevalence estimates. TABLE V-l, PROJECTED PERCENTAGES OF CHILDREN 0.5-5 YEARS OLD ESTIMATED TO EXCEED SELECTED Pb-B CRITERION VALUES (pg/dl) BY FAMILY INCOME, RACE, AND URBAN STATUS, WHO LIVE "INSIDE CENTRAL CITY" OF SMSAs, 1984 Family Income/ Race >15 uo/dl <1 M SI M >20 pq/dl <1 M SI M >25 pg/dl <1 M SI M <$6,000 White 25.7 36.0 7,6 11.2 2.1 3.0 Black 55,5 67,8 22.8 30.8 7.7 10,6 $6,000-14,999 White 15.2 22.9 4.0 6.1 l.! 1.5 Black 41.1 53,6 14,1 19.9 4.1 5.9 S;$15,000 White 7.1 11.9 1.5 2,5 0.4 0.5 Black 26.6 38,2 6.8 10.4 1.5 2.2 aSMSA with population <1 million (<1 M) and SMSA with population SI million (SI M). - V-7 DUP040009607 TABLE V-2, PROJECTEO PERCENTAGES OF CHILDREN 0.5-5 YEARS OLD ESTIMATED TO EXCEED SELECTED Pb-B CRITERION VALUES (pg/dl) BY FAMILY INCOME, RACE, AND URBAN STATUS,a WHO LIVE "OUTSIDE CENTRAL CITY" OF SMSAs, 1984 Family Income/ Race >15 ufl/dl <1 M 1 M >20 uo/dl <1 M '' 1 M >25 ua/dl <1 M 1 M <$6,000 White 19.2 27.7 5.6 8,4 1.6 2.3 Black 45.9 57.8 17,9 24.5 6.1 8.4 $6,000-14,999 White 10.9 16.8 2.9 4.5 0.8 1.2 Bl ack $15,000 White 32.4 43.7 4.7 8.1 10.7 15.4 1.0 1.7 3.2 4.6 0.2 0,4 Black 19.5 28.9 4.9 7.6 1.1 1.7 aSM$A with population <1 million (<1 M) and SMSA with population SI million (SI M). Table V-3 shows the more limited number of strata and the relevant sets of prevalence estimates when Inside/Outside Central City status could not be ascertained. This applied to 196 SMSAs: 34 paired, 161 with populations below 200,000 (with very few exceptions), and Nassau-Suffolk, NY, with a population over 1 million but no central city. The NHANES II Pb-B levels reported and used in calculating prevalences for criterion levels are based on Pb-B determinations for all cases--they are not influenced by initial erythrocyte protoporphyrin (P) determinations and, for cases with elevated EP levels, subsequently selected Pb-B determinations. In earlier analyses, we attempted to apply the national, urbanized compos ite prevalences to each of the SMSAs with the appropriate qualifications as to their reliability. This approach was attempted to best respond to the directive of Section 118(f) that asked for ranking of individual SMSAs. When the scien tific community was reviewing this approach, however, problems were found with the level of permissible disaggregation due to the sample design of the NHANES II survey. For example, the national source-based differences that were implicit but not specific in the original analytic process could not be broken out and reassigned in disaggregation. V-8 DUP040009608 (3) The population in some SMSAs could not be separated by the urban status, 11 Inside Central City," and "Outside Central City." One SMSA did not contain any population center meeting the census definition of "Central City", end the tape failed to distinguish central city residents from all"others for the 17 merged pairs. This necessitated presentation of our findings for three SMSA sets of estimates and also required reanalyzing NHANES II data to accom-^ Biodata this problem since originally the NHANES II data available required stratification by these variables. The data we present is limited to young white and black children because the NHANES II survey did not include enough children of Hispanic and "other race" origins for calculating reliable prevalences. NHANES III plans to correct this but the field work is not scheduled until 198$. Tabulating the tapes for 1980 gave us the distribution of young children in two race and two age categories (0.5 to 2 years and 3 to 5 years) by urban status and family income groups. A further stratification variable, the size of an SMSA's total population as either over or under 1 million, was also known. We applied these 1980 distributions to the number of children established as the 1984 child population 0.5 to 2 years and 3 to 5 years for the two races (see below for construction pf 1984 populations. The two age bands were merged later when prevalences were used.) The 1982 recession and its effect on the economic status of the population (family income) could not be taken into account, since there was no method of establishing its impact on each individual SMSA. When interpreting findings, remember that the actual 1984 distribution by income contained larger proportions of the population in the lower income categories. This is of crucial significance since income is an independent variable in the distribution of Pb-B levels, with the lower income segments of the population constituting a larger proportion of all groups with elevated Pb-B levels than do higher income groups. The most recent natality statistics available were for 1984, and we compiled the white and black child population 0.5 to 2 years and 3 to 5 years as of 1984 by the following steps for each SMSA, We established the actual census counts of children up to 2-years old in 1980 and added to these counts the resident live births minus infant deaths for 1981. This gave us the age group 3 to 5 years. Natality and infant death data were obtained for 1982, 1983, and 1984. The numbers for 1984 were divided in half to yield the 0,5- to 1-year olds for the 0.5- to 2-years-old group. The Census counts and natality V-5 DUP040009609 and infant mortality data ware all available by race. The Division of Vital Statistics of the National Center for Health Statistics supplied the published data for 1981 (US0HHS, 1985a, 1986) and printouts of the as yet unpublished data for the more recent years. Further stratifications (other than race* age, and site of SMSA) that were employed by NHANES II were accomplished by applying the distributions for y Inside/Outside. Central City and three categories of family income as found in the 1980 Census counts for children then 0.5- to 2- and 3- to 5-years old. For example, in a given SMSA, 75% of the black children 0.5- to 2-years old in 1980 lived inside the central city and 25% outside. We applied these percentages to & the black children 0.5- to 2-years old In 1984 in that SMSA. For the 75% living inside the central city in the 1980 Census counts, we established the percent ages for each of the three family income categories and applied those rates to the 75% of the black children 0.5- to 2-years old in 1984. We repeated this process for the 25% of the children outside the central city. Using this process, we could establish fhe J.9S4 child population strata by NHANES II characteristics in each SMSA. We established 24 strata for those SMSAs where the data user tape included details on Inside/Outside Central City residential status. Since the SMSAs population size, over or under 1 million, was also a stratification variable in NHANES II, we established 48 strata for the two larger types of SMSAs. As noted earlier, the data tape did not permit Inside/Outside Central City stratification for smaller and paired SMSAs, and we could establish only 12 strata for these SMSAs. A total of 60 strata resulted. When the two age bands were merged, 30 strata resulted Tor estimating numbers at the selected criterion levels of Pb-B. The NHANES II analyses originally summarized and published Pb-B levels that did not include all the levels of interest to this report, namely; >15, >20, and >25 pg/dl. Chapter IV discussed the rationale for selecting these levels. Further, the original NHANES II prevalences were calculated for 1978, and applying those rates to 1984 populations would overestimate children at risk. These 1978 prevalences are no longer accurate because total lead burdens in the environment have been reduced primarily by the decreases of lead in gaso line and to some extent in food. The NHANES II data shows the impact of the gasoline lead phasedown over 1.976-1980. Because the amount of lead in the environment continues to decrease, a method for projecting prevalences from 1978 to our reference year of 1984 was necessary. Therefore, EPA's Office of Policy V-6 DUP04000S61Q U.S. Bureau of the Census in 1980. The updated and more recent definitions. Metropolitan Statistical Areas (MSAs) and Consolidated Metropolitan Statistical Area (CMSA), could not be used for methodological reasons. We selected 1984 as the reference year for estimating the number of young children at or above selected Pb-B levels because 1984 was the most recent year having all the required counts available to us. The child population data for 1984 give the potential number of children who may be at risk for adverse health effects from exposure to lead and helps us to assess the site of these risk groups across SMSAs. However, this method does not provide a quantitative assessment of the number of children with elevated lead exposure. To estimate the number of children who will have elevated lead exposure, we need data that provide prevalences for each of the demographic and socioeco nomic strata within the child population, which can be applied nationwide. Such variable prevalences are needed because the exposure levels are known to vary significantly and substantially between strata, and an "average national pre valence11' would not estimate accurately the number of children at risk. Findings from the second National Health and Nutrition Examination Survey (NHANES II) give such prevalences since they provide a nationwide picture of lead exposure in children and adults. The NHANES II data base has been used to estimate the number of children and other risk populations having Pb-B levels in the range covered in this report. 1. Estimation Strategies and Methods Three basic steps were involved in the estimates: (1) enumerating the total number of children in each SMSA and allocating them to the selected strata as defined by age, race, income, and, where possible, urbanization categories to match the strata employed in the NHANES II analysis; (2) summing specific SMSA strata populations to obtain national totals for each stratum; (3) multi* plying each stratum population (national total) by the prevalences for the three selected criterion Pb-B levels, after adjusting prevalences from their 1978 levels to 1984 levels, to account for the reduction of lead in gasoline. The NHANES II survey reported prevalence of Pb-B values as a function of socioeconomic/demographic and ethnic strata of children across the nation, but not for specific geographic population clusters, such as SMSAs or cities, or legtl entities, such as municipalities, counties, or states. For example, we V-3 C^n consider white or black children residing inside the central city of an SMSA. with a population of over 1 million who were aged 0.5 to 5 years and in a family with an annual income of less than $6,000, but we cannot consider children in the Springfield, IL, SMSA. The NHANES II data show that Pb-B levels are more similar in children who share the characteristics of a particu lar stratum across the country than children of different strata who live in the same local area. ./ To apply the NHANES II prevalences in a statistically valid manner, we sorted out the SMSA child populatiohs as provided by the 1980 Census tapes into the population strata used by NHANES II. However, since we were interested in child populations in 1984, a more recent year, we proceeded as follows. The actual counts from the 1980 Census are available on data tapes from the U.S, Bureau of the Census. However, these tapes contain selected parts of the information. We used a tape called "Public Use Microdata Samples," which contains the counts for all the 318 SMSAs defined for 1980. To present users with a manageable data tape, the U.S. Census Bureau omitted some of the detail for some of the data units, creating several problems for us. (l) The popula tion figures, originally exact counts, had been rounded off to the nearest hundred. This became a problem when working with the data for black children since the total number of black children in many SMSAs is quite small,, and frequently their distribution among the required socioeconomic strata results in totals below 100 in a given stratum. In these cases, the tape showed zero as the number in one or more of the race/age/urban status/family income catego ries. This left us without a basis for assigning proportions of children into strata, and consequently we could not estimate the numbers of children at selected criterion values of Pb-B for these particular eases. This proved to be a particular problem in SMSAs with populations of less than 200,000. This particular problem of allocation is less significant when SMSAs are viewed collectively and not individually, as we had originally hoped to be able to do. (2) In the available data tape, 34 of the SMSAs were merged into 17 pairs; making it impossible to separate the data for the pairs. These 17 pairs are listed in the introduction to Appendix C, The selection of the pairs appears to control for geographic location, population size, and other characteristics. Examples of such pairing are Bangor and Lewiston-Auburn, ME, and Midland and San Angelo, TX. These paired SMSAs account for all except one SMSA with popula tions below 100,000. V-4 DUP040009612 V. EXAMINATION OF NUMBERS OF LEAD-EXPOSED CHILDREN BY AREAS OF THE UNITED STATES Section 118(f)(1)(A) of the Superfund reauthorization legislation calls for an estimate of the numbers of children exposed to lead levels high enough to cause adverse health effects. The numbers are to be arrayed by Standard Metropolitan Statistical Area (SM$A) or some other geographical unit. As noted in Chapters II and IV, exposure can be defined as the level of lead in whole blood (Pb-B), and "exposure sufficient to cause adverse health effects" is defined as a Pb-B level at or above which such effects are mani fested. The specific reference Pb-B values, which we use to define adverse health effects, were presented in Chapter IV. In Section 118(f)(1)(A), lead exposures are defined in terms of adverse health effects as we now understand them. Since the levels of acceptable lead exposure in terms of blood lead con centrations are continuously being lowered in response to new evidence of lowlevel lead effects, these indices may decline even further. The reader should bear this in mind when examining findings in this and other chapters in the report. Low-level lead effects occur across a range of Pb-B values, that is, 10, 15, 20, and 25 pg/dl, and these ranges are considered where it is appropriate. The obvious response to the Congressional directive (i.e*, tabulating Pb-B levels gathered for each child in each geographical unit) is not possible at present. Such information does not exist at this time. A response would be easier to achieve if current data representative of the prevalences of Pb-B levels in highly defined geographical areas and socioeconomic/demographic strata within those areas were available, but here also, information is not readily available. We then are required to base estimates on whatever informa tion is available. To evaluate lead exposure, i.e., elevated Pb-B levels in populations, we used "enumerations11 or actual physical counts of subjects, or else the most reliable derivations of numbers based on estimates for groups. For estimates. V-l DUP040009613 we can employ Pb-B prevalence modelling in tandem with population strata. When combined these data give estimates of the number of subjects that have Pb-B levels above different Pb-B criterion values, whatever these criterion values actually mean in terms of toxicity or toxicity risk. As a simple example, we can determine the actual numbers of children stratified by certain socioeccinomic/demographic categories at a national or other level, based on census enumerations. If a second data set tells us that children in one of the above y categories have a prevalence of 25% for Pb-B levels above, say, 15 pg/dl, then a simple multiplication of the census number by the prevalence fraction gives us the number of children estimated to be at Pb-B levels above 15 pg/dl in this stratum. for enumerations, we will present the number of children actually identi fied with elevated Pb-B levels in various screening programs. Since these pro grams were conducted in discrete geographical locations, their results can be included as a response to the Congressional directive. Estimates and enumerations appear in Sections A and B, respectively. In working with available data, we found that we could also quantify the U.S. Census-enUmerated children in each pf the 318 SMSAs who may have been exposed to lead through leaded paint in their houses or housing-related environment. Although the report presented in Section C for these children differs from the reports in Sections A and B, insofar as we cannot assess actual exposure through their Pb-B levels, they represent actual, essentially metropolitan depictions of child exposure risk for leaded paint-related exposure as of 1980. In their case therefore, we are combining a geographic variable with a source variable. Section D summarizes the various exposure examination methodologies and their respective results. A. ESTIMATED NUMBERS OF LEAD-EXPOSED CHILDREN IN SMSAs BY SELECTED BLOOD LEAD CRITERION VALUES In this section, we estimate the number of children living in the SMSA segment of the country who have been exposed to lead at levels large enough to affect their health. We focus on the risk of urbanized populations in the United States, rather than the entire population, since Congress judged this population segment to be of concern. To enumerate this urbanized population, as described below, data was used on children in the SMSAs as defined by the V-2 DUP040009614 the Interested reader is referred to a comprehensive review of this work In Air Quality Criteria for Lead (U.S. EPA, 1986a, Chapter 12). We have a rather good understanding about the persistence of the effects induced in the heme biosynthesis pathway when exposure is maintained. In popu lations at high risk for lead exposure, EP elevation is a chronic problem (see U.S. EPA, 1986a). Furthermore, elevation of EP can persist beyond early childhood. Persistence in EP elevation is particularly likely in cases where Pb-B levels remain elevated because of resorbable bone lead. One need only examine Figure IV-2 to realize the potential for extended persistence of effects in a myriad of other systems, when the heme pool in the body remains disturbed. In summary, then, and in response to the relevant language in Section 118(f), we can state that various adverse effects of lead do persist, or can potentially persist, over extended time periods. Furthermore, such persistence need not be of long duration to have implications for future deleterious effects on physical and psychosocial development. IV-25 DUP040009615 TABLE VI-2. Age Group (yr) SUMMARY OF Pb-B LEVELS (pg/dl) OF A RELATIVELY HOMOGENEOUS WHITE POPULATION IN THE UNITED STATES*b Bj. ' x.Bil a:,, Geometric Mean (pg/di) Median (pg/dl) 99th Percentile (pg/di) Geometric Standard Deviation (pg/dl) _y" 0..5-6 6-18 .18+ (Men) 18+ (Women) 12.9 10.6 14.7 10.0 13.0 10. Q 15.0 10.0 32.0 24.0 35.8 23.0 1,43 1.46 1.44 1.46 "Adapted from U.S. EPA (1986a). EPA internal analysis of ayaiTable NHANES II ItLa sets. "Sample size (vertical order): 752, 573, 922, and 927. From a toxicological standpoint, the distribution of lead levels within target organs (the Central nervous system of children, for example), as a function of a given Pb-B value is important for illustrating the distribution phenomena. These distributions are not found in present epidemiological approaches to lead exposure. However, their importance can be seen by studying another metal toxicant, cadmium. Kjellstrom (1985) discusses target organ distributions of cadmium (measured in vivo) including biological indica tors and population dose-response curves. The distribution of lead in major body components such as bone is another important biological factor, because lead can become mobilized and re-enter the blood (Chapters III and IV). The characteristics of this distribution in young children over time are of particular interest. 3. Human Behavior and Other Factors in Source-Specific Population Exposures to Lead In the relevant literature, discussed in detail by U.S. EPA (1986a) and in critical studies and reviews cited in the EPA document, we find that, given a specified and significant degree of external lead contamination, a number of socioeconomic/demographic variables can affect the relationship between lead in the environment and blood in children. The interrelationships of several of these variables can amplify the degree of adverse interaction between the Vl-8 DUP040009616 BLOOD LEAD LEVELS, ms /AI Figure VI-1, illustrative log-normal Pb-B distribution curve. Values from WHO (1086): Median 10.5 ng/div 98% * 20.0 ug/dl. Shaded area * 2%. How do these estimates fit available information on the recent or current median Pb-B values for adults in the U.5. population? In the WHO/UNEP world survey of Pb-B levels, included in the Global Environmental Monitoring Survey (GEMS), the u,S. adult median Pb-B level in 1981 was 7.5 pg/dl (Friberg and Vahter, 1983), judging from the various projections and other data from the U,,S. EPA (1985, 1986a), this median Pb-B value has declined in recent years. For a given Pb-B level and a given cumulative frequency, the values for children would probably be higher than for an adult population, because distri butions of Pb-B levels among members of a population are also age-dependent; that is, young children have a different distribution from adults, especially in heterogeneous populations. Adult/child differences occur even in rather homogeneous populations. U.S. EPA (1986a) shows these differences using NHANES II data (Table VI-2). VI-7 DUPO4O0O9617 in food, for example--we cannot identify any specific inputs; we can only say that human activity, collectively, adds considerably to lead levels. The relative impact of these lead sources varies greatly, both by source and by different geographic/demographic/socioeconomic strata. These strata refer to numbers of subjects and not necessarily to the intensity of exposure at a contaminated site. Any population of children having significant contact with lead in dust and soil is also highly likely to have significant contact with lead in air and paint. This category, however, is mainly included to identify a significant pathway for childhood lead toxicity and to evaluate the source for dust and soil in linkage with its primary sources. ; 8. NUMBERS OF CHILDREN EXPOSED TO LEAD IN PAINT Many reports address the role of leaded paint in lead poisoning and con sider paint lead poisoning to be a public health issue (see, for example, CPC, 1985; U. S. EPA* 1986a). The cause-and-effect relationship of leaded paint to severe lead poisoning dates back many decades. Evidence has long been available to show radio-opaque (lead) paint chips in the abdomens of children who had both high Pb-B levels and severe poisoning and who had not been in contact with any other source of lead. Although the total number of acute, very severe U.S. cases of lead poisoning has declined greatly, the basic epidemiological picture characterizing paint lead-associated toxicity has not materially changed for chronic interaction. The problem can still be described as it has been in some recent studies. In their prospective study pf inner-city children in Cincinnati, OH, Clark et al. (1985) found that child Pb-B levels varied across housing categories and children who lived in the worst housing had the highest Pb-B levels. The housing-quality category accounted for more than 50% of the Pb-B variability in 18-montH-old children. In a prospective examination of Baltimore children treated for lead toxicity, Chisolm et al. (1985) observed that children returned to housing where work had been done to remove leaded paint showed significantly higher Pb-B levels than children returned to public housing free of leaded paint. Furthermore, little decline was noted in the Pb-B levels of children who lived in lead-abated units over an extended period--indicating that current efforts to abate lead fall short of public health goals. Both lead paint-contaminated and deteriorated housing units are included in the lead VI-10 DUP04000961S child and the contaminated environment. Such factors affect the relative results that investigators find in relating such exposure indices as Pb-B to some measure of adverse effect. For example, one can understand that if children are residing in a heavily contaminated environment and are at the age when they are orally exploring their environment, then the degree of lead exposure via such exploration will be influenced by parental attention to child activity, extent of mouthing, and ingestion of lead-containing material. We ? might then expect inverse relationships between quality of parental care and degree of lead exposure and some measure of outcome, at least under conditions of moderate lead exposure. Such studies, however, do not imply that lead exposure does not occur or does not significantly contribute to an adverse effect. They simply imply that the degree of exposure interacts with other factors. Examining modifying factors for scientific reasons is appropriate and necessary, but we should not assume that it will neutralize the effect of lowlevel exposure in the overall lead problem. These assumptions would be illogical add can detract from a simple rule of health risk management: abating the:lead sources removes or reduces the risk for all children, whatever their socioeconomic or demographic status. Such caveats against misinterpreta tions of the above-noted studies are even stronger when we examine the signif icant rise in the number of lead toxicity cases associated with urban "gentrification," where children of upper socioeconomic status families reside in lead-contaminated environments formerly occupied by children of lower socio economic status (Rabinowitz et al., 1985). 4. Organization of the Chapter In the main body of this section we estimate and discuss the numbers of children exposed to six different lead sources: paint, gasoline combustion, stationary emissions, soil or dust, water and food. We do not include rela tively limited sources of lead (such as exposure from painted toys or hobbies) or contact specific to an ethnic group (as seen in some types of folk medicine). This approach does not imply that these sources are unimportant In certain circumstances, particularly with newly arrived ethnic groups. However, these sources are difficult to quantify and do not affect the overall effect of the major sources of lead described below. For some of these six categories--lead VI-9 DUP040009619 There is a general dearth of nationwide studies that estimate the number of children living in lead paint-containing homes who have elevated Pb-8 levels, and much of the information relating leaded paint in the environment to Pb-B levels is not in a form suitable for our analyses. Reasonable data for our needs are available in two forms. The first is a comprehensive unit-by-unit screening conducted in Chicago in 1978 as part of the city's lead-screening program for that year. Although screening was confined to one metropolitan area, it was a comprehensive study, involving more than 80,000 housing units, to determine both Pb-8 levels and the presence of leaded paint in the chil dren's houses. The second approach projected (to 1984) prevalences from NHANES II data for Pb-B levels in those socioeconomic/demographic strata where paint is likely to be the major, if not entire, source of exposure. These prevalences were presented in the previous chapter. EPA's Office of Policy Analysis {U.S, EPA, 1985) used the Chicago data to estimate the likely percentage of children in Chicago (under 6 years old) who would have a Pb-B level greater than 30 pg/dl due to leaded paint exposure. Using estimates of the probability of lead in paint occurring in a home with a child having lead toxicity and the probability of lead in paint occurring in the survey housing in general--both parameters were determined in the Chicago survey--EPA employed Bayes' theorem to determine the probability of elevated Pb-B at the then current toxicity risk level. This prevalence value, 12.8% of all children in the survey, has limited use since it is a dated estimate, represents a Pb-B level too high fpr our present purposes, and may not represent a best estimate for that year.. One can, alternatively, use prevalences for more appropriate Pb-B levels than the rather high Chicago survey criterion value of 30 pg/dl. In Chapter V, prevalences updated to 1984 are tabulated at Pb-B levels of >15, >20, and >25 pg/dl for young children id various socioeconomic/demographic strata. We have taken the number of young children enumerated by the U.S. Census as living in deteriorated housing with 1C0% high lead paint, and applied the most logical prevalences for the stratum that would apply to Children in deteriorated housing. We assumed that children in 100% deteriorated, high lead-paint housing conform to the stratun that is in the inner city* in the densest population areas, and in the lowest income category. We also assumed that many of these children would be black. VI-12 DUP040009620 problem. These units have the largest exposures and they also represent affordable housing for a sizable fraction of inner-city children and parents. Public health officials have long viewed leaded paint as a lead source in the child's home. However, they should also consider older public buildings used as day-care centers, kindergartens, elementary schools, etc., as potentially serious exposure hazards, X. Estimation Strategies and Methods As indicated in Table VI-1, estimates of U.S. children exposed to lead In paint are based on degrees of potential risk and on estimates of the numbers of children predicted to have actual elevated risk because of paint-associated elevations ip their Pb-B levels. For potential risk of lead exposure via leaded paint, estimates are given for children living in units with leaded paint and children living in units with an elevated probability of actual exposure because of peeling paint, broken plaster, or other deterioration. The data sets used include calculations by Pope (1986) and the estimates of categories and numbers of lead-painted units with problems from the American Housing Survey of the U.S. Bureau of the Census, 1983 (U.S. Bureau of the Census, 1986), Pope (1986) first determined a child density factor for each unit (i.e., numbers of Children per lead-painted residence) by examining the child popula tion under 7 years of age and the number of housing units in the nation. The child-density factor is specifically the ratio of children under 7 years of age per 1000 housing units. This number, given by Pope (1986), is 287/1000 or 0.287. National figures for housing yielded a value for the fraction of housing units containing leaded paint as a function of age: pre-1940, 1940-1959, and 1960-1974, Furthermore, data from the American Housing Survey, U.S. Bureau of the Census, provide three criteria for unsound units that are relevant for lead paint exposure: peeling paint, broken of cracked plaster, and holes in walls. The data source also provides the fractions of the total units that these units represent. We therefore have estimates of: (1) the total number of children in homes with lead paint; and (2) the numbef of children in homes with leaded paint that are in disrepair, thus maximizing lead exposure. In addition to Pope's best estimate, we also used Pope's national upper bound. Pope also estimated children by four major regions: Northeast, Midwest, West, and South. VI-11 DUP040009621 of data, we then can obtain the percentage of all young children who reside in urbanized housing. This percentage is about 80%. In considering the numbers of children who live in deteriorated housing that contain leaded paint, Pope (1986) classified the housing according to Census Bureau designations for unsound housing within the three house age groups. Table VI-4 shows the best national estimate and the national upper' bound for children in deteriorated, lead-painted houses and the number of these houses as a function of age and condition, along with the totals. From Table VI-4, we can calculate that the best national estimate and the national.; upper bound estimate of children under 7 years old living in unsound lead" painted housing are 1,772,000 and 1,996,000, respectively. Table VI-5 shows young children exposed to peeling paint (the only sign of deterioration) in lead-based painted homes by the four major geographic regions, as given by Pope (1986). As expected, the older developed areas, specifically urban areas in the Northeast and Midwest, have the highest and next highest figures: Northeast, 174,000; Midwest, 139,000 for children in homes with peeling leaded-* paint as the survey criterion for deterioration. The South with 130,000 ranks third, while the West has the lowest figure, 77,000. TABLE VI-4. NUMBERS OF U.S. CHILDREN RESIDING IN UNSOUND AND LEADrB PAINTED HOUSING RANKED BY AGE AND CRITERIA FOR DETERIORATION3115 ' Unsound Category Age of Home Number of Unsound Lead-Based Painted Houses Number of Children Peeling paint Total Pre-1940 1940-1959 1960-1974 Pre-1980 964.000 758.000 250.000 1.972'ood 277.000 218.000 72,000 567,000 Broken plaster Pre-1980 1,594,000 458,000 Holes in walls Pre-1980 2.602.000 747.000 Grand Totals Pre-1980 6,199,000 . (6,|54,000)a 1,772,000 j (1,996,000) aAdapted from Pope (1986), bHousing data from 1983 Housing Survey, (U.S, Bureau of the Census, 1986). cChildren under 7 years old. ^National upper bound to the numbers. WT-.1 A DUP040009622 From the relevant tabulation In Chapter V, the Pb-B prevalences (Pb-B level percentage) for the 0.5 to 5-year-old/inner-eity/higher urban density/ lowest income/black stratum are: *15 pg/dl, 67.8%; >20 pg/dl, 30.8%; >25 pg/dl, 10.6%. 2. Results To estimate the total numbers of young children living in lead-paint hous ing, we can first estimate the percentages of housing having paint with lead greater than or equal to 0.7 mg/cm2 as: pre-1940, 99%; 1940"1959, 70%; and 1959-1974, 20% (Pope, 1986). Given a total housing inventory of 80,390,000 in 1980 <0.5, Bureau of the Census, 1983 Survey), we arrive at a final tally of 41,964,000, or 52% of all residential housing units have lead paint greater than or equal to 0.7 mg/cm2. This figure for the lead-paint concentration is based on the 1985 CDC statement (CPC* 1985), A count of children less than 7 years old in homes with lead paint is shown in Table VI-3, as given by Pope (1986). The national best estimate of the number of children in all leadpainted housing, regardless of the age or state of repair, is 12,043,000. The national upper-bound estimate is higher"13,579,000, When compared to the number of children ranked by age of housing and SHSA as given in Chapter V, and taking into account some differences in children's age in these two sets TABLE VI-3. NATIONAL BEST ESTIMATE AND UPPER BOUND OF NUMBERS OF CHILDREN UNDER 7 YEARS OLD IN LEAD-BASED PAINTED U,S, HOUSING BY AGE OF UNITS3 Estimate Type Housing Age Number of Lead-based Painted Houses (Thousands) Number of Children (Thousands) Best Estimate Total Pre-1940 1940-1959 1960-1974 Pre-1980 20,505 16,141 5,318 41,964 5,885 4,632 1.526 12,043 Upper Bound Total Pre-1940 1940-1959 1960-1974 Pre-1980 20,712 20,753 5,850 47,315 5,944 5,956 1,679 13,579 aAdapted from Pope (1986). VI-13 DUP040009623 lower bound to the child density per unit by simultaneously increasing the number of units* thereby offsetting distortions. The above estimates of numbers of children potentially exposed to leaded paint minimize the contribu tions to the total numbers that would arise from children exposed to lead because older housing is being renovated--the so-called urban gentrification phenomenon. Reliable figures for quantifying this aspect of childhood lead . exposure are not available. In considering estimates of these children exposed to lead in paint who have elevated Ph-B levels because of this exposure, we first chose to combine the numbers in Tables VI-4 and VI-5 for children in unsound, lead-based painted*; housing with the 12.8% of children >30 pg/dl Pb-B calculated by EPA for all children residing in these units who represent a large urban area. This approach gives an estimate of about 230,000 children; however, the relative accuracy is unknown for reasons already stated. Next, the results of using selected lower Pb-B criterion values--15, 20, and 25 pg/dl--using NHANES II projected prevalences for values that would be plausible for a group of children living in 100% deteriorated, high lead-based painted housing combined with base numbers of such children are tabulated in Table VI-6. The numbers for Table VI-5 are reasonable estimates but are still likely underestimates (see next paragraph). The rationale for assuming the demographic/socioeconomic profile of children likely to reside in such housing is also reasonable. The number of children in such housing having Pb-Bs above 15 pg/dl is around 1,200,000 while the corresponding figures for Pb-B limits of above 20 and 25 pg/dl are around 545,000 and 188,000, respectively. Numbers in Table VI-6 do not give us an estimate of exposed children in old housing with high paint lead levels but lacking specific criteria for deterioration. The totals in this case may be substantial, since Section C, Chapter V noted that many families in old housing are not in the central city and not in poverty and the homes of these children are not in a deteriorating state. For this reason, these figures in Table VI-6 should be viewed as possible lower bounds (pr underestimates) to the true count. Similarly, the stratum of NHANES II selected aj? appropriate for assignment of these children in order to obtain actual prevalences may represent percentages, after projec tion to 1984, which are actually from a mix of housing quality. In other words, the true projected"Pb-B prevalences for present-day children in 100% deteriorated, high lead paint housing may be considerably above that set of Pb-B prevalences actually selected for estimates in Table VI-6. VI-16 DUP040009624 TABLE VI-5. REGIONAL BEST ESTIMATE LEAD-BASED PAINTED HOUSING BY AGE AND OF NUMBERS NUMBERS OF OPFEECLHINILGDRPEANINTINUlUNiltNITTSpSOwUN UD', c,d Region Number Peeling Paint Number of Age Lead-Based Painted Houses Chi1dren Northeast A Total Pre-1940 1940-1959 1960-1974 Pre-1980 432,000 203,000 51,000 686,000 110,000 51,000 13,000 174,000 Midwest Total Pre-1940 1940-1959 1960-1974 Pre-1980 264,000 159,000 47,000 479,000 74,000 47,000 14.000 139,000 West Total Pre-1940 1940-1959 1960-1974 Pre-1980 92,000 127,000 44,000 236,000 27,000 37,000 13,000 77,000 South Total Pre-1940 1940-1959 1960-1974 Pre-1980 156,000 203,000 80,000 439,000 46,000 60,000 24.000 130,000 aAdapted from Pope (1986). ^Estimates of housing from U.S. Census Bureau (1983). cCbildren under 7 years of age. ^These figures do not include children in units meeting other criteria for unsoundness but only for peeling paint. One can ask whether these figures are not Actually lower bounds when com pared with estimates that might be made by summing, across SMSAs, all young children in the known socipeconomic/demographlc risk categories. Sums of the SMSA-specific tabulation in Chapter V, Section C, indicate that this is not the case. The estimates of housing (based on Pope) used here include non-SMSA housing stock. Non-SMAS housing should not be in any better condition than SMSA housing. For example* the fraction of substandard homes in rural America is about 41% (2+ million/5 million), according to Lerman (Economic Research Service, USDA, 1986). "Substandard" is technically different from "unsound" in these surveys, but the fraction of houses with peeling paint and cracked plaster as well as lead-based painted surfaces is probably significant in substandard rural housing. Toxicologically, these factors determine the level of lead exposure, not definitions of housing, per se. We may be placing a VI-15 DUP040009625 been lodged in ecosystems where it can lead to human exposure, for example, through dust and soil. A chronological look at such inputs is provided in Table V|"7, For the 10 years shown in Table VI-7, more than 1 million metric tons of gasoline lead were dispersed just in the United States. A comparison of leaded paint and leaded gasoline indicates the full, insidious nature of the lead problem. Leaded paint can cause very high ^expo sure, with overt poisoning, in a rather confined area and can also induce chronic toxicity due to lower persistent exposure. In contrast, lead from vehicular exhausts can cause sufficient exposure, related to chronic health effects, over a large area, Evidence showing that leaded gasoline was enough of a human health risk to require further regulatory changes in the existing ambient air standard was compiled in the 1977 EPA Air Quality Criteria for Lead (U.S, EPA, 1977). In addition to assessing the scientific literature related to leaded gasoline, the document also included concepts and perceptions that were then beginning to figure in health risk assessment and biomedical practice as applied to environmental health. Relevant environmental health phenomena, such as bipod lead distribution in the population, were discussed. Aggregate exposure to pollutants was defined and discussed. In addition, subtle adverse effects of lead--particularly as noted by the pediatric medical community--were examined. TABLE VI-7. RECENT CONSUMPTION OF LEAD IN GASOLINE5 Calendar Year Leaded Gasoline Volume (109 gal) Lead Consumed (IQ3 ton)0 1975 1976 1977 1978 1979 1980 1981 1982 1983 1984 92,5 87.0 79.7 75,0 68.1 57.5 51.0 52.5 47.5 43.8 167,4 171.4 168.9 153.0 129.4 78.8 60.7 59.9 52.3 46,0 Total 654.6 1,087.8 aFrom U.S* EPA (1986a). u Consumption in metric tons. VI-18 DUP040009626 TABLE VI-6. ESTIMATED NUMBERS OF U.S. CHILDREN LIVING IN UNSOUND,. LEAD-BASED PAINTED HOUSING ABOVE INDICATED Pb-B CRITERION VALUES3'0 Category Housing Age Total Children >15 >20 >25 Peeling pa.i nt Total P re-1940 19401959 1960- 1974 Pre-1980 277,000 218*000 72,000 567,000 187,800 147,800 48,800 384*400 85,200 57,100 22,200 174*500 29,400 23,100 7,600 60,100 Broken plaster Pre-1980 458,000 310,500 140,900 48,500 Hole in wall Pre-1980 747.000 506,500 229,800 79.500 Grand Total 1,772,000 1,201,400 545,200 188,100 3Total child count from Table VI-4. Selection of NHANES II stratum for use of specific prevalences fs discussed in text. Prevalences are from Table V-l> Using both of these factors, the true count of children with elevated Pb-B levels could be underestimated considerably. On the other hand the estimates may overlap in Table VI-6. Units with peeling paint may also have been counted as having broken plaster, etc., in a number of instances. C,, NUMBERS OF CHILDREN EXPOSED TO LEAD FROM LEADED GASOLINE The combustion of leaded gasoline by motor vehicles and the dispersal of lead from exhausts have had a major role in the status of lead as a public health issue. The recent debate on air quality criteria, health effects, and the leaded gasoline phasedown is only the latest episode of a controversy dating back to 1925, when lead additives had just been introduced. The Hamilton et al. (1925) review of the new leaded gasoline problem from a public health standpoint voiced many concerns that applied equally to the 1950s, 1960s, or 1970s (for a public health perspective on 60 years of leaded gasoline see Rosner and Markowitz, 1985). Since about 60 years ago when lead additives for gasoline were introduced mini ions of tons of lead from the combustion and dissipation of leaded gasoline in the United States have entered the environment. Much of this quantity has VI-17 airborne lead inhaled directiy and air lead ingested after fallout, such as by children who take in dust and soil. Given the continuing interest in the impact of airborne lead on Pb-B levels, numerous studies have been conducted on the blood lead to airborne lead ratio; that is, the amount of change in Pb-B one might expect from a unit change (pg/m3) in airborne lead. Basically, such a ratio is an oversimplified, only partially integrative depiction of systemic exposure. It permits a quick, but imprecise, look at the effects of changes in a community's airborne lead levels on the systemic exposure of child and adult populations. The blood lead/airborne lead ratio is lowest when (1) the ratios are exa mined experimentally in test chambers where the only exposure pathway is inhaled airborne lead, or (2) the ratios are examined for adults, a group with little secondary entry of airborne lead via dust and soil. This ratio rises consider ably when children are comprehensively examined for all impacts of airborne lead (Brunekreef, 1984). Direct inhalation of airborne lead yields ratios of about 1 to 2. When children are examined for both direct (inhalation due to emitted lead particulates) and indirect (entrained dust/soil inhalation or ingestion of dust and soil) effects, a ratio of 5 to 6 or even higher is measured. That is, for each 1 pg/m3 increase, the Pb-B level rises 5 to 6 pg/dl, Because dust ingestion and gut absorption vary so much among children, the contribution to individual children varies widely around these figures. Since internal, or systemic, lead exposure comes from several sources, it is necessary to determine how much exposure comes exclusively from airborne lead. This measurement was conducted using an isotope tracing method, the isotope lead experiment OLE, Fachetti and Geiss, 198:2). Such studies indicate that airborne lead contributes at least 20 to 2536 of total Pb-B in adults with inhalation as a principal route. Such estimates are considered lower bounds since a significant fraction of lead within this isotopic ratio, when absorbed, moves to the bone, where it joins a large lead burden. This mixture mow loses any isotope identity in blood by a significant "isotope dilution." A sizable fraction of this short-term lead deposit will move from the bone back into blood (U.S, EPA, 1985a). Collectively, the above data indicate (1) that past gasoline lead inputs produced airborne lead that added significantly to atifioipheric and soil/dust/ food burdens; (2) airborne lead added significantly to blood lead by direct and Indirect routes, yielding 20 to 25%, as a lower bound, based on isotope VI-20 DUP0400Q9628 Between the 1977 and 1986 EPA flip Quelity Criteria for Lead Documents, information on the lead problem accumulated; much of it Concerned lead from the combustion of leaded gasoline. For example, the quantitative relationships of blood lead to this source were studied; the knowledge about the adverse ef fects; of lead at lower levels was expanded; and the Mechanisms of toxicological action were examined. Host of these subjects lie beyond the scope of this report. Gasoline lead makes a sizable contribution (about 90 to 95%) to the total atmospheric lead burden in developed countries such as the United States. By using lead isotope ratio tagging for lead in gasoline, we can follow that fraction of lead not only into the environment but also into humans. The best estimate of leaded gasoline Contributions, using isotope ratios in urban Italy, is about 90% (Fachetti and Geiss, 1982). As expected, air lead levels related to gasoline combustion and auto density are highest in areas of highest traffic volume, urban and suburban com muting, and commercial activity zones. The most extensive data set of U.S, ambient air levels over the years was compiled by the National Filter Analysis Network and its predecessors. Such surveys have shown that ambient air-lead levels in remote parts of the United States are 2 ng/m3 and that in urban areas, levels are often 1 to 3 pg/m3, some 1,000-fold higher. The trend in these air-lead levels is downward, particularly with the leaded gasoline phasedown that EPA implemented in about 1975, The current allowable lead content of leaded gasoline is 0.1 g/gallon (F.R., 1985, March 7), From 1975 to 1984 U.S, gasoline lead consumption decreased 73%, and estimated lead levels in ambient air showed a similar decrease. Dispersal of gasoline-based lead from air into food,soils, and dust via fallout has been amply documenJted and critically evaluated (U.S, EPA, 1986a; WHO, 1986). Airborne lead fallout associated with traffic, as well as lead levels in exterior dust, house dust, soil, and plants are highest near traffic arteries in urban and suburban areas. This observation parallels the findings for ambient air lead from urban stationary sources, such as secondary smelters and municipal incinerators. The quantitative relationships between airborne lead from leaded gasoline combustion or other sources and a biological indicator such as Pb-B have been the object of numerous studies, and they are discussed at some length in Chapter 11 of U.S. EPA (1986a). This report focuses on the relative impact of VI-19 DUP040009629 below selected criterion values due to continued declines in leaded gasoline use over a number of years. The EPA Office used logistic regression analyses based on NHANE5 II data. These regressions were estimated for both black and white children and for the rather broad age band of children at risk, 6 months to 13 years old. Assuming that a log-normal Pb-B distribution would occur with the decreased user of leaded gasoline, EPA generated estimates of the mean and variance of trans formed (normal) distribution for determining percentages above specific Pb-B levels, logistic regression estimates of the children with Pb-B equal to. or above 30 pg/dl, and computer estimates of the mean of the log-normal distri bution (SAS/SURREGR). A more detailed discussion of this method is beyond the scope or purpose of this report, and appears in the original EPA document (1985). Since much of this methodology is relevant to Chapter V, these techniques also appear in Appendix G of this report. 2. Results As indicated, we restricted our count of children at risk of exposure to leaded gasoline to the 100 largest U.S, cities. These cities had a 1984 esti mated total population of 50,597,300, of which 5,565,700, or 11%, were children less than 7 years old. This estimate of some 5.6 million children at risk cannot be related directly to the following discussion on the impact of leaded gasoline on Pb-B levels, because the children are different ages and possess inherent differences. Table VI-8 shows the numbers of U.S. children, 6 months to 13 years old, whose Pb-B levels will fall below selected toxicity levels when projected to 1990. The numbers are significant, showing expected increases as the Pb-B level is lowered. Smaller numbers of children occur at higher Pb-B criterion levels* since the numbers originally above these levels were smaller. These values represent nationwide projections for a 13-year age band in children. Since Pb-B distributions are age-dependent in this age band, especially in younger children, it is riot easy to divide out these figures into narrower age bands from the values in Table VI-8. One difficulty with the broad age range for the number of affected children is that the numbers of very young children are not available to the reader. A second factor, evident in Table VI-8, is the prevalence of the numbers of children with Pb-B levels below expected Pb-B levels in the years long after the the leaded gasoline phasedown: gasoline VI-22 DUP040009630 tracing and up to 50% based on NHANES II data. In children, blood lead/airborne lead ratios of 5 to 6 and even higher indicate that the airborne lead input to blood lead can be very significant. Therefore, we would expect alterations in airborne lead, paralleling reductions of lead in gasoline, to reduce lead in blood. This relationship is indeed the case, and major support for this statement is the very high correlation between the decrease in Pb-B levels in the general population seen in the NHANES II survey for all segments of the population and declines in the use of leaded gasoline. Specifically, the correlation indicates that decreased use of leaded gasoline over 1976-1980 is the reason for the lower Pb-B levels. Regional data supporting the above national trend were presented by Rabinowitz and Needleman <1982) for a large sampling of newborn cord blood levels in the Boston, MA, area. 1. Estimation Strategies and Methods If we examine the total potential of direct (inhalation) and indirect (fallout) childhood exposure to leaded gasoline, we mainly examine large urbansuburban areas with denser traffic, i.e., urban population centers, in which airborne lead levels have been high enough to add a potentially significant burden to dust and soil. Since such parts of the environment can retain lead for long periods (U.S. EPA, 1986a), a population of children can be exposed to lead lingering from this source long after airborne lead levels have started to dec'l l he. To examine the number of children 6 years old or younger who were poten tially exposed to airborne lead via inhalation or dust/soil lead, children less than 7 years old in the 100 largest U.S, cities were counted from Census Bureau 1984 estimates of total population, and 11% of the population was determined to be under 7 years old. No children are exposed to lead exclusively from leaded gasoline, and we estimate imprecisely the fraction of children exposed to lead via this source. We can conclude, however, that children whose blood lead levels have changed due to the decreased use of leaded gasoline can be said to have sufficient eontact with lead by this route to meet the intent of Section 118(f), As noted earlier, Pb-B levels are declining, and efforts have been directed to quanti tate this decline as a function of the decreased use of leaded gasoline. As part of this effort, EPA's Office of Policy Analysis (U.S. EPA, 1985) performed projection analyses of the number of children whose Pb-B levels will fall VI-21 DUP040009631 by U.5. EPA (1986a). Airborne lead levels near lead smelters and refineries, and in some cases up to 5 to 10 km away, reached 5 to 15 pg/m3 in past periods, particularly before emission controls were installed in the 1970s,. In impact zones, lead levels ranged up to 100,000 ppm (10% by weight) where emission con trols were minimal, and near smelters in Missouri, soil lead levels reached levels up to 60,000 ppm. Today, soil and dust levels range between 500 and 5,000 ppm in areas near point sources. The levels decrease exponentially with distance from the operation. Results of numerous studies document that children sustain marked increas es in. blood lead and body lead burdens when they live hear stationary leademitters., particularly lead smelters. This relationship can be seen in the investigations of Yankel et al, (1977), who evaluated Pb-B levels in children 1 to 9 years old living near a smelting operation in Silver Valley, 10, in 1974-75. Table VI-9 shows the results of the biological and environmental monitoring in this smelter area. These overall blood lead results were extremely high, especially the percentage of levels over 40 pg/dl. Airborne lead levels were alsp very high, even at 10 km from the operation. In the zone adjacent to the smelter, about 100% of the Pb-B levels were above 40 pg/dl. Elevated Pb-B levels have been found in children living near other smelter sites, both in the United States and elsewhere (U.S. EPA, 1986a). TABLE VI-9. GEOMETRIC MEAN Pb-B LEVELS (pg/dl) BY DISTANCE FROM SMELTER (AREAS 1-6) FOR CHILDREN* NEAR IDAHO SMELTERP Area and km from Source 1 0-1.6 2 1.6-4.0 3 4.0-10.0 4 10.0-24.0 5 24.0-32.0 Airborne Lead (pg/m3) 18.0 14.0 6,7 3.1 1.5 Geometric Mean Pb-B (GSD) (pg/dl) 65.9 (1.30) 47.7 (1.32) 33,8 (1-25) 32.2 (1.29) 27.5 (1.30) % Pb-B >40 98.9 72.6 21.4 17.8 8.8 6 ~75 1.2 21.2 (1.29) 1.1 aAges 1-9 years. bPA analysis of Yankel et al. (1977) data, Vi-24 DUP040009632 1. Estimation Strategies and Methods'' The interim OAQPS numbers are derived from dividing the stationary sources into three categories; primary smelters, secondary smelters, and lead-acid battery plants. Estimates for each1 group were collected for different radii around the operations, which1 reflect differences in lead dispersal patterns. The numbers are for total subjects and the fraction of children less thdh 7 years old, 10.4%. The LIA study differs from the OAQPS study in terms of inventory of units still operating, quadrants surveyed, and radii around the operations. The LfA study mainly made its estimates based on ambient airborne lead levels. The LIA assessment did not count Closed facilities. But in assessing the net and continuing lead exposure of children around stationary operations, closed facilities must be included because past lead emissions continue to have an impact. These sources must be included to avoid underestimating the risk of lead exposure. the LIA study narrowed the radius of exposure population considerably, compared with the OAQPS model. The LIA Considered airborne lead movement for the dominant wind direction at the emission point, but did not allow for changes in wind direction on soil and dust levels in sectors not in the dominant path. Data in fable VI-9 show that at 10 to 24 km away from a smelter, with an airborne lead level of 3.1 gg/m3, the geometric mean Pb-8 level In children was 32.2 pg/dl, with almost a fifth of the lead levels above 40 pg/dl. If children are also examined for uptake pathways 10 to 24 km from the smelter-- distances well beyond both the LIA and the OAQPS plottings--the Pb-B/Pb-Air ratio is almost 6 when the levels are normalized to those of a group of control children in this zone. This ratio strongly suggests heavy additional input into Pb-B above that contributed by inhalation, i.e., dust and soil lead contributions. Angle et al, (1984), for an Omaha smelter area, reported a value of 8 to 7 for total inputs to children's Pb-B levels by lead exposure through air inhalation, dust, and soil. The above estimates by LIA and OAQPS were for potential exposure subjects. Actual Pb-B prevalence data for such sites as primary and secondary smelters also exist. The recent smelter community studies in Montana and Idaho (CDC, 1986a, 1986b), as cited earlier, show that both dust and soil levels and Pb-B VI-26 DUP040009634 Recent surveys carried out in two smelter communities, Montana (COC, 1386a) and Idaho (CDC, 1986b), as a joint effort by COC, EPA, and the respec tive states, indicate that considerable levels of residual dust and soil contamination linger after former active, high atmospheric inputs. As a consequence of this lingering exposure problem in a smelter community in Idaho (COC, 1986b), the survey found that; (!) Children who lived close to the smelter in the Silver Valley area of Idaho had a higher geometric mean Pb-B (20 pg/dl) than children farther away (11 pg/dl), (2) Detailed statistical analysis of the data base showed that the only significant environmental contributor was lead in the soil, and its contribution was via lead in household dust. Soil lead near the smelter had a geometric mean level of 3,472 ppm, while a mean level of 481 ppm was measured for sites farther away; the corresponding geometric mean for lead dust was 3,933 near the smelter and 1,138 ppm farther away. (3) At the time of the survey, the ambient air level had mean values, by area, of 0.10 to 0.28 pg/m3. (4) The percentage of children living near the smelter whose Pb-B and EP levels exceeded the CDC risk criteria for 1985, i.e., Pb-B 25 pg/dl and EP 35 pg/dl, was 26%, While the corresponding figure for those farther away was 2%. These two comprehensive studies conclusively document that previous lead fallout remains a main contributor to lead exposure in .general, and contributes to body lead burden of children in particular. We turn now to estimates of U.S. children who are either potentially at risk to lead exposure from fixed operations or actually have elevated Pb-B levels due to exposure from stationary sources. Such population data are surprisingly meager. Only a limited number of reports have helped us to quantify this aspect of the U.S. lead problem. One preliminary report, for EiPA's Office of Air Quality Planning and Standards (OAQPS) (GCA Corporation, 1986), provides the larger of the two data sets for the total number of children living near stationary sources in potential exposure to lead. The data set of the Lead Industries Association (TRC Environmental Consultants, Inc., 1986) provides a markedly different estimate of children from that of EPA, These data sets are for potential exposure. VI-25 DUP040009635 TABLE VI-10. EXTRAPOLATED PEDIATRIC POPULATION ESTIKATES.FOR STATIONARY LEAD SOURCES: TRC/LIA AND ERA APPROACHES3'0 Source Operating Facilities Number of Children Extrapolated for TRC Distances1* 1.0 pg/m3 0.5 jjg/nr* Extrapolation for EPA Distances Primary smelter 5 616 1,946 6,154 Primary refinery 1 7 553 8,961'' Secondary smelter 23 141 2,377 19,738 Tetraethyl lead 1 37 122 365 ... Battery Plants Total 98 IML 3,293 2,448 8,291 15.827 51,045 "Adapted from TRC, In: LIA study as submitted to QAQPS/EPA (TRC, 1986). ^Using 8,291 as the best estimate of potentially exposed subjects, distances from point source as defined in ERA and TRC reports. TABLE VI-11. GCA/GAQPS ESTIMATES OF TOTAL AND CHILD (<7 YEARS) POPULATIONS EXPOSED TO STATIONARY SOURCES OF LEAD3 Source Radius Around Plant (km) Total Population Number of Children Primary lead smelters 5 200,000 21,000 Secondary lead smelters 2 1,800,000 187,000 Lead-acid battery plants 1 240.000 25.000 Total 2,240,000 233,000 aAs tabulated and submitted to OAQPS/EPA, April 8, 1985. Radii to estimate potentially affected population are preliminary and are under re-examination. VI-28 DUP040009636 assuming a 4% prevalence above 20 pg/dl reported for the Dallas survey. We cannot estimate the numbers with elevated Pb-B levels near the lead-acid battery plants because data do not exist. E, NUMBERS OF CHILDREN EXPOSED TO LEAD IN DUSTS AND SOILS In previous sections, the three major contributors to lead in dusts and soils were evaluated according to a ranking of childhood lead exposure by source: lead paint, gasoline lead, and stationary lead emissions. Dusts can be further classified into soil dusts, street dusts, and household dusts. In various exposure environments, the relative importance of these types for childhood exposure differs. In summer, street dusts are probably more impor tant because of the amount of time children spend outdoors; in colder weather, household dusts are probably more important. Children may be further exposed to lead In dust via dust brought home on the clothing of working parents and relatives. These occupational dusts may have high lead content, reflecting fairly concentrated amounts of substances such as lead oxide (Hilar and Mushak, 1982), As noted earlier, lead levels in household and street dusts vary as a function of their primary contributors; these levels can range well above 1,000 ppm in many urban areas (see U.S. EPA, 1988a, for a detailed discussion). Brunekreef et al. (1983) determined, in a study in the Netherlands at sites without major point sources, that household dust increased in lead content by 400 to 700 ppm for each 1 pg/m3 increase in airborne lead. A major problem with reported studies of lead in dust and soil in relation to body lead burdens is the absence of any current standard method for collect ing samples at the test site. For soils, current core samples or surface scrapings can be taken; multiple sites can be sampled or hot spots can be emphasized. Near stationary lead sources, lead levels in dust respond more dramatical ly to changes in airborne lead levels (Yankel et al,, 1977; CDC, 1986a, 1986b). Soil lead content is also considerably affected by airborne lead fallout from mobile and stationary sources. Lead levels in soil can rise considerably with fallout, but the levels generally are lower than in dusts because the nonlead fraction dilutes the soil samples more (see, e.g., CDC, 1986b). An important aspect of soil contamination is the uptake of lead onto plants, which is mainly deposited on the surface with some uptake through the root system. Plant uptake becomes significant when assessing lead exposure in plants that are an VI-29 DUP040009639 X2 - the airborne lead level, X3 = the level of lead in dust, X4 = the lead level in soil, and is a random error term. Unfortunately, no study to date has produced this type of general regres sion equation. Available equations either omit leaded paint (Angle et at., 1984; Charney et al,, 1980; Walter et al., 1980; Yanke! et at., 1977), aifiome lead (Charney et al., 1980; Oalke et al., 1975), or lead in dust (Galke et al., 1975; Yahkel et al., 1977), Some of these omissions reflect regional differ ences. for example, leaded paint is not an important contributor to children's blood lead levels in the western U.S., and, therefore; it Is absent from the multiple linear regression models for children In Idaho (Yankel et al., 1977) and Nebraska (Angle et al., 1984). Other environmental measurement omissions, however, reflect limitations in study design. To successfully use a regression approach for estimating the number of children exposed to hazardous levels of lead in dust and soil would require* at a minimum, an extensive effort In urban and rural areas in the four U.S. regions: West, Midwest, Northeast, and South. The purpose of this effort would be to test children's Pb-B levels and uniform ly collect household-specific data on lead levels in paint, air, dust, and soil. These data would form the basis for constructing regional-specific regression equations to predict children's Pb-B levels In urban and rural areas. A survey of a representative sample of dusts and soils from urban and rural areas of each region is necessary to establish the prevalence of leadcontaminated dusts and soils. Using the regional- and urban- or rural' 'Specific regression equations, one could determine "safe" lead levels in dust, i.e., levels which do hot cause children's Pb-B levels to exceed 25 pg/dl (the present criteria level), or any such level in the future. This determination would be possible by using average lead levels in paint, air, and soil to solve the equation for a "safe" lead level in dust. Similarly, one could solve the equation for a "safe" lead level in soil by using average lead levels in paint, air, and dust. Once "safe" dust- and soil-lead levels are determined for urban and rural areas in each region, an estimate of the number of children living with higher lead levels of dust and soil can be made. By definition, this estimate would be the number of children exposed to dust and soil lead levels at concentra tions sufficient to cause adverse health effects. VI-32 DUP040009640 point sources of lead with heavily contaminated soil and dust, the fraction of atmospheric lead uptake through these indirect sources would presumably be much greater. 1. Estimation Strategies and Methods The numbers of children exposed to lead in dust and soil Cannot be sepa rated, as noted above, from the numbers exposed to airborne lead (gasoline or stationary emissions) or leaded paint. Direct exposure to lead, i.e., airborne lead or leaded paint, also foretells simultaneous exposure to dust and soil; therefore, we should sum across estimates for these contributing sources for both potential and actual risk, this summing will lead to overestimates in the numbers of children, clearly making the totals upper bounds. One can determine a lower bound for the estimate by Selecting the number of children exposed to the single, main contributor. An alternative estimating process which avoids double counting, uses multimedia regression analysis. A regression approach, which separates the contributiohs of lead from various sources to children's blood lead levels, would yield a more precise estimate than the cumulative approach, A regression approach, however, would require (1) establishing a set of regression equations for urban and rural settings in different U,S. regions, (2) determining the prevalence of lead-contaminated dusts and soils in these regions, and (3) using the regression equations and the prevalence data to estimate the number of children exposed to dust and soil lead levels at concentrations large enough to cause adverse health effects. The general type of regression equation needed simultaneously identifies the independent contributions of leaded paint, airborne lead, lead in dust, and lectd in soil to children's blood lead levels. The form of this equation is Y * AQ + C6 X6 + C2X2 + e3x3 + C4x4 where Y = a child's blood lead level, A - a constant, 0 C:L-4 = the relative contributions of the independent sources of lead, XL -- the leaded paint level. VI-31 DUPQ40009641 contaminate the water at three points; (1) the water source itself-"rivers, reservoirs, and groundwater; (2) the distribution system from water supply to living units, ie-, water mains, and (3) the plumbing in the home, e.g., lead solder. Actually, contamination rarely occurs in water sources from service connection lines and goose necks (connectors for main street to house line), and little is associated with the distribution system. By far, most of the contamination comes from domestic plumbing and plumbing in such public buildings as elementary schools, day-care centers, kindergartens, etc. Specific sources are lead pipe service connections, lead-based solder in copper plumb ing, and corrosive (lead-dissolving) water in the plumbing. While lead in drinking water is usually considered a source in the child's home,, a potentially significant exposure risk also exists in such public facilities as elementary schools, kindergartens, day-care centers, etc. One potentially important but little recognized problem in schools and other public facilities is lead contamination of drinking water obtained through taps., water fountains, and coolers. There are several reasons why water in schools could be a hazardous exposure source for young childrens 1. Water-use patterns in schools (school periods, weekends, vaca tions) involve long standing times of water in these units, which permit leaching. 2. Both water cooler-fountains and building plumbing may have lead-soldered joints and other sites of leachable lead, such as lead-containing surfaces in cooling tanks or loose solder fragments in pipes. 3. Unlike the case with lead-containing plumbing in private residences, which affects only the Occupants, a single leadcontaining cOoler-fountain Could expose a large number of users. These findings mean that young children can ingest lead from water at sites other than the home and that the numbers of children and other risk groups exposed to water lead may be expanded to the school-age group. The magnitude' of lead-contaminated drinking water as a public health problem can be seen in the situation that prevailed until recently for half the population of Scotland. The problem was traced to interactions between soft, plumbpsolvent water from sources such as Loch Katrine, the city of Glasgow's water supply, and lead pipes and lead-lined tanks in the homes of residents. VI-34 DUP04Q009642 2. Results The numbers of children potentially exposed to lead in dust and soil, but without determining numbers of Pb-B elevations, are taken as the sum of totals exposed to primary contributors to dust and soil: Faint lead in pre-1940 housing with highest lead content Gasoline lead in 100 of the largest U.S, cities Stationary Source Emissions 5.9 Million children 5.6 Million children 0,2 Million Children Total 11.7 Million Children As already noted, this total of 11.7 million is an overestimate of unde termined magnitude, since some fraction of children exposed to leaded paint have also been exposed to other sources. Alternatively, one can select the largest number of children exposed to a single primary source of lead in dust and soil or leaded paint, and consider this number an underestimate. This method may he used because not all children exposed to leaded paint have contact with the other primary generators:. This number is 5.9 million children. As an overall estimate, between 5,9 and 11.7 million children are potentially exposed to dust/soil lead. Estimates of children exposed to lead in dust and soil sufficient to elevate Pb-B levels to potentially toxic ranges cannot be readily obtained in any precise way. One can achieve totals at each Pb-B value, e.g., 15, 20, or 25 pg/dl, for the primary contributors--paint, gasoline, and stationary source emissions as given in earlier sections. A major difficulty for estimating such Pb-B elevations is finding a reliable method for apportioning of a given Pb-B value to either the primary contributor, e.g., paint, or to the receiving pathway, dust and soil. F. NUMBERS OF CHILDREN EXPOSED TO LEAD IN DRINKING WATER Studies in the United States and elsewhere have shown that drinking water is a potentially significant source of human lead exposure. Lead can VI-33 DUP040Q09643 between meals or on an empty stomach in the morning. For lead food intake by adults,, 10 to 15% of the lead is absorbed, but for water, 35 to 50% or a higher percentage, is absorbed (U.S. EPA, 1986a), Viewed in the context of risk assessment for the case of adults, lead in water presents three to five times the risk for systemic exposure as does lead in food--given the same concentra tions of lead. Relative absorption rates are generally higher in children, apd the difference may result in rates from water well above the estimate of 50%^ in children for lead in food (see Chapter III). 1, Estimation Strategies and Methods As noted earlier, there are three levels of exposure from lead in drinking water that can be defined for U.S, children: potential exposure; some actual exposure at a measurable but not necessarily toxic level; and actual exposure at high toxic risk levels. In the first approach, estimates of the numbers of children at potential risk of exposure to unhealthy levels of lead from drinking water differ in precision. Several estimates are given below. The estimates of the Division of Housing and Demographic Analysis, Housing and Urban Development (HUD), also include inventories of older housing units (which, as stated earlier, tend to have lead pipe segments at service connections) and provide an index of the persistence of such units in the national housing inventory. Nlext considered is ah estimation of the numbers of children consuming waterborne lead at some elevated level. According to the analysis by EPA`s Office of Policy Planning and Evaluation (U.S, EPA, 1986b), 42 million people in the United States may receive drinking water with lead levels that exceed the proposed EPA maximum contaminant level (MCL) for lead, 20 pg/1, at the tap. With this estimate, one can use Census Bureau data to calculate the number of children at risk for elevated Pb-B levels from water lead levels above 20 pg/1. EPA's analysis of the extent of lead Contamination of tap water uses data on water samples collected by the Culligart water softening company in a cooper ative study with EPA. Laboratory analyses were performed by the Illinois institute of Technology, These 772 grab samples taken at random times during the day were collected in 580 cities in 47 states. They indicate that 16% of the water from U.S, kitchen taps contain 20 pg/1 of lead or more. In addition, newly Installed plumbing Is at particular risk of elevated lead levels because VI-36 DUP040009644 Exposure was widespread, and prevalences for elevated Pb-B levels were high. The epidemiology of human lead exposure via drinking water is discussed in detail in EPA's lead criteria document (1986a, Chapter 7 and 11). In the United States, interactions between drinking water and..residential plumbing involve either lead connectors (goosenecks) and service lines (commonly used before 1920) entering the home or copper piping with lead-based solder in the joints--a form of solder that came into use about 1950. Some lead service lines and connectors may have been used after 1920, and lead service connections were occasionally installed until 1986. Published reports, both in the United States and the United Kingdom, indicate that five major factors contribute to the problem of lead-contaminated drinking water: (1) the length of the time water is in contact with the piumbing--the first water drawn from a standing column of water that has been in contact with lead in plumbing can have a high concentration of lead; (2) water temperature--hot water from pipes containing lead or joined with lead solder lead has more lead than cold water; (3) age of the solder--copper plumbing with lead solder that is less than 5 years old causes higher levels of lead in wafer than copper plumbing with lead solder that is older; (4) signif icant lengths pf solid lead pipes--water from long sections of lead pipes has high levels of lead; and (5) corrosive water soiirce--all of the above conditions are intensified when the water source is corrosive. The most corrosive water is acidic, soft, or nonalkaline. Many investigators, both in the United Kingdom and in this country (U.S. ERA, 1986a), have examined the quantitative relationships of Pb-B levels to lead in drinking water. These relationships, reflecting the complex interac tions of lead with biological responses, are often described by cube-root and other mathematical functions, Worth et al. (1981) examined residents in Boston, MA, where lead plumbing is still relatively common. These workers found a clear association between lead levels in water and Pb-B levels in children under 6 years old. Children exposed to tap water with lead levels above the U.S. standard of 50 pg/1 of water had elevated Pb-B levels, as a group, above 35 pg/dl. These differences were observed during a survey period before corrosion controls were implemented to reduce the lead levels in tap water significantly, Toxicokineticany, lead in drinking water is probably absorbed more completely than lead in food or other media, especially when the water is drunk VI-35 DUP040009645 TABLE VI-12. NUMBERS OF CHILDREN LIVING IN HOUSING CLASSIFIED BY HOUSING AGE* Age of Housing (% Total) <5 Years Old 5-13 Years Old Total Pre-1940 (29%) 5.2 M 8.7 M 13.9 M 1940 - 1949 (9%) 1050 - 1059 (16%) 1.6 M 2,8 M 2.7 M 4. 8 M =4.3 M y ' 7,6 M 1960 - 1969 (20%) 3.6 M 6.0 M 9.6 M 1070 - 1983 (27%) 4.6 M 7.8 M 12.4 M ' Total 17,8 M 30,1 M 47.9 M aSonrce: Statistical Abstracts, 1985: Table 27 (July 1, 1983) and Table 1315 (Fall, 1983). TABLE VI-13. CHILDREN POTENTIALLY AT RISK FOR LEAD EXPOSURE BY HOUSEHOLD PLUMBING, BY AGEa,D Number of Children Age of Housing 19?3 ISIS IMS Exposure Profile Total (Number) 14 M 19 M 21 M In housing built: Pre-1920 (%) 13 13 13 Lead pipes (+ lead paint) 1920-1949 (%) 25 25 24 Iron pipes (+ lead paint) 1950-1984 (%) 54 55 59 Lead solder (+ lead paint) Within past 2 years (%) 874 Fresh lead solder aSource Totals: Special tabulations from 1973-1983 Annual Housing Surveys. Percentages from Special Report: Division of Housing Demographic Analysis, HUD, Communicated January 7, 1987. source. For example, about 40% of the oldest, lead service connection (pre-1920) homes are still occupied. This may be an upper-bound estimate because old plumbing has been replaced In some of this old housing stock, but exact Information for this is not available. VI-38 DUP040009646 TABLE VI-14. ESTIMATED NUMBERS OF CHILDREN AT GREATEST BISK OF EXPOSURE TO LEAD IN HOUSEHOLD PLUMBING New Housing Population at Risk 8.8 million people in new housing with lead soldered piping9: (8.8 M)(7.6% of population less than 5 years old) (8.8 M)(12.8% of population 5-13 years old) Total number of children at risk in new housing Old Housing*3'0 = 0,7 M 1.1 M 1,8 M If one-third of housing units built before 1939 contain lead pipes,** then (0.33)(0.29) = 10% of housing have lead pipes. (0.10)(17.8 M children less than 5 years old) -= 1.8 M (0.10)(30.1 M children 5-13 years old) =! 3.0 M Total number of children at risk in old housing 4.8 M aSource: Reducing Lead in Drinking Water: A Benefit Analysis (U.S. EPA, 1986b, based on 9.6 mi11ion in new homes and 92% of these homes with metal plumbing). ^Source: Derived from Statistical Abstracts, 1985; Table 27, and Table Vi-12 of this report. cTtris group is a subset of the category of children living in housing built before 1939, "Source: David Moore, Office of Policy Development and Research, U.S. HUD, Submissions to ATSDR, January, 1987 and U.S. EPA. TABLE VI-15. PERSISTENCE OF AGING HOUSING STOCK IN OCCUPIED U.S. HOUSING INVENTORY (MILLIONS)9 Cumulative Total Bui Tt 1920 1930 Census of 1940 TSSO 1960 1970 1980 Pre-1920 24 21 20(E) 9(E) Pre-1930 30 30 29(E) 26(E) Pre-1940 35 34(E) 31 27 21 Pre-1950 43 39 36 30 tabulated values of Division of Housing and Demographic Analysis, HUD: Special Report of January 7, 1987. (E) = Estimated by authors of HUD report. VI-39 D U P040009649 r Contamination of drinking water by lead in other public facilities has also been reported. Unpublished preliminary data on lead levels in water from drinking fountains/coolers at two U.S. Naval facilities have been made available to the U.S. EPA and ATSDR (see Table VI-16). Of the approximately 90 fountains/ coolers sampled by the Navy contract laboratories, water lead levels above the current EPA 50 pg/1 limit were found in about 35% of combined first-flow, 1-minute, and 2-minute draw samples. Of these fountains/coolers, over 60 were major brands; the remainder were not identified by brand. In this survey "first-flow" refers to the first water obtained from the source at various times during the day. Thus, such samples may not have been the first flush of water after overnight standing. Of 39 first-flow samples, 23 (58%) were at or above a proposed EPA goal of 20 pg/1, and 31 (72%) were at or exceeded the level of 19 pg/1. For the 1-minute draw samples, 26 (72%) were at or above 20 pg/1, while 30 (83%) were at or above 10 pg/1. While it is not fully clear how much of the lead in these samples was contributed by the fountains/coolers and how much by the buildings' plumbing, water from some fountains/coolers ip the Navy survey coptaihed additional lead above that expected based on water Ifead levels from plumbing lines or taps in the same building. TABLE VI-16, LEAD LEVELS IN WATER SAMPLES OBTAINED FROM WATER FOUNTAINS/COOLERS AT NAVAL FACILITIES IN MARYLAND* Parameter Lead in First Flow Parameter Lead in 1 or 2 Minute Flush High Mean Median Low N = 39 570 pg/1 101 pg/1 39 pg/1. <5 pg/r High Mean Median Low N = 90 830 pg/1 69 pg/1 30 pg/lh <5 pg/r aSource: Based on data obtained from u.S, Navy (1987). Analytical detection limit of 5 pg/1. The above data from two separate states' surveys of schools and from Naval facilities in Maryland raise important questions about the potential for significant lead exposure from sources of potable water in public facilities. Systematic evaluation of this potential problem will be needed to determine its scope and any appropriate corrective measures. VI-42 DUP0400Q9650 obtained after weekend of holiday periods. In Phase II, samples at five of the original sites were examined for both first-flush and post-flushing lead levels. First-flush levels ranged from 2.2 to 500 pg/1 with a mean of 141 pg/1 (median = 38 pg/1). After 1-minute flushing* the mean value was 9.5pg/1 (median = 6.7 pg/1). The first survey was followed up with a much larger statewide survey, which has just been completed. Preliminary summary statistics provided by the x M0H indicate that two first flush samplings, 30 days apart, were obtained from 104 (25%) of Minnesota's 414 school districts. These repeat samplings con sisted of 1,157 and 1,051 water samples respectively. In the first data set, 74 samples (6.4%) exceeded the existing EPA limit of 50 pg/T and 166 samples (14.3%) exceeded the proposed 20 pg/1 goal. For the second sampling, the corresponding exceedences were 85 (8.1%) and 150 (14.3%), respectively. In neither Survey was the nature of the tap water drinking source specified, e.g., non-refrigerating fountain, electric cooler, or other sources. In a similar type of survey, the Maryland Department of Health and Mental Hygiene (MDHMH) examined drinking water lead levels in three stages in the summer of 1986, as described in Maryland Department of Health and Mental Hygiene news releases (September 22, 1986 and September 30, 1986), These schools were characterized as buildings less than four years old or units where new plumbing was installed in the last four years. Leap leaching was such that flushed water lines began to accumulate the toxicant after two hours of standing without further use. In July 1986, a survey of 45 schools, including a number of schools In the city of Baltimore, showed that 20 of them (44%) had lead levels above the EPA limit of 50 pg/1. In September 1986, MDHMH reported that a second survey yielded 33 (30.5%) of 108 schools with lead levels exceeding the EPA limit of 50 pg/1. Further examinatibn of MDHMH's summeiry data as provided in the releases indicates that water samples from 72 (67%) of these 108 schools were at or above the proposed EPA goal of 20 pg/1. In a third stage of the Maryland school survey, carried out in September 1986, 30 schools were examined for the first time* and two of them exceeded the 50 pg/1 limit. However, examination of the MDHMH summary data indicates that 9 (30%) of the schools were at or above the proposed goal of 20 pg/1. From the available information it appears that the new lead soldering in school plumbing and/or lead contamination in fountains themselves are suspected sites of lead leaching into water. VI-41 DUP040009651 employed for projections of children whose Pb-B levels would decline from specified Pb-B levels from phasedown of gasoline lead (U.S. EPA, 1985). In this analysis of the benefits of reducing the lead standard for drink ing water, U.S. EPA (1986b) estimated that 241,100 children had Pb-B levels above 15 pg/dl due to lead in their water as a result of the action of corro sive water on aged plumbing. Of these, EPA estimated that 100 children have.. Pb-B >50 pg/dl as a result of waterborne lead, 11,000 have Pb-fi levels between BO and 50 pg/dl, and 230,000 have Pb-B levels between 15 and B0 pg/dl. G. NUMBERS OF CHILDREN EXPOSED. IQ LEAD IN FOOD / Dietary lead can account for a significant portion of the total body lead burden in populations not having sizable exposures to the sources already discussed, in many people, it can add enough to cause an elevation in Pb-B levels. Dietary lead intake is important because it is a source of exposure for the entire population. Since food is ingested in relatively large amounts, lead concentrations in food at the parts-per-biTlion (ppb) level correspond to intakes of microgram quantities. For example, an average food content of 50 ppb of lead yields an intake of 50 pg/day when 1 kg of food is eaten. These 50 pg will elevate the Pb-B level by a measurable amount, about 8 pg/dl, using one relationship Cited in U.S. EPA (1986b). Over the centuries, lead ip food and beverages has provided much of the toxicologic record for lead poisoning, especially when lead was used in Targe amounts as an adulterant (see, for example, Wedeen, 1984). At present, lead enters food at production, harvesting, processing, and distribution steps (U.S. EPA, 1986a). In addition, beverages and other liquids can be contam inated by improperly glazed pottery (Klein et al., 1970) and various utensils. We cannot determine how much of the total food lead is due to human activity without knowing the background level. Wolnik et al. (1983) gathered background or near-background levels in cereals, grains, vegetables, and several meats. When we relate the results from these Studies to current food consumption surveys conducted by the FDA, we find that production and processing increase the lead content of food 2-fold to 12-fold. Sources of lead at the production stage include fallout onto plants, some lead uptake through the root system, and lead in forage and soil in areas where livestock graze. Lead enters in food processing mainly via lead-soldered cans. VI-44 DUP040009652 Table VI-17 shows EPA`s preliminary calculations of the relationship of tap-water lead in homes as a function of both pH and age of house. As expected,, first-flush samples are more apt to have excessive lead concentra tions than fully flushed collections. The more acid, i..e., more corrosive, water produces the greater lead contamination at values above 20 pg/1, the EPA proposed standard. Although the frequency of elevated lead samples decreases with the age of the home, there are still unacceptable first-flush percentages for corrosive and neutral waters, i.e., 51% and 14%, respectively, in houses 6 years and older. Equally important is the finding that in houses up to 2 years old that have corrosive water with a pH 6,4, 51% of the samples of fully flushed water contained more than 20 pg/1 of lead. TABLE VI-17, PERCENTAGE OF VARIABLY COLLECTED WATER SAMPLES EXCEEDING 20 pg/1 OF LEAD AT DIFFERENT pH LEVELS AND BY AGE OF HOUSE3 Age of House Percent of Samp! es >20 pg/1 Fully Flushed pH First Flush (2 min) 0-2 years 6.4 93 51 7.0 - 7.4 83 5 *8.0 72 0 2-5 years 6.4 84 19 7.0 - 7.4 2D 7 >8.0 18 4 6+ years 6.4 51 4 7.0 - 7.4 14 0 *8.0 13 3 aSourc;e:: U.S. EPA Office of Drinking Water (1987c); preliminary results from "Lead Solder Aging Study." Estimations for the category of actual exposure to water lead sufficient to cause Pb-B levels with toxicity risk are those employed by U.S. EPA (1986b) in its examination of numbers of U.S. children who would be above certain cri terion values because of drinking water lead levels above 20 pg/1. U.S. EPA (1986b) employed logistic regression analyses techniques analogous to those VI-43 DUP040009653 In the Belolan (1982) study, Table VI-18, the three age groups had mean intakes of 15, 59, and 82 pg/day. The corresponding lead intakes expressed as a function of body weight (kg) were 2.7, 6.1, and 5.6 pg/kg. Bander et al. (1983) found that children had a mean intake of 62 pg/day lead on a subject basis and 22 pg/day on a caloric or food mass basis. Parti tioned by age, the intake ranged from 49 pg/day for infants to 74 pg/day for 5-year-olds (Table VI-19). Because of the continual reduction in the lead' content of foods, estimates of current dietary lead intake are smaller. TABLE VI-19. MEAN DAILY DIETARY LEAD INTAKE IN PRESCHOOLERS CLASSIFIED AS TOTAL OR NORMALIZED DAILY INTAKE* Age (years) Total Mean (pg/day) Mean/500 kcal Mean/500 c Food <1 49 17 16 1 55 24 21 2 56 22 20 3 65 22 22 4 65 22 21 5 74 20 22 "Adapted from Bander et alt (1983), Based on food lead measurements in 1980. 1, Estimation Strategies and Methods The number of persons potentially exposed to some level of lead in food includes the entire U.S, population because a centralized food production and distribution system Serves virtually all parts of the nation. Each food processing step adds to the amount of lead in food (U.S. ERA, 1986a). There fore, all U.S, children under the age of 6 are at potential risk. We calculat ed the number for the 1985 estimated population, using the lowest projection method and found 9% of the total population to be under 6 years of age. This amounts to about 21 million children. We used the following strategy to evaluate the number of children exposed to lead levels in food that are high enough to elevate the Pb-B so that it approaches some toxicity level: (1) The Pb-B level associated with lead in food should not be more than 10 pg/dl, given other inputs such as from drinking water, contact with dust and soil, and even direct inhalation--all of which also contribute to VI-46 D UP040009654 In the late 1970s, the use of lead to solder the seams in cans began to be phased but, and consequently, the lead in canned food has significantly de creased. With infant foods, for example,-lead levels in evaporated milk have declined, on the average, from 0.5 pg/g wet Weight in the early 1970's to 0.07 pg/g in 1981. Similarly, lead levels in some juices have declined about 95%.. The daily dietary intake of lead in young children has been examined in several surveys. Beloian (1982, 1985) has proposed and used a food consumption model for evaluating daily contaminant intake* The elements of this model include the numbers of times Specific foods are Consumed in 14 days, lead content, and size of portions. Three age groups of children were examined: 0 to 5 months, 6 to 23 months, and 2 to 5 years* Lead levels in food groups were averaged over the period 1972-1978. Table VI-18 shows data reported by Beloian (1982). They include the mean daily lead intakes and the distributions of lead intake by indicated percen tiles, with food lead data for 1973-1978. Mean values are moderate, but at the higher percentiles the lead intakes are sizable. Which emphasizes the impor tance of considering distribution phenomena. These numbers are based on older, higher food lead measures than may exist currently:. TABLE VI-18, DAILY MEAN DIETARY LEAD INTAKE BY PERCENTILES3 Age group Mean Intake (pg/day) 50 Percentiles 90 95 0-5 months 15 11 31 36 6-23 months 59 54 89 110 2-5 years 82 79 120 130 aAdapted from Beloian (1982). Based on averaged data from 1973-1978. 99 55 140 170 Bander ei al. (1983) conducted a nationwide 7-day food consumption survey of .371 preschool children 0 to 5 years old, using food intake levels provided by the National Food Processors1 Association in 1980. Table VI-19 shows the means of lead intake, the means related to kilocalories, and the means per unit mass of food as a function of age. VI-45 D U P040009655 analyses and the lower levels of lead at the 95th percentile for younger children, the Bander et al. (1983) results are consistent with those of Beloian (1982). Uncertainties are inherent in these approaches for estimating the numbers of children who are exposed to lead in food to a degree sufficient to cause measurable elevations in Pb-B levels. First, the percentage of decline in food ' . y' lead from 1973-1978 to more recent periods is difficult to determine. We cannot specifically compare data gathered before 1981-1982 with more recent survey findings. The lead content of certain categories of foods has been markedly reduced (see Chapter IX), but changes in the overall dietary.intake of: lead are difficult to measure. Second, the direct/indirect air lead contribu tions are difficult to measure. Third, the criterion Pb-B value selected for calculating background levels is not a precise measure. Finally, selecting a single value for lead intake in food about a given percentile affects the margin of toxicological safety. If the current value is .significantly below about 63 pg/day at the 95th percentile of the distribution then the resulting Pb-B will be lower, and the other levels must be adjusted accordingly. 2. Results The number of children under 6 years is estimated to be 21,405,000 (World Alamanac, 1987); this number is based on the Census Bureau projections for 1985 by the lowest of three methods. Since we exclude infants 0 to 5 months old from our calculations, the base population is reduced to about 19,474,000. Of this estimated number, a maximum 5%, or 973,700 children under 6 years old, receive enough lead from food alone to constitute a potentially unaccept able lead burden, as indicated by Pb-B levels. If the increase in Pb-B from food is lower than the one selected here (i.e., less than 10 gg/dl), then the numbers of children at risk would be lower for a given daily lead intake. On the other hand, the reference Pb-B level of 20 pg/dl selected for the estimate is not the lowest criterion level for the purpose. H. SUMMARY AND OVERVIEW In this chapter, estimates of the numbers of lead-exposed young children, arranged by the source of exposure, are derived and described. These estimates VI-48 DUP040009656 Pb-B and push the final level unacceptably close to 20 to 25 pg/dl, the lead toxicity risk levels identified by the COC (1985) and WHO (1986). (2) A relationship of lead in food to Pb-B in infants and toddlers deHved from published data (Ryu et al, (1983) is Pb-B (pg/dl) = 0.16 x diet Pb/day (pg/day). From this relationship, a Pb-B less than or equal to 10 pg/dl from food requires a lead in food intake of less than or equal to 62.5 pg/day. (3) The percentage of children who have lead intake at or above about 65 pg Pb/day should then be selected from those studies whose results can be applied to the nation as a whole. Surveys by Beloian (1982) and Bander et al. (1983) were designed so that they can be applied nationally for the years when the lead levels in foods were measured. Given the centralized food system, any comprehensive tJ.S, survey of lead levels in food becomes a national survey. The Beloiah (1982) data. Table VI-18, show that the 95th percentiles of daily lead intake are 36, 110, and 130 pg/day for children aged 0 to 5 months, 6 to 23 months, and 2 to 5 years, respectively. If overall declines for average lead levels in food are assumed to be at least 50% from 1973-1978 to the present and across the entire distribution, these levels would now be 18, 55, and 65 pg/day. Uniform downward changes across the entire distribution are reasonable, assuming a centralized food supply and ho major changes in general food intake habits from 1973 to the present. The last value, about 65 pg/day, is the upper limit of lead levels in food to produce Pb-B levels lower than 10 pg/dl. For the 6 to 23 months group, 55 pg/day is also close enough to the limit of concern for the 95th percentile. While we are not sure about the relative vulnerability of the very young (0 to 5 months old) to lead exposure, this youngest group has a very low intake and is not included in the analysis. This approach allows us to say that, at most, 5% of the children under 6 years of age, excluding children 0 to 5 months old, are at or approaching a dietary lead exposure that pushes their body burden close to that associated with early toxicity if they are also exposed to other typical lead sources. In general, the Belonian percentiles agree with other data. Bander et al. (1983) noted that 8.9% of children had daily lead intakes of at least 100 pg/day. Most of these children were 4 to 5 years old. Considering that this study was conducted more recently and used food processors' data for 1980 VI-47 DUPO4OO09657 children will be in residential units having leaded paint meeting a minimal definition of exposure: greater than or equal to 0.7 mq/cm2. In so doing, we determined that the best available data for this analysis provided 3 "national best estimate" of about 12 million children potentially exposed to lead in paint, with about 13.6 million children for the upper bound. Qf these, about 5.9 million children are in pre-1940 residential units. In this case, we did not address leaded paint in the presence of those factors that might additionally enhance childhood lead paint exposure, for example, deterioration indexed by peeling leaded paint, lead-painted broken plaster, etc. Such indices of deterioration are not required before leaded paint exposure becomes a problem. For example, children can readily gnaw and chew on lead-painted woodwork such as window sills, even if the painted surfaces are in good repair. The next level estimated involved enumeration of children determined to be residing in unsound/substandard housing. Here we would expect that the proba bility for lead exposure sufficient to elevate blood lead, to some level would be much higher than it would be through a simple housing count, where undeteriorated and deteriorated housing is combined. Using figures from one study, the best national and upper-bound estimates for the numbers of children in such lead-painted, unsound residential units are about 1.8 and 2.0 million children, respectively. These figures are probably an overestimate since units having one characteristic of disrepair would also have others, yielding double .counting in at least some cases. These figures complement the numbers of children presented as census data enumerations by SMSA presented in Chapter V, Section C. For example, the total census count of Children in the 318 SMSAs who live in residential units built before 1950 amounts to about 4.4 million (Table V-20). From Table VI-3, the number of children (national best estimate) in all pre-1940 housing is approxi mately 5.9 million. Taking into account all factors of differences in the two analyses, approximately 75 be 80% of all children in older U.S. housing having leaded paint are found in urban areas. The numbers of children in unsound housing tabulated in this chapter do not include those children of families who are now moving back to older housing in cities and rehabilitating such housing as part of the phenomenon of gentrification. This number may be sizable but it is not possible to estimate such a subset of the urban Child population. VI-50 DUP040009658 define different degrees of exposure, both within an exposure category and across exposure categories. Overall, the data sets used for these source-based analyses vary highly in their precision and accuracy, in their assessment and definition of actual versus potential exposure, in their representativeness for childhood exposure nationwide, and, finally, in the relationship between the degree of exposure and some toxicity risk. With regard to the accuracy and precision of numbers relative to source of lead, it is not possible to measure the level of estimation error for each of the source categories. For example, in some cases we deal with actual counts of individuals, while in other cases we are confined to combining various elements of an estimation analysis, each having variable and relatively unde fined precision. Some estimates are also judged to be upper or lower bounds for actual values. In a number of the estimation procedures, available data for the prevalence of elevated Pb-B levels among children are derived from either regional analys es or reasonably matched strata of children from NHANES II, and their represen tativeness for the actual census of source-exposed children must be carefully appraised. Finally, the various source-based estimates of actual exposure to lead will differ as to how closely measures such as blood lead can be related to what we term some toxicity risk. In some cases, a Pb-B criterion value associ ated with presently understood toxicity risk is used, while in others we can only say that a blood lead elevation is predicted to occur at some undefined upper value. It should be noted that definitions of toxicity in terms of Pb-B values have been declining. For this reason, multiple Pb-B values are used where calculable. Fjor purposes of summary and discussion, each source-based estimation analysis is treated separately. 1. Paint Lead as an Exposure Source We have presented three levels of estimates for young children exposed to lead in paint. The first two analyses involve actual U.S. Census and housing counts and can be taken as reasonably accurate enumerations of children who are at least potentially, if not actually, exposed to lead in paint. The most general approach was to determine U.S. Census enumerations of young children (less than 7 years old) and then compile which portion of those VI-49 DUP040009659 declines below Pb-B criterion values are shown. With data displayed in this manner, the effect of gasoline lead reduction is focused on relative toxicity risk., that is, the Pb-B criterion values. 3, Lead From Stationary Sites as an Exposure Source / The numbers of children exposed to lead from, stationary source emissions have not been well catalogued and related to potential exposure risk. One study found that approximately 230,000 children are in the exposure zones -i4- associated with operations such as smelters, refineries, acid-lead battery' plants, etc. A range of estimates for the number of children actually exposed to lead from such sources was also presented where prevalences were restricted to results from several specific smelters. A likely national best estimate could not be derived from the limited data. For primary smelter operations, preva lences range from 1 to 26% (Pb-B 25 gg/dl and 35 pg/dl EP). The corresponding figure for secondary smelters, based on one survey, is 4% (Pb-B >20 pg/dl). The corresponding numbers for primary operation communities range from 210 to around 5,500 children. With secondary smelters, the number is approximately 7,5Q0 children. 4. Lead in Oust and Soils as an Exposure Source To estimate the number of young children exposed to lead in dust and soil, we combined the numbers of children exposed to the primary generators of this source category, i.e., lead in paint and lead from stationary/mobi1e (gasoline) lead sources. As described in the report, the upper limit of young children potentially exposed in this category is approximately 11.7 million and the lower limit is 5.9 million. The number of children actually exposed to dust/soil lead levels sufficient to cause elevated Pb-B levels that are also distinguishable from elevations due to paint, etc., cannot be easily determined by the various methods for obtaining estimates. 5. Lead in Drinking Water as an Exposure Source One estimation method shows that approximately 1.8 million children less than 5 years old and 3.0 million children 5 to 13 years old have potential risk VI-52 DUP040009660 To examine the number of children estimated to have actual lead exposure sufficient to cause Pb-B elevation, we have employed prevalences of different iPb-B .criterion values for children in inner-city housing and derived from either a survey of Chicago housing (Pb-B >30 pg/dl) or NHANES II projected prevalences at Pb-B levels >15, >20, and >25 pg/dl. The Chicago-based preva lence of 12.8% applied to children in deteriorated housing yields a total of ^ approximately 230,000 children with Pb-Bs above 30 pg/dl. The numbers of children in such housing with Pb-B levels above 15, 20, and 25 pg/dl were, respectively, about 1.20 million (15 pg/dl), 0.55 million (20 pg/dl), and 0.19 million (25 pg/dl). Although we recognize that leaded paint in elementary schools, kindergartens, etc., will pose potential risk for young children, we cannot as yet quantify this segment of the leaded paint problem. Similarly, leaded paint inputs to dusts and soils around public facilities are not readily quantifiable* 2. Gasoline lead as an Exposure Source Estimating the numbers of young children with potential exposure to lead from combustion of leaded gasoline is not a straightforward process. In this report, an estimate was based on the numbers of children living in the largest U.S. urban areas where vehicular traffic is expected to figure significantly in childhood exposure. For the largest 100 U.S. cities and for children less than 7 years of age, this figure is approximately 5.6 million children. To examine numbers of children having exposure to gasoline lead at various Pb-B criterion values, this report relied on data from EPA's Office of Policy Analysis, The EPA report derived numbers of children predicted to fall below indicated Pb-B values with the phasedown of lead in gasoline, and projections were extended to years beyond 1987. For 1987, for example, 563,000 children up to 13 years old will have Pb-B declines to below 20 pg/dl. The corresponding number for a Pb-B level of 15 pg/dl was approximately 1,6 million. Please note that in this case the age interval for defining children extends to 13 years of age. It is not possible to adjust these figures to the age interval up to 5 or 6 years employed in most cases, since Pb-B distributions are child age-dependent and do not permit a simple linear fractionation of these figures. Estimates provided by EPA do not reveal specific Pb-B values for the children in the analysis, but rathjer shifts in Pb-B levels sufficient to cause VI-51 DUP040009661 different estimation approaches, the precision of the estimation process, and the definitions of potential and actual lead exposure and the size of the age intervals employed in source-specific estimating. When specifically estimating actual lead exposure, any rigid ranking of children exposed by source can be misinterpreted with underestimates of particular concern. A good example of this is the data for children exposed to lead in paint at levels that elevate Pb-B to the toxic range where at least two factors would militate in the calculation of a low' estimate. We can provide the following general findings and conclusions about lead sources for childhood exposure and in utero exposure. p in terms of both quantitative impact and persistence of the hazard, as well as dispersal of the Source into the population, leaded paint has been and remains a major source for childhood exposure and intoxication. o Following close to leaded paint as a troublesome and persistent lead source is dust/soil lead, dispersed over huge areas of the nation. o Prinking water load is now recognized as a potentially signifi cant exposure source in both the home and in schools and other pub 1ie facilities; a particular hazard is electric water cool ers, as documented in the section on drinking water. o From examining the above lead sources, they are all related, collectively as multi-source exposure in old housing and partic ularly old housing in varying stages of disrepair. o Gasoline lead is declining significantly as a major lead source, particularly since the 1970s when it was adding about 40 to 50% to total Pb-B levels in the U.S. population. o Stationary sources provide a very limited, though potentially high, source of lead exposure. o Lead in food is declining in importance as a general exposure source, but daily intakes for recent years are still enough to add measurable amounts to total Pb-B levels of children. o Time did hot permit the detailed quantification of fetal expo sure, via pregnant women as the surrogate risk group, in terms of source-specific exposure. o With pregnant women, lead from food and water would be the main contributors to Pb"B levels above those considered "safe" for fetal protection. VI-54 DUP040009662 for lead exposure from parts of old residential plumbing. For new homes with new and Teachable plumbing lead solder* the corresponding numbers are calculated as 0.7 million and 1.1 million, respectively. Next, the estimate for numbers of children having drinking water lead exposure sufficient to cause some Pb-B elevation but not necessarily to toxic levels is given. As derived from EPA's statistics, 20% of public drinking ^ water supplies exceed the proposed Maximum Contaminant Level (MCJL) of 20 pg/1, which eventually yields a total of about 3.8 million children. These children will have Pb-B elevations calculated as being at or above 3 to 6 pg/dl, based on the .relationship between ingested lead and Pb-B [Pb-B " 0.16 x pg Pb/day (from water)] with daily intake of 1 or 2 liters of water at or above 20 pg/1. At this time, we estimate that 241,000 of these 3.8 million children would have a Pb-B level above 15 pg/dl, with 230,000 between 15 and 30 pg/dl, 11,000 over 30 pg/dl, and 100 over 50 pg/dl. 6. Lead in Food as an Exposure Source When we examine this category of source-specific lead exposure in young children, we not only have a large affected population base for potential exposure, but one that is the focus of much activity to reduce the lead in this medium. With respect to potential lead exposure from food at even some modest level of contact, virtually all young children will ingest some measurable amount of lead: that is 21 million children. The children estimated to have a lead exposure risk sufficient to cause some rise in Pb-B is approximately 5% of this base population, about 1 million children. This number is based on both lead levels in foods measured in the 1970$ and on those levels adjusted for declines in more recent times; therefore, it may be an overestimate to some extent. 7. Ranking of Lead-Exposed Children by Source It is not possible to rank rigidly the numbers of lead-exposed children from each lead source, a difficulty that applies to both potential and predicted actual lead exposure. For health assessment, it is more useful to consider the overall impact of each category and to rank qualitatively their specific characteristics. The reasons for this are related to the nature of the VI-53 DUP040009663 Since food and water lead primarily produce the projected Pb-B levels and total exposure counts for the four pregnancy catego ries in Chapter VII, we can estimate the joint contribution of food plus water to produce these numbers. VI-55 DUP040009664 1- Methods The following specific steps were taken to establish the required infor mation for the populations and estimates of prevalences of blood lead levels among them: 1, U.S. Census Bureau population projections for 1984 were used, as well as 1980 census data on residential distribution, to esti-x mate the number of white and black women aged 15 to 19, and 20 to 44 years of age and who live in SMSAs. 2, From the Division of Vital Statistics of the National Center for ; Health Statistics data, the numbers of live births occurring in SMSAs in 1984 were counted, and fetal deaths for 1984 appor tioned to SMSAs. Data for legal abortions for 1984 are not yet available, and other data from CPC (1983, 1986c) were utilized. The number of pregnancies regardless of outcome were estimated for the four race/age strata of women in SMSAs. 3, Estimates of prevalences of Pb-B levels of interest in pregnant women for 1984 were provided by the U.S, EPA Office of Policy Analysis, Washington, D.C., (J. Schwartz and H. Pitcher) using the same methodology as cited to project Pb-B level prevalences in young children for 1984.' The Pb-B criterion values of con cern were >10, >15, >20, and >25 pg/dl. The estimated preva lences for use in 1984 were necessitated by the observed declines occurring in Pb-B from the time of the NHANES II survey period to more recent years. With respect to the outline of approaches employed in this chapter, several points require discussion. The selection of the two age categories for women of childbearing age is based on the fact that women below 20 years of age tend to have a high risk of pregnancies With poor outcomes in general and without specific reference to the blood lead status of the mother (National Research Council, 1987). Further, the NHANES II data for women of childbearing age indicate not only that blood lead levels showed variations for white and black women, but that women of either race showed variation by age. We therefore examined four categories in this population: white, aged 15 to 19; white, aged 20 to 44; black, aged 15 to 19; black, aged 20 to 44. VI1-2 DUP040009665 VII. EXAMINATION OF NUMBER? OF LEAD-EXPOSED WOMEN OF CHILDBEARING AGE AND PREGNANT WOMEN In pregnant women, lead readily crosses the placental barrier early in gestation (see Chapter III). In utero exposure therefore occurs at periods of embryo logical development when important organ and system elaboration can be affected adversely by lead uptake. Such adverse in utero effects have been known for many years and low-level lead effects remain a public health problem. These effects were documented earlier in this report, in Chapter IV, and by such critical assessments as EPA1 s lead criteria document (U.S. EPA, 1986a). Two important points can be made now concerning in utero lead exposure:: in utero impact can be irreversible and the adverse impacts of maternal blood lead have been found at low levels, between 7 and 17 pg/dl, based on current studies (see Chapters III and IV). Pregnant women are recognized as a high risk population segment because of in utero exposure of the fetus. These risk definitions imply that every pregnancy potentially represents a fetus at risk if the mother has a blood lead level of 10 pg/dl or higher. Since the composi tion of pregnant women is not a predictable segment Of the population, women Of childbearing age are also examined in this chapter. A. STRATEGIES AND METHODS We have first established numbers of women of childbearing age and preg nant women by two race and two age groups. We decided to examine women residing in SMSAs and of childbearing age for 1984, a relatively recent date that matches pur examination of young children, and for which relevant Pb-B prevalences could be estimated. In addition, estimates of pregnant women for that year were obtained to illustrate the extent of risk to fetuses at any given time. VI I-1 DUP040009666 TABLE VII-2. ESTIMATED HUMBER OF WOMEN OF CHILDBEARING AGE AND ESTIMATED NUMBER OF PREGNANT WOMEN AND PROJECTED NUMBERS ABOVE FOUR SELECTED Pb-B CRITERION VALUES (pg/dl). BY RACE AND AGE, IN ALL SMSAs, 1984 Race/Age (YrS) Number Pb-B fua/dll >10 >15 >20 >25 Women in SMSAsa White 15-19 20-44 5,478,000 29*740,000 504,000 27,400 2,864*800 535,300 5,500 119,000 if6QQ 29,700 Black Totalb 15-19 20-44 1.098.000 4.984.000 41,300,000 90,000 981,600 4,460,600 14,300 184,400 761,400 2,200 34,900 161,600 500 10,000 41,800 Pregnant Women in SMSAs8 White 15-19 20-44 433,000 2,380,000 39,800 230,900 2,200 42,800 Black 15-19 20-44 187.000 595.000 15,300 117,200 2,400 22,000 Totalb 3,595,000 403,200 69,400 ^Method of calculating explained in text of Chapter VII, ^Totals by addition, not estimated. 400 9,500 400 4,200 14,500 100 2,400 100 1,200 3,800 These projections for women should be viewed in light of the method ological variables that will contribute to both overestimations and underestimations. The logistic regression analysis accounts for the declines in women's blood lead due to the phasedown of lead in gasoline, but does not account for the reductions of lead in food over this time span* This would result in an overestimation. The original NHANES II survey did not include enough women of "Other Race" to establish statistically reliable prevalences of blood lead levels. Consequently, this total population is excluded from the estimates presented, which are restricted to white and black women. Women of "Other Race" constitute sizable segments of the female populations in SMSAs in the West and Southwest of the country. Finally, the women not residing in SMSAs, about 20%, were omitted entirely from the calculations presented and result in significant underestimations. VII-6 DUP040009667 TABLE VII-1. ESTIMATED PERCENTAGES OF WOMEN OF CHILDBEARING AGE EXCEEDING SELECTED Fb-B VALUES, THEIR GEOMETRIC MEANS AND STANDARD DEVIATIONS (pg/dl) BY RACE AND AGE, FOR POPULATIONS IN ALL SMSAs, 1984' Race/Age (Yrs) Pb-B (pq/dl) >10 >15 >20 Geometric >25 Mean Geometric so White 15-19 20-44 9.2 0.5 0.1 0.03 9.7 1.8 0.4 0.1 3.4 5.2 1.78 1.65 Black 15-19 20-44 8.2 1.3 0.2 0.05 19.7 3.7 0.7 0.2 5.1 7,3 1.62 1.54 ^Estimates of prevalences provided by J. Schwartz and H. Pitcher, U-S. EPA Office of Policy Analysis, Washington, D.C. approximately one microgram for each decade of age increase. The differences in geometric means for young and older women in each of the racial groups amounts to about 2 ug/dl. The prevalence estimates were then applied to the estimated population strata, and the findings are presented in Table VlI-2. 2. Results Census projections for 1984 and demographic distributions for 1980 were utilized to estimate the 41,300,000 white and black women of childbearing age who lived in SMSAs in 1984. The estimated numbers of these women in the four .race/age categories above the selected Pb-B levels were: >10.pg/dl, 4,460,600; >15 pg/dl, 761,400; >20 pg/dl, 161,600; and >2$ pg/dl, 41,800. The estimating procedure outlined above yielded a total of 3,595,000 preg nant women for 1984. Of these, 403,200 are estimated to have a Pb-B level above 10 pg/dl, 69,400 above 15 pg/dl, 14,500 above 20 pg/dl, and 3,800 above 25 pg/dl. Estimated prevalences of Pb-B at these selected levels for 1984 are lower than those obtained from the survey data collected during 1976-1980, which is attributable to the reduction in ambient air lead pollution, (see Chapter IX). However, recall that women have a smaller uptake Of airborne lead than children on a body weight basis. Unlike children, they obtain the major portion of the total body burden of lead from food and water; a smaller fraction is derived from paint, dust, and soil lead. Lead in the food of adults, providing exposure for teenage and adult women, may not be reduced fay the same amounts as for infants and toddlers (see Chapter IX), although reductions are certainly occurring across all age groups. VII-5 DUP040G09668 Women of childbearing age represent about 45% of the total female pop ulation. The prevalence rates for Pb-jB levels significant to the impairment of healthy fetal development equate to about 4,460,600 women in the urban population., At any given time, almost 9% are pregnant, and in a given year, about 400,000 pregnancies are at risk for adverse health effects from maternal lead `(>1.0 pg/dl Pb-B). Since pregnant women and this population segment are continuously changing and not readily identifiable, the same quantitative problem recurs until abatement reduces the lead in the environment of these women. In other words, no fixed, identifiable group of individuals has a one-time exposure risk. Over $ 10-year period,, for example, the cumulative number of individual fetuses at risk will be 10 times thait of a single*year VII-7 DUP040009669 Source B are still useful. One can lower the Pb-B level from 25 to 20 pg/dl, which is still below the selected Pb-B toxicity index. Several approaches to the problem of the aggregate impact from various sources of low lead concentrations need to be examined. National or regional surveys of blood-lead levels would, of course, reflect the total integrated amount of lead absorbed from all sources across national or regional population groups; such surveys could set baselines for comparing changes. Methods for tracing specific sources of blood lead need to be further explored, and the impact of lead distribution in a given source low in lead need to be further evaluated. Quantitative metabolic models of lead intake, uptake, and systemic distribution that permit the factoring p.f all inputs to Pb-B levels beyond what is now available need further development. A. NATIONAL/REGIGNAL SURVEYS OF BLOOD LEAD LEVELS; BASELINE LEVELS AND SOURCE-RELATED CHANGES IN SURVEY BASELINES In this section, the impact of regulatory actions on both lead sources and blood lead levels are examined. National survey-based approaches that permit simultaneous examinations of lead source and blood lead trends, as lead sources are regulated, are very useful. These approaches are, however, expensive and complicated. The best example of this approach, and one that has figured heavily in policy with regulatory aspects of the U.S. lead problem, is the NHANES II national Pb-B survey. The observed declines in national blood lead levels during the survey have been very highly correlated over time with declining use of lead in gasoline. Figure VIII-1 shows composite plots of Pb-B declines over the course of the NHANES II survey, 1976-1980, and the declines in consumption of leaded gasoline. These declines included both annual and seasonal changes (Annest et al., 1983). The overall level of blood lead declined by 37%. The change was distributed rather uniformly across age and sociodemographic groups and was caused by a pervasive, host-independent source. This is discussed in detail in EPA documents (U.S. EPA, 1985, 1986a). As a consequence of the quantitative relationships between the rate of decline for leaded gasoline use and Pb-B levels in children (see Chapters V and VI), reductions in the number of children who had some toxicity risk due to VJIJ-2 DUP040009670 VIIL THE ISSUE OF LOW-LEVEL LEAD SOURCES AND AGGREGATE LEAD EXPOSURE OF U.S, CHILDREN In Chapter VI, we presented an approximate categorical source ranking for childhood exposure, including some dominant sources or cluster of sources, for example, dusts and soils*' This qualitative comparison was reasonable because of the high lead concentrations in the source. However, the impact of low-level lead sources such as food or water cannot be assessed without simultaneously considering all lead inputs to the body. Exposure estimation strategies based on aggregate lead exposure risk for food intake were employed in Chapter VI. Concern for total input from multiple low-level sources recognizes that lead enters the body from various sources and presents a unified toxicological threat since absorbed lead is toxicologically independent of source. For such multiple low-level intakes and uptakes, we need to examine source contributions as well as changes in PbHB that occur with changes in low-level sources. A cumulative exposure approach also requires us to examine various para" meters associated with different body organs and functions (e.g., lungs versus the gastrointestinal tract) in the same population group or among various groups (e.g., children versus adults). Details of the metabolic factors appear in Chapter III. The effect of a smaller amount of lead deposited in a body compartment that releases a large percentage of it into the bloodstream may be more severe than a larger amount lodged in a body repository that better retains it. The issue of aggregate exposure to low-level lead sources has both scien tific and regulatory policy aspects. With respect to policy, these aspects include the degree of exposure remediation possible for various lead sources. For example, a blood-lead level of 25 pg/dl can be considered as one index of toxicity. Let us assume that Source A contributes the equivalent of 20 pg/dl, or 80% of this Pb-B, whereas Source B contributes 5 pg/dl or 20%. In theory, removing Source A can lower the Pb-B level by the greatest amount. If this is not possible, but lead reduction in Source B is achievable, then reductions in VIII-1 DUP040009671 leaded gasoline consumption could be projected. This approach did not require any prior Knowledge about the significance of gasoline lead in a steady-state lead-exposed population; one simply examined the results when the relative input of gasoline lead was reduced. Post hoc judgments about the original impact of this particular source can then be made. B.. USE OF SOURCE-SPECIFIC TRACING METHODS y Various geochemical and biochemical principles can be used to develop what are called tracing methods. For instance* atomic lead is composed of various stable isotopes, usually in a fixed ratio, particularly 204: 206; 207: 208. Occasionally, there are isotopic ratios that differ from those in the main stream of lead-bearing pathways. In that case, one can theoretically "orchestrate*1 an exposure situation where such an isotopic ratio "tracer" can be used to measure the impact of a specific lead Source by using it to examine changes in body lead isotope ratios when the lead first enters the body; we can do this by Ipojcing at isotope data in Pb-B. Simple mathematical equations then depict the total body lead burden that arises from the source being traced. In the Isotopic Lead Experiment (TLE) performed in the Piedmont and the city of Turin in Italy, lead isotopes with an isotope ratio quite different from that in local food and water were used in leaded gasoline, through the cooperation of the lead additive manufacturer and the oil companies {Fachetti and Geiss, 1982; Fachetti, 1985). The lead isotope ratios in ambient air and blood lead levels in communities away from Turin and within Turin were examined over the time that the special mixture in leaded gaspline was used in this area. Such techniques require a knowledge of the toxicokinetic behavior of lead in human populations. As noted earlier, any portion of this "ratio tag" enter ing survey individuals and moving to bone for subsequent release (a sizable fraction, as noted in Chapter III), will not appear in the estimates. The bone lead reservoir, where large amounts of lead are stored, contains so much "old ratio lead" that the new ratio lead entering bone cannot survive statistically when it is resorbed into the bloodstream as' fully randomized atoms. Therefore, it is lost to any toxicokinetic accounting, VIII-4 DUP040Q09672 AVERAGE BLOOD LEAD LEVELS, p g /d l Figure VI11*1. Parallel decreases in blood lead values observed in die NHANES 11 Study and amounts of lead used in gasoline during 1976-1980. Source: Anneet et al. (1983). VIII-3 DUP040009673 technical parameters of that specific study. One can extend this approach, with combining of data sets, as the basis of some systematic biokinetic modeling techniques as indicated in the next section. 0. BIOKINETIC MODELS OF THE IMPACT OF LEAD SOURCES ON. BLOOD LEAD In the area of lead toxicokinetics and toxicology, there have been numerous attempts to derive precise models of how external lead relates to body burcien and various biological indicators of that burden (e.g., blood lead, see 0.5* ERA, 1986a, for a detailed discussion). Such modeling attempts have differed In their complexity and applicability across a range of exposures. For relatively moderate lead exposure, the model of Kneip et al. (1983) accounts for transfer and absorption coefficients relevant to the developing child and Involves manageable first-order kinetic solutions. This multicompartment model, developed from (infant) nonhuman primate metabolism of ingested lead, is depicted in Figure VIII-2, One advantage of such quantitative estimation models is that if knowledge of external media lead content is available, data for such lead levels can be inserted into the computations used to obtain Pb-B levels. This practice involves use of computers and specialized computer programs. Using models to examine Pb-B levels is useful in obtaining at least general assessments of a population's risk for lead exposure/toxicity When field studies, such as the screening for elevated Pb-B levels, are not or cannot be done. The U.S EPA Office of Air Quality Planning and Standards, (OAQPS) has applied the Kneip et at. model to young children to depict short~term exposures (U.S. EPA, 1986C; Harley and Kneip, 1985; Johnson and Paul, 1986), This U.S, EPA model 'is defined by its name: Integrated Lead Uptake/Biokinetic Model. The model assesses relative impacts of lead from different sources by integrat ing the data for all absorbed lead via different media and different absorption rates and by allowing the grand total of absorbed lead to be metabolically integrated to yield levels of lead in the bloodstream and other parts of the body. Since blood is also the biological monitor, it reasonably expresses What is going on internally. In fact, a major use of modeling is to provide the theoretical underpinning for choosing among biological monitors. This topic iis discussed in detail elsewhere (Mushak, 1986; Elinder et al. , 1987). VlII-6 DUP040009674 table VIII-1 shows the estimated lead fraction from leaded gasoline and the portion of this airborne source in blood lead. During the study period, leaded gasoline in Turin was estimated to contribute 87% to ambient air lead and a minimum of about 22% to blood lead; this latter fraction is dependent., of course, on the total Pb-B level. In Turin, the values were in the 20 to 29 pg/dl range. In a population with a Similar level of leaded gasoline use, but with a total Pb-B of 10 pg/dl, this contribution wduld be 47% of total x Pb-B. Hence, about 22% would probably be a lower boundary for values in communities with lower total blood lead levels. The fractional value of about ZZ% is a minimal percentage estimate on metabolic grounds, as noted above. ' Also, note that these values are for adults;eomparable information for children is presently not available. TABLE VIII-1. ESTIMATED CONTRIBUTIONS OF LEADED GASOLINE COMBUSTION TO BLOOD LEAD BY VARIOUS PATHWAYS3 Location Mean Pb-B (pg/dl) Pb-B from gasoline (%) Inhaled fraction Turin 21,8 4.7 (21.4) 0.6 <25 km 25.1 2.9 (11.4) 0.2 25 km 31.8 3.2 (10.1) 0.1 aAdapted from U.S. EPA tabulations (U.S. EPA, 1986a) with Fachetti (1985) update. C. THE USE OF SOURCE-BASED DISTRIBUTIONS OF LEAD INTAKE AND SOURCE-BLOOD LEAD RELATIONSHIPS IN ASSESSING AGGREGATE INTAKE AND POPULATION RISKS The methods discussed in the previous two sections dealt with the assess ment of source-specific inputs into blood lead and will, therefore, be most useful when change occurs only in a specific source or when ascertaining the relative input of one source Into total Pb-B levels. To factor more than one changing source into the inputs to Pb-B levels is complicated. With multiple, low-level lead sources, one can attempt to measure the lead content of each source and use an empirically derived mathematical relationship to relate source lead to some specific Pb-B level in exposed individuals. This is usually done with source-specific regression equations. Being derived from experimental data, these equations are most relevant to the actual design and VI11-5 DUP040009675 Table VIII-2 presents the varying intake/uptake (absorption) estimates for 2-year-old children under three exposure scenarios and the resulting different Pb-B levels. The data utilized are currently available for air quality, soil, dust, and dietary lead levels among such children. The three scenarios are: (1) urban non-point source area; (2) point source impact area; and (3) urban area with leaded paint. Household dust from chalking was used as the source of leaded paint expo sure in the table's scenario, which markedly underestimates overall leaded paint input, since the ingestion of leaded paint (for example, eating flaking paint or gnawing lead-painted woodwork by children) is not included. Such exposure . ?! would be difficult, to quantify in any case. This scenario also does not include exterior paint weathering. Direct and indirect (fallout) impacts of airborne lead emissions from nearby sources are shown in the table. Distance and wind direction from point sources Cause sharp differences in lead exposure. The situation illustrated in the table only represents a portion of the sensitive population who may be exposed around a given source. When comparing urban children exposed to lead from paint (third column; all other exposure sources being held constant) with urban children not exposed to leaded paint (first column), the first group has upper and lower Pb-B bounds approximately 3.3-fold higher than the latter. In lead toxicity assessment, distribution of Pb-B levels within a risk population is of special concern, perhaps even more than the actual mean values. The EPA model produces geometric mean blood levels, and the OAQPS draft report indicates how to derive distribution estimates from these modelbased means, given geometric standard deviations (GSDs) for the typical log normal distributions of Pb-B values. To be useful, models must be validated with empirical information. The validation exercise done to test the predictive accuracy of the Uptake/Biokinetic Model drew upon results of a 1983 survey around the primary lead smelter in East Helena, MT (COC, 1.986a). The Survey was conducted jointly by CDC, EPA, and the Montana Department of Health and Environmental Services. Study area parameters, at various distances from the smelter, were examined including dust, soil, and blood lead concentrations of children up to 5 years old. Available aerometry and emissions data were used to estimate airborne lead exposure at different locations in the area. VI11-8 DUP040009676 INTAKE --GUT 0 EXCRETION 5 X12= 0.34 (IN FANt) - 0.11 (JUVENILE) X2i" 1.73 x 103 Xi3 0.10 X31= 0.03 Xu* 0.03 X4J*' 0.07 Xis* 0.08 XM= 0.01 X 6i= 0.23 Figure VII1-2. Schematic model of lead metabolism in infantbaboons, with compartmental transfer coefficients. Source: Kneipet al, (1983). VI11-7 DUP040009677 The mode] described here yield? geometric mean and median Pb-B levels in children having multimedia lead exposure. The model's predictive power increases with the level of certainty about all source variability. GAQPS has used exploratory analyses to examine prediction/observation comparison runs for two cases (Run 1, Run 2) where individual dust/soil measures inside and outside of homes were included. In the exercise, a third run also generated prediction curves when a generalized measure of soil/dust lead was included.,Figure VIII-3 depicts predicted versus measured Pb-B levels in children 1 to 5 years old living within 1 mile of the smelter operation. Measured soil and dust levels were used a$ analysis inputs to obtain Figure VIII-3. Plots.based only on estimated soil and dust lead levels show similar patterns, although Pb-B levels closest to the smelter are slightly underestimated. QAQPS is con tinuing to examine these data. Table VIII-3 presents predicted versus measured Pb-B level in the two areas (Area 1, SI mile; Area 2, 1 to 2.25 miles) a$ a function of measured versus estimated soil/dust lead levels. Overall, there was reasonably good agreement between the two values. In response to ATSDR's request for testing the mode] in other exposure cases, OAQPS compared the model estimates with earlier empirical information for Omaha, NE, and for Silver Valley, ID, two areas in which extensive studies have been done on children affected by lead operations. Table VIII-4 presents predicted versus measured/reported data for the Omaha investigations (see Angle et al., 1984, and references cited therein). Mote that although the predicted values and measured values are similar in the suburban site, the model underestimates the levels in the mixed commercial/ residential area:- One problem with the Omaha data is the nonspecificity of the soil/dust measures, measures that are present and precisely established in the East Helena survey used to validate the model. In Omaha, furthermore, socio economic and other factors may have increased blood lead levels beyond those predicted by the model. For example, much higher historical airborne lead exposures than during the study year were noted. Table VIII-5 shows predicted versus measured Pb-B values in the Silver Valley, ID, area, where much childhood exposure information was gathered in the 1970s (Yankel et al., 1977). Note that agreement increases with distance from smelter (Area I is closest. Area VII is furthest), as would be expected, given that the Pb-B versus lead-intake relationship is based on linear kinetics that VIII-10 DUP040009678 TABLE VII1-2. ILLUSTRATIVE MODELING BALANCE SCHEMES FOR AVERAGE L INTAKE AND UPTAKE IN 2-YEAR-OLD CHILDREN UNDER THREE SCENARIOS ' Parameter Urban Non-Point Source Area Point Source Impacted Area Urban Area With Leaded Paint 1. Outdoor air lead (pg/m3) 2. Indoor air lead (pg/m3) 3. Time spent outdoors (hours/day) 4. Time weighted average (pg/m3) 5. Volume of air respired (m3/day) 6. Lead intake from air (pg/m3) 7. % Deposition/absorption in lungs 8. Total lead uptake from lungs 0.25 0.08-0.2 2-4 0.09-0.21 4-5 0.4-1.1 25-45 0.1-0.5 (pg/day) 9. Dietary lead consumption (pg/day) a) from solder or other metals 6.1 b) atmospheric lead 4.5 c) natural lead, indirect atmos- 4.4 pheric undetermined sources 10. % Absorption in gut 30-40 11. Dietary lead uptake (pg/day) 4.5-6.0 12. Outdoor surface soil/dust lead 55-200 (m/s ) 13. Indoor dust lead (pg/g) 14. Time weighted average (pg/g) 15. Amount of dirt ingested (g/day) 16. Lead intake from dirt (pg/day) 17. % Dirt lead absorption in gut 18, Lead uptake from dirt (pg/day) 19. Total lead uptake from lung and 85-225 80-217 0.085-0.13 6.8-28.2 40 2,7-11.3 7.3-17.8 gut (pg/day) 20. Average blood lead (pg/dl) 3-7 1.0 0.3 2-4 0.36-0.42 4-5 1.4-2.1 42 0.6-0.9 6.1 4.5 4.4 30-40 4.5-6.0 400-975 785-1350 721-1225 0,085-0.13 61.3-159.3 20 12.3-31.9 17.4-38.7 6-15 0.25 0.08-0.2 2-4 0.09-0.21 4-5 0.4-1.1 25-45 0.1-0.5 6.1 4.5 4.4 30-40 4.5-6.0 55-200 2000 1352-1700 0.085-0.13 114.9-221.0 20 22.9-44.2 27.6-50,7 11-20 aRange of average blood lead levels at age 2 reflect exposures from birth. Uptake estimates for first 2 years of life are calculated and incorporated but not displayed here. Differences in earlier years are due to: (1) higher urban air, soil, and dust lead levels in early 1980s; (2) lower uptake levels during the first year from irijadvertent dirt, consumption when hand to mouth activity is relatively low; and (3) higher dietary lead consumption rates in early 1980s before reductions of lead in canned foods that have continued over the years. Age-specific exposure parameters used for first 2 years of 1ife are as follows: Age: 0-1 year 1-2 years Time spent outdoors (hours/day) Volume air respired (m3/day) Dietary lead consumption (pg/day) % absorption in gut Amount of dirt ingested (g/day) 1-2 2-3 11.5 42-53 0-0.85 1-3 3-5 12.2 42-53 0.085-0.13 Calculations as provided by the EPA Standards, October, 1987. ce of Air Quality Planning and VITI-9 DUP040009679 2I-IIIA fX n f-ftot > m 01 cr tfk 0 fCt ll eft 3 n m SI 3 (ft 01 T ffl. o << ft > ft W ft o< Hi o *4* "U 3 </) O >'s. CL* fTI 3 Pi . > ft 3 (0 ft ft rt 3 *> ZT ft --DJ i pi 3 SC ft in ft ft ft X (ft << ft * (ft .* (ft o o IS: ft (ft w* o O ;3- 0 (C ft <Q ft &H 3 LO ft 00 ft Nt SI al Hb H m p. ft 0w. w CL e:ift ft ft o o o '. 330 (ft ,0 ft em 0 "5W3 3<t*.-<5 ft ft .4* m wi o ct 3 n. PI 0 CL Vi 3 c: ft 4"IPX <: si 6 ft rt o << ft ft c 0 ft M 3 ft U> O* ft 'Hi w 1 JO ft L-*fO ' (> CL 3 ft con <+ ^ 3:q ft 0. 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Advwwns `3 *Aai[A 4aA[ts ui 8 6 pue j seaay ui uaas se uoiqenqis aansodxa q6tq AaaA aqq oq A[qei[aa paqB[pdeaqxa aq qouuBo [apoui Aq paq&iuiqsa sueaui punoq-aaddn pye -aaMO[ qo aSeyaAe squasaadaa g-qg ueaui paqoipaag^ 86I `aaqoqsg `sasA[eue Vd3/SdbV0 :aoanosq T*22 9*52 - 9-91 2*02 9*02 - *9T 9*02 - -91 uoiqduinsuog pooj ui peaq Z-Z 2-t 1-0 1-0 (saeaA) aBy : (69861) Vd3 *S*n ui pazA[eue eqep uoiqdtunsuoa pooq pue pea[ pooq vgj uo paseq !$bZ6T A[aea Buianp saqis qqoq aoq (Aep/sufeaBoaouu) Bipqdn peat Aaeqaip paqBuiiqs3B m 259 (uidd) pea[ qsnp asnoq aSeaaAv on 212 (uidd) peat [ios a6eaaA\/ LZ' 0 92 "0 (gui/6i1) peat aiB aBeaaAy 8*n 5*8T sp[o aeaA z (tp/5ri) g-qd 3ueaui paqoipaad 9*tT 9*S2 sp[o aeaA 5-1 ([P/6H) g-qd UBatu paAaasqo aqig UBqanqns aqiS paxiw aaqauiBaed S13A31 loanos DNIOniONI ONV aBSN0I10ia3yd 13G0W 3U3NI)(0ia/3SVldn a3JLW93J.NI *SA 46t-IZ.6I `3N `VHWWO NI Q3anSV3W S13A31 0V31 00018 S,N3aaiIH3 'fr-IIIA 3iaJ. DUP040009683 computer programs. If Pb-B levels are estimated as high, then scenarios that reduce Pb-B in various media can be examined. At present, such modeling approaches for moderate overall exposure appear encouraging in the case of children. Modeling of aggregate exposure risk for the fetus (due to elevated body lead in pregnant women) is potentially more complex. For such modeling approaches to be useful, they have to account for the Pb-B distributions arising for a set of individuals having identical exposure. Approaches beintJ developed now attempt to do this. A related approach uses distributions of lead levels from a given source, if available, to define risk populations by source intake and uptake above some cumulative frequency distribution of Pb-B levels. As the index of lead body burden, i.e., blood lead level, is revised furfiber downward in terms of perceived unacceptable toxicity risk, the problem of cumulative impacts of only low-lead sources becomes magnified. For example, yfhen we say that a Pb-B level of about ID pg/dl is associated with onset of toxicity risk in the human fetus, we can return to our earlier example of five low-lead sources and substitute contributions of only Z pg/dl each to yield a total that is equal to the criterion Pb-B level of 10 pg/dl. If we accept 10 pg/dl in pregnant women to be the maximum tolerated, for valid reasons given in Chapter IV, then the average Pb-B in the population necessary to avoid this must be considerably lower than ID pg/dl. the same concerns apply for young children. The implication of this is that control options increasingly will center on producing reductions in ever smaller Pb-i increments. VII1-16 DUP040009684 have a measurable Pb-B of 30 pg/dl For a young child or a pregnant woman (fetal exposure), a Pb-B of 30 jig/dl poses an unacceptable toxicity risk and requires immediate reduction. Following comprehension of the above problem's impact, the question of how best, to manage such low-level sources remains. When there is one large lead source or a dominant source associated with severe lead intoxication, the exposure abatement remedies are more apparent and justifiable. With the above example, which of the five low-level sources first should receive attention? In reality, we qualitatively recognize that a number of low-level lead sources are operating in the human environment. However, we often do not know their quantitative impacts on Pb-B levels unless we track one source environ mentally and/or metabolically or use an integrated approach in which we measure all levels and estimate Pb-B contributions from each of these sources. In this chapter, both approaches were described and their relative value and limitation discussed. Single-source changes can be examined by careful trend analysis of Pb-B changes versus trends in the source contributing to Pb-B, The observed high correlation between declines in leaded gasoline use and declines in nationwide U.5. Pb-B levels illustrates this, A second, conceptually distinct strategy is to trace source-specific lead through the environment and after it enters the human body. An example is the Turin, Italy, gasoline lead experiment studying a distinct elemental isotope composition used as a tracer. The net result of both of these approaches was the determination that gasoline lead as a nationwide exposure source was contributing at least 25 to 50% of body lead in all members of the population, and gasoline lead reduction in response to regulatory initiatives will, cumulatively, reduce or avert unacceptable levels of Pb-B in millions of young children. The two approaches presuppose that only one lead source, or one main lead source, is being changed in some fashion, e.g., total level of lead or its isotopic composition. When all or most lead sources with which individuals have contact are changing, assessment of these changes becomes more complicated. One strategy being pursued by various researchers and agencies is the use of a cumulative metabolic model. In such idealized modeling approaches, as presently defined, levels in each exposure medium are measured and the data employed to calculate a total Pb-B level, using appropriate mathematics and VII1-15 DUP040009685 TABLE IX-1. CATEGORICAL TABULATION OF THE COMPONENTS OF PRIMARY AND SECONDARY PREVENTION OF LEAD EXPOSURE IN CHILDREN AND RELATED U.S. RISK GROUPS Type of Prevention Method Components of the Method I, Primary A, Environmental 1, Lead in paint 2, Lead in ambient air (a) Leaded gasoline combustion (b) Point source emissions 3, Lead in dusts/soils 4, Lead in drinking water 5, Lead in foods ^ B. Environmental/Biological Source controls augmented by communitynutrition interventions, i.e., nutri tional supplementations, for: (a) Calcium and (b) Iron II. Secondary A. Environmental 1. Case finding 2. Screening programs 3. Environmental follow-up 4. Event-specific exposure abatement B, Environmental/Biological Nutritional assessment and follow-up on ad hoc identification basis C. Extra-environmental Legal actions and strictures Primary and secondary types of prevention of lead exposure and public health risk draw upon classical distinctions made between the two in community medicine (see, g.g-., ETinder et al., 1987), Primary prevention strategies span from the very beginning of the commercial existence of a potential human toxicant and extend to controls on the amount of the toxicant permitted to enter both human exposure pathways and the mainstream of economic activity; for example, discontinued use of leaded paint and.removal of old paint. Secon dary methods of prevention are technically reactive in nature, i.e,, a cluster of responses to existing and identified problems. These include preventing the flaking of old paint, maintaining a high level of hygiene, preventing access of children to paint flakes, and minimizing contact with lead in dust. Also, screening for actual lead exposure is considered secondary prevention. IX-2 DUP040009686 IX. METHODS AND ALTERNATIVES FOR REDUCING ENVIRONMENTAL LEAD EXPOSURE FOR YOUNG CHILDREN AND RELATED RISK GROUPS Section 118(f) of SARA directs that ATSDR examine methods and alternatives for reducing environmental lead exposure in young children. This topic encom passes many environmental and social issues and only a limited number of them can be discussed In this report. The collective sense of the earlier chapters is that a significant problem remains with certain source-specific lead exposures and toxicity among young children and other U.S. risk groups. -With other sources, specific measures with large consequences for exposure control have been put in place in the United States, These are helping to reduce some of the original levels of exposure and toxicity in identifiable segments of the risk populations. Questions surround the issue of adequate envirpnmental lead reduction. Is it simply bringing exposed populations below some Pb-B value associated with some adverse health risk? Alternatively, is it reducing population exposure to a level that also allows some modest margin of safety? This safety margin is desirable for obvious reasons, not the least of which is minimizing toxicity risk. Any likelihood that future information will cause further downward revi sions in acceptable levels of Pb-B is a second reason. One can only surmise what the positive public health benefits of Safety margins might have been earlier, when toxicity was deemed to be at Pb-B levels of 60 to 80 pg/dl. An additional point is the unique position of lead in terms of safety margins among human toxicants. There is virtually no margin between observed levels measured in the population and the level at which effects appear. The topic of exposure prevention methods and alternatives is best addressed in two parts: primary prevention and secondary prevention. It is a common practice to classify prevention strategies into primary, secondary, and tertiary approaches. However, for our purposes, tertiary strategies are more clearly presented under parts of secondary prevention. The components of each type of prevention method are depicted in Table IX-1. IX-1 DUP040Q09687 wherever the land-use changed from residential use and badly contaminated soils and dust areas were made unavailable to children or paved over. Such measures may, on balance, abate risk for a given group, but they pose the ultimate question of where to deposit or dump the lead-bearing material. A. PRIMARY PREVENTION MEASURES FOR LEAD EXPOSURE -y This subsection is divided into environmental measures aimed at preventing exposure, and environmental/biological measures aimed at minimizing the effects. 1. Primary Prevention Using Environmental Measures This subsection is organized by environmental source category. Of parti cular interest are data showing how refractory each source may be to collective exposure abatement and control. Primary prevention as applied to the lead problem has actually been a hybrid of classically defined primary 'prevention measures and post hoc decisions for exposure reduction that resemble secondary prevention approaches. a. Lead in Paint Leaded paint was introduced in the United States with little Consideration of any future environmental health concerns. National and other actions to control leaded-paint exposure were only instituted after lead poisoning problems had been recognized (see the history of lead in the United States in Chapter II). Discussion of these levels of action are divided into Federal and non-Federal controls. Federal Actions in Preventing Paint Lead Exposure in Young Children. Federal actions directed to primary prevention of leaded paint exposure in children concern mainly those taken by the Department of Housing and Urban Development (HUD) and the Consumer Product Safety Commission (CPSC), The main action of the CPSC relevant to this topic was to mandate reduc tion of lead in paint to 0.06% lead in 1977, This move primarily affected the rate of further input of leaded paint into the housing stock. The Conran*ssion's IX-4 DUP040009688 In no small measure, past and current problems with lead as a health risk are traceable to failures in primary prevention mechanisms. For example, ade quate safety assessments for leaded paints and leaded gasoline, as we now define them, were not originally applied to these sources. According to both Rosner and Markowitz (1985) and Hamilton et al. (1925), reviewers examining the use of leaded gasoline at either end of a 60-year span, the introduction of / tetraethyl lead as a gasoline antiknock additive was permitted in the absence of any credible public health risk assessment. Present U.S, regulatory practices would not permit very many uses of lead if it were in new products, given either the earlier (1920s, e.g., Hamilton et al., 1925) or current toxicology literature on results from experimental test animals and production worker exposure. As Farfel (1985) has noted, we can further define two approaches under the rubric of primary prevention that have a bearing on lead exposure: passive measures or community-level exposure preventionj and active measures, which require the individuals' participation and changes in their behavior. Active approaches are more difficult to accomplish given both the pervasive nature of lead exposure and requirement for adherence to a preventive behavior pattern. Behaviors of people* however, can be positively changed with intensive public education, as demonstrated in the case of cigarette smoking. One can also dichotomize primary and secondary prevention strategies along lines of environmental exposure exclusively or environmental control in tandem with biological reduction of in vivo exposure and toxicity risk. This approach combines environmental lead control and biological factors to achieve protec tion greater than that obtainable from environmental abatement alone. For example, nutritional factors in young children can reduce to some degree lead absorption from the gastrointestinal tract, e.g., adequate iron, calcium, and phosphorus. It is crucial to note that optimizing nutrition is no substitute for environmental control action. In addition to specific primary and secondary measures for preventing lead exposure, other actions can have the net effect of being prevention measures without being defined as such. For example,.the national urban renewal pro grams of the 1960s and 197Qs had the net effect of removing large numbers of inner-city, lead-painted hqusing units and associated dpst/soil surfaces. Whatever the larger societal merits of such measures, at least some degree of lead exposure was removed for inner-city children. Further benefits occurred IX-3 DUP040009689 Collectively, these new actions address virtually the full spectrum of U.S. housing activity in which HUD has some assistance role. However, no Federal action exists to reach directly into fully private sector housing beyond the lead level in paint offered for sale. The Veterans' Administration and the U.S. Department of Agriculture apparently have not addressed the problem. The actions concerning public and Indian housing include required4nspections for defective paint surfaces in units with children less than 7 years old and required inspections for ehewabie and defective surfaces if a child has am elevated Pb-B level. The test threshold for paint lead in all cases.; is 1 mg/cra2 1ead. Recognized problems with the lead detectors, pointed out by HUD in all of the Federal Register notices, cause Concern about such testing. Only a limited number are available in the country and their accuracy may be questioned. Current usual operator skills require uniform training and protocols for testing them by a central authority to ensure widespread imple mentation of the hew rules, thh hew action for public housing requires hazard abatement, i.e., leaded paint removal, when a child is identified with an elevated Pb-B In the dwelling, in common areas, or in public child care facil ities within control of purlin housing. The degree of abatement is linked to such factors as the Pb-B level, local and state practices, and feasibility. While abatement methodologies are hot specified, they require that the hazard be "thoroughly removed on covered." public housing authorities may request Federal funds to carry out Abatement if other support is not available. New HUD activity on the leaded paint hazard in FHA and related housing supported by Federal assistance has a 1973 construction cutoff, i.e., housing built in this year and earlier is covered under the action. Inspection for defective surfaces, as with the public/Indian housing action, does not require X-ray fluorescence analysis, but the ehewabie, protruding surfaces do. The many components to this rulemaking and the bulk of detail are beyond the scope of this report* They are published in the Federal Register notice (52 FR 1876: January 15, 1987), However, note that testing and abatement actions for FHAassisted housing are triggered by change in ownership status and continuation of Federal mortgage insurance. Presumably, if a leaded paint-contaminated unit remains in its present ownership status or is bought through non-Federal financing, then the particular requirements do not apply. IX-6 DUP040009690 mandate does not allow addressing the preexisting paint lead burden in U.S. housing stock. Reduction to a level of 0,06% followed an unofficial voluntary restriction by the manufacturers themselves to a 1% lead content in the late 195Qr. However, between the 1950s and 1977, paint stocks in excess of this lead level continued to be produced. This level of 1% (a$ dry solid) still amounted to 10,000 ppm lead, a level well above that associated with elevated Pb-B levels (see Chapter VI). In contrast to the role of CPSC, HUD has been primarily concerned with leaded paint already present in public housing or any other housing involved in any type or level of Federal assistance; however, HUD did restrict the use of high-lead levels in paints in housing stock under its jurisdiction. The Lead-Based Paint Poisoning Prevention Act (42 U.S.C. 4801 et seq, ) authorized HUD action to prohibit the use of leaded paint in Federal or Federally assisted construction or rehabilitation; relevant HUD regulations were adopted in 1972. A major statutory step forward in HUD's responsibilities was mandated in Section 302 of the Act, added in 1^73, which required HUD to set up procedures for leaded paint abatement in existing housing stocfc, Here also, jurisdiction was limited to Federally connected housing. In 1973 and again in 1976, HUD acted in two ways under provisions of Section 302: (1) warnings to purchasers and tenants of HUD-associated housing as to "immediate hazard" in housing built before 1950, and (2) prohibiting lead-based paint at a level above 0,5% (prior to the 0,06% level as of June 22, 1977). Recently, HUD has become even more involved as a result of 1983 court action (Ashton vs. Pierce, 716 F.2d 56/B.C, Cir. 1983), This action challenged HUD regulations to include essentially all lead-painted surfaces as an "immediate hazard" rather than just the criteria of conditions associated with deteriorating surfaces and the dwelling in general, HUD has, at present, promulgated three rules that extend considerably its activities in this area: (1) lead paint hazard elimination in public and Indian housing (51 FR 27774: August 1, 1986; effective September 23, 1986); (2) lead paint hazard elimination in FHA single- and multi-family units and Section 8 housing/housing voucher and rehabilitation, FHA single- and multi-family property disposition (foreclosure) programs (52 FR 1876: January 15, 1987; effective date, March 2, 1987); and (3) lead paint hazard elimination in various community-based Federal grant and related programs (52 FR 4870: February 17, 1987; effective date, March 19, 1987). IX-5 DUP040009691 8-Xi Aft n> OW Qft" ft II 9 a. .-4 Oct Aft CO H> CO -5 OO 3 M .i ac 3U 'mm* WW 0| -j. n om 3 H O CO cn ' Oft .o <S# I ch cn 4k 3 C '3' cr ISJ <0 cn C O O Hi E .3 fOTt CO 3 Q. oo b CO ai ft b Q. w* V> 4k : CP > c n CQ a* --h rt 'CSDT ft CP w. co ct ' mm* o4k 00 o -* o IS) CO <3 OM <4* * M .4* * at CO 3 Q. t* O r+ 1-1 co cn M Hi CO to q* cn O i o i M |H CO to >4 cn ro to M HM 4* wM cn cn co co Si co at H* IS> C* O 00 cn w 0o*1 CO P* s5 Ni MM wi#M <Ti Uft Cl oob 00 is> cn .C O N) M 4k 4* cn no si cn o o HO 3 ,<A -< ft I eD H M Oft c CO ' o cn o .f-*t o . 00 H* USIi rz !..p to -n 3--< --4 30>3 o (0 X mm / S --u Mi* ' i\3 . wz. 3 CD o < x r-- HO. (A c: 3 r*2> >m cs>o >4 O ft mi. ; 3tfl - <*h in w S3 -H ma mm2 T3 2 3> ~H .wcn ^z.oCoO --J --i Uft Z ' o SC Co to o co .W< : 3. 7m0.3> <n/z5 Za ft ap z in i c -5 . -on'o C O -4k ----1 oo -J. VI n (D .H, * --ri oz b c+ in ; --I 3V> 3 *H ta co W n -n 3o topo +-< o M rs> Z CO to - o =c O E --in< f;; 3 . ' H o"o -mn .CO 50 i-- m fO.--ZI 1.01 o O --1 ' no c n " si z o ft , --* O --*.o c: 3 P ft* 3 ft sin-^ in 2ff>nomo7H0 mto o 4k M Co zo* b 3 . 3a 3 3> n v-s nzyt wf<--4t* *- cn o* to .e cn o '-J -.------ oin r+ ft < c--n4* i3n ft m S> <n DUP040009692 With respect to the various community grant-based. Federally assisted programs, most elements of the new rules operationally overlap with the other two sets of actions described above. In brief, this action requires that Community Development Block Grant* Urban Development Action Grant, Secretary's Fundi Section 312 Rehabilitation Loan, Rental Rehabilitation and Urban Home steading Program applicants must carry out lead paint analysis and abatement steps in order to receive funds within the programs. Both this cluster of HUD community grant programs and that involving FHA-rel.ated assistance primarily place abatement costs on the private sectors involved in the housing trans actions. While these recent actions suggest a new comprehensive effort to attack the leaded paint hazard, quantifying the likely or estimated impact of the three rulemaking actions is Still necessary. Table IX-2 provides estimates of the number of units and associated abatement costs in public housing, at a paint lead removal action level of 1 mg/cm2 (Wallace, 1986). About 308,000 units are estimated to' require abatement across all unit age categories with an aggregate cost of $380.1 million. Tablei IX-3 presents the estimated number of units requiring lead abatement for each year, 1987-1991, and the projected cost in these years for FHA singlefamily units. For all housing ages, 171,300 units are estimated to require abatement for each of the 5 years, and total 856,500 units with a cost of about $2 billion. Single family, FHA-insured units are but one category in this particular HUD action. Miller and TouTmin (1987) have estimated that for 1987-1991, all of these FHA categories will involve an outlay of $2.57 billion. Of these amounts, about 95% will have to be paid by buyers and/or sellers in the private sector. i* ` Municipal and $tate Actions in leaded Paint Exposure. In 1951, the City of Baltimore prohibited leaded paint use on interiors of dwelling: units and,xin 1958, required warning labels on cans of leaded paint already in the market pipeline (Baltimore City Health Department, 1971). By that time, the paint industry had introduced titanium dioxide as a substitute pigment for lead carbonate in paint, but the advantages of coverage and perceived surface freshness of leaded paint (see Chapter II) assured its persistence at some concerttratii on into the 1970s. Retroactive regulation at any level of jurisdiction, i.e., states or Cities, for paint lead already in U.S. housing stock has been infrequent and IX-7 DUP040009693 TABLE IX-4. SUMMARY OF TOTAL PRE-1940 LEAD-PAINTED HOUSING VERSUS DELEAQING ACTIVITY IN SELECTED MASSACHUSETTS COMMUNITIES FOR 1982-JUNE 30, 1986a City Pre-1940 Units*3 1982 Units Oeleaded In: 1983 1984 1985 1986c Total Boston Worcester Springfield New Bedford Fall River Somerville Lynn Lowell Lawrence Newton TOTAL 179,391 43,555 36,239 29,536 28,502 26,806 26,006 23,356 19,916 18,516 450,339 221 175 148 100 40 41 9 21 6 91 20 23 - "*- 01 453 379 136 201 99" 142 23 34 16 10 21 14 21 35 .- - 10 305 427 152 885 67 556 2 146 1 57 0 14 9 30 12 117. - 153? 300 02 243 2260 aSummary Statistics: Childhood Lead Poisoning Prevention Program, Commonwealth of Massachusetts, as provided by Cosgrove to ATSDR, 12/10/86; communities ranked by number of pre-1940 units bAll pre-1940 units are assumed to have leaded paint at significant levels, cTo June 30. ^Total only supplied. Statutes such as that of Massachusetts can be employed in Concerted action by community groups. In 1981, a tract of high-risk, lead-painted housing in the Jamaica Plain area of Boston was systematically examined, the children were screened for lead toxicity* and then 50% of the suspect housing was treated to remove lead. This was brought about by the joint efforts of the Harvard School of Public Health, which did the community assessment, and the Legal Aid Society, which used the Massachusetts statutory sanctions to force the property owners to comply (Harvard School of Public Health, 1981), A lingering problem with leaded paint is the disposition of old retail stock that has high lead content* CPSC, for example, cannot take action against salvage, close-put, and bankruptcy sales if stock was manufactured before the June 22, 1977 effective date of the 0,06% standard. Because of this and other reasons, high lead-level paints are still circulating in retail channels. The Connecticut Department of Consumer Protection, for example, has noted that lead-based paint can reach the market in higher amounts than expected (Communi cation of Department of-Consumer Protection, State of Connecticut to Dr. Jane S, Lin-Fu, Department of Health and Human Services, September 17, 1985). IX-10 DUP040009694 TABLE IX-3. ESTIMATED ABATEMENT COSTS AND NO. OF UNITS FOR DIFFERENT SITE CATEGORIES AT A LEAD PAINT THRESHOLD OF 1.0 mg/cm2 IN SINGLE-FAMILY FHA HOUSING UNITS3 Year Built 1987 Year of Abatement-Number of Units 1988 ' *' 1989 1990 1991 1960-1972 20,500 20,500 20,500 20,500 20,500 1950-1959 55,900 55*900 55,900 55,900 55,900 Pre-1950 Total No. 94,900 171,300 94.900 171,300 94,900 171,300 94,900 171,300 94.900 171,300 Total Cost ($ Thousands) 388,400 388,400 388,400 388,400 388,400 Cumulative Cost 388,400 ($ Thousands) 776*800 1,165,200 1,553,600 1,942,000 3Source: Miller and Toy]min (1987). variably enforced. In the early 1970s, Philadelphia, PA, had a primary prevention ordinance directed at removing leaded paint up to 5 feet above the floor In any unit with leaded paint. However, the city eventually discarded such prophylactic removal in favor of abatement only after demonstrated toxicity in child residents. Among the states, Massachusetts banned Lead in any unit in which children younger than 6 years of age were living, but the combined effect of organized opposition from real estate interests and limited funding for enforcement resulted in secondary prevention'--that is, intervention only after demonstrated instances of toxicity (Needleman, 1980). The Massachusetts statute typifies primary prevention legislation that has been rendered ineffective, for whatever reason. Summary statistics pro vided by the Commonwealth of Massachusetts to ATSOR, shown in Table IX-4, permit some observations. Of interest is the activity Level of Lead removal programs, compared with the number of pre-1940 housing units, that is, leadpainted units with high lead content. The table indicates that the selected cities of the Commonwealth have a total of 450,339 pre-1940, high Lead-painted units. Over the period January 1982 to June 1986, only 2260 or 0.5% of these units were subjected to lead abatement. We are not aware of the level, if any, of lead removal carried out under Massachusetts statutory provisions but occurring outside the reported programs. IX-9 DUP040009695 In 1982, EPA promulgated new rules (47 FR 49331 October 29, 1982) that, among other things, reduced the lead content of gasoline to 1,1 grams per liquid gallon. This intermediate action coincided with reports of the adverse health effects of lead on children and adults, which argued for still further action, as did the disturbing rate of "misfueling," whereby leaded gasoline was used in vehicles built to use unleaded gasoline. Further action was taken and, effective January 1, 1986, EPA promulgated the phasedown of lead in gasoline'to 0.1 g per liquid gallon. The decline in gasoline lead that these actions will bring is expected to impact the number of children whose Pb-B levels fall below certain toxicity ;< risk ceilings, including the 1985 CDC action level of 25 pg/dl, Tabulations in Chapter VI show expected sizable declines in the numbers of children with Pb-B levels above 15, 20, and 25 gg/dl. EPA is also examining its 1978 lead standard of 1.5 gg/m3 in ambient air, with a likelihood of reducing it. This will reduce atmospheric inputs, mainly in the proximity of stationary sources. As is also the case with post hoc controls on leaded paint, controls on lead inputs from mobile and stationary emissions mainly abate additional exposure.. In both cases, populations will continue to be at risk for exposure from lead-contaminated dust and soil , arising from past air lead fallout and lead paint flaking, weathering, and chalking. c, Lead in Dusts and Soils The primary prevention measures for exposure to lead-contaminated dust and soil have been directed at the generators of lead for these sources, that is, paint, leaded gasoline, and stationary source emitters. These measures, again, will primarily reduce or eliminate further inputs from these sources. At present', limited regulatory action seems specifically directed at con trolling lead in dust and soil. Chapter X describes Superfund activity and, in Appendix F lists sites that are due for cleanups and which also contain lead in soil. Several factors have contributed to this lack of regulation. First, dust and soil traditionally have not been recognized in public health actions or policy as specific, potentially major sources or pathways of child hood lead exposure. These sources are complex and still need quantitative characterization. Second, legal and other societal sanctions that are not IX-12 DUP040009696 In the Connecticut investigation, some of the lead-based paint found during 1985 on retail shelves was over 22 years old. Furthermore, discount and salvage outlets will buy close-out inventories and keep lead-based paint in the consumer pipeline. Of particular concern is the fact that paint producers are permitted to market a "sludge" paint from new materials plus "residues from vats." If these residues are from lead-containing industrial' products, then the ultimate lead level in the sludge paint may exceed the CPSC limit, of 0.06%. b, Lead In Ambient Air: Leaded Gasoline Combustion,And Point Source Emissions SPA has had regulatory authority over the use of lead in gasoline since 1973 (24 CFR 965,705(D)(2)), In 1975, EPA classified lead a$ a criteria pollutant, a designation reserved for pollutants whose public impact is such that control is required by ambient standards rather than by site-specific emission controls. Several parallel actions were being pursued in 1975 under the aegis of either Section 108 or 109 of the Clean Air Act, as amended, USC 7408 and 7409, which authorized the EPA Administrator to set ambient air standards for lead. In addition. Section 211(c)(1) of the Act authorizes the Administrator to: "control or prohibit the manufacture.of sale of any fuel additive" if its emission products cause or contribute to "air pollution which may be reasonably anticipated to endanger the public health or welfare" or "will impair to a significant degree the performance of any emission control device or system...in general use." Since the mid-1970s the lead use in gasoline began to decline mainly as a result of the increase of lead-sensitive, emission control-equipped vehi cles in the U,S. domestic fleet. This downturn has been reasonably established as a significant factor in Pb-B level changes among U,S. population groups, as determined by national (NHANES II, CDC screening data) and regional observa tions, The NHANES II data; indicated a generalized, cross-population decline in Pb-B levels of 37%, an average drop of about 5,4 gg/dl (see U.5. EPA, 1986a, for a detailed discussion). In 1978, the ambient air lead standard of 1.5 pg/m3--a considerable drop from the earlier standard--was promulgated. This standard also provided, a means for controlling point-source emissions from smelters and similar operations. IX-11 DUP040D09697 the necessary population surveys were discussed. A workshop report was prepared and lays considerable groundwork for future selection of actual demonstration sites and for this general area of exposure assessment. Recently, a limited but illustrative draft report of alternatives and issues of soil cleanup was prepared by EPA Region I in Boston, with assistance of the Harvard University School of Public Health (Ciriello and Goldberg, 1987). Given the useful nature of the material, the draft report is presented as Appendix E and is only summarized in this chapter. The report evaluates five proposed remedial alternatives for lead' contaminated soil in urban residential areas. They consist of: (1) removal and off-site disposal of contaminated top soil, with uneontanrinated soil coverage and revegetation; (2) the same approach with on-site disposal; (3) covering contaminated points with low-lead topsoil and then revegetation; (4) removal, decontamination, and on-site placement with revegetation; and 0) rototilling soil and revegetation. To assess the impacts of the five alternatives, a typical site in Boston was identified for each option and comparisons of costs and results attempted. Steps already proposed or implemented at Superfund or other sites also were described and examined. Conclusions of the report include: (1) Excavation of lead-contaminated soil and on-site decontamination is too costly and operationally unwieldy. (2) The effectiveness of soil lead abatement steps such as capping, rototilling, excavation, and on-site disposal are uncertain for soil lead levels of 1,000 ppm or higher. On the other hand, they may work for soil with lead levels below 1,000 ppm. (3) Excavation of lead-contaminated soil with off-site disposal, aug mented with Pb-8-level testing for children in the affected residences, seem best for protection; cost and off-site disposal impacts, however, may be a problem. Note that these strategies represent a limited effort and options germane to the Boston urban area. IX-14 DUP040009698 Corrosivity of drinking water, i.e., softness. Tower pH, etc.. Is an environmental factor that affects the presence of waterborne lead other than from lead in plumbing. U.S. EPA (1986b) has estimated that about 62 million LI.S. people receive such water. If we assume that 11% of these individuals are children under 7 years of age, then about 6.8 million such children are in homes where corrosive water is liable to mobilize lead to some unquantifiable extent. To estimate the numbers of children exposed to drinking water with suffi ciently high lead levels to elevate Pb-B levels, we assumed that children receiving drinking water that exceeds 20 pg/1 are at risk of some Pb-B eleva* tion (U,S, EPA, 1986b), A total of $2 million people are estimated to receive water with lead having more than 20 pg/1 of water. Census Bureau data indicate that 9% of the U.S. population are children under 6 years of age. Therefore, S,;78Q,Q00 children under 6 years of age are exposed to drinking water lead above 20 pg/dl. In addition to exposure in the home, other sources of water lead exposure may exist during time spent by children in public facilities. Precise numbers of preschool and school age children who may be exposed or are exposed to lead in drinking water in schools, day care centers and other settings cannot now be accurately estimated, given that the necessary survey data are not available. However, exposure to lead in drinking water in these settings can be important. As noted earlier in this section, water use patterns in schools are different from those in homes and they fayor the accumulation of leached lead after long lapses in use, for example, summer and holiday break periods and weekends. Such water standing in school plumbing may increase the risk of excessive lead exposure through ingestion of potable water. With regard to the overall problem of lead in school drinking water, state-level education and health units in two states have reported results from school drinking water lead surveys within their jurisdictions. The Minnesota Department of Health (MDH) recently carried out two surveys of lead in drinking water in Minnesota schools. The first and smaller survey (Minnesota Department of Health, 1986) consisted of two phases. In Phase I, 31 schools in 30 Minnesota cities were surveyed, including 24 elementary schools or schools with elementary grades. Of the 67 water samples collected and analyzed, 17 (25%) exceeded the Current EPA limit of 50 pg/1 and 27 (40%) exceeded the proposed goal of 20 pg/1. These were 11 first-flush" samples VI-40 DUP040009648 there has not been sufficient time for a film of calcium carbonate to build up on the inside of the pipes, which produces a protective barrier between the water and the materials of the plumbing system. New homes were not included in the Culligan data. Therefore, EPA included the Inhabitants of housing built within the past two years to be an additional subpopulation at risk of elevated lead levels in drinking water. Since this national exposure analysis was completed in 1986, EPA has X collected data on local conditions throughout the country. Data on lead leaching rates and contamination patterns in many places confirm that the occurrence of high levels of lead in drinking water is widespread, and may indicate that the national projections underestimate actual exposure (U.S. EPA, 1987c). A significant omission in the national estimate is the prevalence of high lead levels in drinking water in schools. 2. Results Table VI-12 shows the most general estimates of numbers of U.S. children under 5 years old and those 5 to 13 years old tabulated by age of housing. Using Census Bureau data, U.S. EPA (1987a) estimates that 5.2 million children under 5 years old and 8,7 million children 5 to 13 years old are in older housing, some fraction of which would have old lead service connections for water supply. The data tabulated in Table VI-12 are of the most general form. A more refined estimation of the numbers of children exposed to water in leaded plumbing is given in Table VI-13, which provides more relevant housing age categories for greatest risk, independent of the corrosivity of water, i.e., homes built before 1920 and the newest units built within the past 2 years. In Table VI-13, the most recent column of age/data is for 1983. In 1983, of the 21 million U.S. children under 6 years of age, 13% or 2.73 million lived in units that had lead water service connections. Similarly, 4% or 840,000 children lived in homes built within the last 2 years, which is the housing fraction having lead-soldered new Copper plumbing. Table VI-14, a tabulation from EPA, is similar to that of Table VI-13, but expands the childhood age bands to age 13 and has a 1-year difference in the younger age band. In Table VI-15, the tabulation shows the relative persistence of aging housing stock. Such data indicate the persistence of the lead service connec tion problem by virtue of persistence of older housing containing this exposure VI-37 DUP040009647 Important part of the human diet. Lead in soi] also impacts lead levels in livestock; when the animals forage lead-contaminated crops or ingest soil lead, lead may enter the food chain. A number of reports have addressed the quantitative relationships of lead in soil and dust to Pb-B, and U.S. EPA (1986a) has summarised these reportsIn general, lead in dust and soil at levels of 500 to 1,000 ppm begins to affect children's Pb-B levels (Baker et <*1- 1977; Mielke et al., 1984); a number of investigators have found a highly significant correlation between Pb-B levels and lead levels in dust and soil (see, for example. Angle et al,, 1984; Reels etal., 1980). Results from U.S.-based investigations of these relationships have been confirmed and extended to other countries (Duggan and Iqskip, 1985), In the study of the Silver Valley, ID smelter reported by CDC (1986b), the difference in the Pb-B means for children near the smelter operation vs. those farther away was 9 pg/dl (20 pg/dl vs. llgg/dl, respectively). The average soil levels for the sites differed as much as 3,000 ppm. Calculations show that, a 1 pg/dl rise occurred in the Pb-B level for each 330 ppm of soil; the corresponding relationship for lead in dust was essentially the same, 310 ppm. Recent data of Bornschein et al. (1987b) and Clark et al. (1987) show that lead in soil and paint contributes to lead in dust; dust lead transmitted via children's hands to their mouths accounts for a significant fraction of Pb-B increases. Also, an increase of lead by 1,000 ppm raises Pb-B by 6.2 pg/dl. The relationships of lead in soil and du$t to Pb-B levels in various studies (see U.S. EPA, 1986a; Bornschein et al., 1987b) show a range of values, generally changing between 3 and 7 pg/dl for every 1,000 ppm change. Note that some of these studies derived Pb-B response data for Pb-B levels which are higher than those now judged as unacceptable. In the Baker et al. (1977) study, for example, lead levels in dust above 1,000 ppm caused a rise above 40 pg/dl. This observation implies that a lower Pb-B threshold for reference would have been associated with lead levels below 1,000 ppm. A determination of the direct and indirect contributions of airborne lead to Pb-B, that is, the fraction from direct Inhalation and that from fallout, has been noted in the lead isotope ratio study In Turin, Italy (Fachetti, 1985); results showed that 6G% of the amount enters adult subjects via inhala tion and 40% via indirect routes. In children, especially those living near VI-30 DUPO4OO09638 levels of children remain elevated even when airborne lead levels have dropped to very low levels (0.10 to 0.28 pg/m3). These results showed that about 1% (1/98) of the children within 1 mile (1.6 km) of the East Helena smelter and 2631 (11/43) of the children within 1 mile (1.6 km) of the Kellogg smelter met the 1985 CDC criteria for some level of lead toxicity: a Pb-B level of at least 25 fig/dl and an EP level of at least 35 pg/dl. Further, results of a systematic - ' / survey iri Dallas, TX showed 4% of the children living near secondary smelters iii the area had Pb-B levels above 20 pg/dl (City of Dallas, 1985). 2. Results Table VI-10 shows the values from the LIA study (TRG, Inc., 1986) for potential numbers of exposed children; Table VI-11 shows the Interim OAQPS estimates of the same potential exposure group (GCA, 1985). The OAQPS data are probably more useful in accounting for the indirect impact of stationary source emissions on present and past levels in dust and soil. If results of other studies, such as the Yankel at al. (1977) Silver Valley, ID, study and the CDC East Helena, MT, and Silver Valley, Idaho studies (CDC, 1986a, 1986b), are exa mined together, the OAQPS tabulation may be a conservative estimate of the . total exposure population for primary smelters. Dispersion radii for secondary smelters are usually shorter than for primary smelters, but such operations tend to be in densely populated urban areas. OAQPS is reanalyzing and updating information on impact zones around different point sources. Table VI-11 provides the best guide for estimating the total number of children v/ho may have potential lead exposure due to proximity to stationary sources. To estimate actual exposures, we used the rates of 1% and 26% for primary smelters and 4% for secondary smelters, as noted earlier. These rates give differences among the point source emission characteristics, geography, neighboring communities, etc. Extrapolating the results Of the East Helena primary smelter study--where 1% of the children had Pb-B levels over 25 pg/dl--yields a total of 210 children for alt primary smelters. The corresponding prevalence recently found in Idaho, 26%, gives a figure of around 5,500. In 1984, in Herculaneum, MO, 18% of the children living within 1.5 miles of the primary lead smelter had Pb-B levels above 25 pg/dl (communi cation, OAQPS/EPA to ATSDR). Using this factor yields a total of around 3,800. Likewise, an estimate of 7,500 is the corresponding figure for children sufficiently affected by secondary smelters to have Pb-B levels above 20 pg/dl. ' VI-27 DUP040009637 TABLE Vl-8. ESTIMATED NUMBERS OF U.S. CHILDREN (THOUSANDS) FALLING BELOW INDICATED Pb-B (pg/dl) LEVELS AS A RESULT OF Pb-GASOLINE PHASEOUT3*- Blood lead (pg/dl) 1985 1986 1987 1988 1989 1990 25 72 172 157 144 130 119 20 232 563 518 476 434. 400 15 696 1,726 1,597 1,476 1,353 1,252 aFi'om U.S. EPA (1985). Based on regulatory action beginning January 1, 1986, to achieve 0.1 g/galby January 1,1988. ^Tabulations in original U.S, EPA (1985) analysis were extended only to 1990 for this table. lead phasedown alone will not bring all Pb-B levels down to acceptable Tow levels. Table VI-8 shows, even in terms of the 25 pg/dl level, that sizable numbers of children are projected to fall below these various Pb-B ceiling levels from 1986-1990 and that large declines are expected for criterion levels of 15 and 20 pg/dl, D. NUMBERS OF CHILDREN EXPOSED TO LEAD FROM STATIONARY EMISSION SOURCES As noted in Chapter II, stationary sources mainly refer to fixed operations that emit lead into the atmosphere and, consequently, into other ecological areas. Such sources include primary and secondary smelters, incinerators, and operations involved in coal and waste oil combustion. In terms of impact, these operations mainly affect neighboring communities, but they can cause severe lead contamination. The United States has 11 mines, 5 primary smelters and refineries, 60 secondary smelters, and 132 plants where lead-acid batteries are manufactured. For these sources, we have to consider that contamination occurs even after the facilities have closed. . Over the years, a lead-emitting operation will add a heavy ecological burden to nearby areas. Of particular concern is lead fallout from smelters transferring to nearby soil, dust, and forest coyer. The evidence linking lead emissions from stationary operations to the elevated body lead burdens of young children is well established. These connections have been derived from studies of a number of major U.S. smelter operations (includ ing ones in Idaho, Montana, and Nebraska) that have been extensively examined VI-23 DUP040009633 where manufacturing, processing, or disposal of lead has taken place. This can be seen graphically in Table X-l, relating the twelve most common activities at NIPL sites with observed lead releases from waste. Actual disposal of waste accounts for the largest proportion by number of sites, with manufacturing, ore processing, and battery recycling at the bottom of the list. B. URBAN AREA SITE ERA has carried out a preliminary assessment and site investigation of a Boston area to prepare an HRS package for scoring the site. The site;, consists of a rectangular area encompassing approximately 5 square miles where children are believed to be exposed to lead from both interior and exterior paint and from elevated lead concentrations in the soil surrounding the houses. This site was chosen because it contains areas that have been designated by the City of Boston as Emergency Lead Poisoning Areas (ELPAs). An ELPA is an area of one or more city blocks where a higher than average number of children were found to have elevated blood lead levels. The areas consist mostly of triple-story houses of frame construction. Most have been converted to six apartments, causing a high population density in the area. Because the houses are separated by only a few feet, lack of sunlight inhibits the growth of grass or a suitable cover for the soil, and the lead is available to children playing in the dirt in these areas. Data were gathered for two housing units within the area specifically to be evaluated under the HRS, Scoring was done for the unit expected to score highest under the HRS. This unit has greatly elevated soil lead levels both in front and behind the house, but no evidence of peeling paint. The lead concen trations in the front of the house near the street exceed the concentrations in the back of the house, indicating that a portion of the lead may have resulted from auto emissions. The data for this area have been processed through the Hazard Ranking System as if it were a hazardous waste disposal site to be evaluated for the NPL. The data were collected by Region I personnel and scored prior to transmission to headquarters. This original scoring package passed through the quality assurance and quality control process without revisions, and the assigned score of 3,56 was affirmed. The minimum HRS score needed for listing on the NPL is 28.5, X-4 DUP040009712 \ enforced allow primary contributors, such as leaded paint to continue to con taminate residential dusts and soils. One impediment to regulatory or legal control of lead in dusts and soils has been the relative paucity of studies shovring how specific primary contributors affect given dust and soil contamina tion levels. Duggan and Inskip (1985) have reviewed dusts and soils versus childhood exposure in detail and their review provides further information. Recent data indicate that some general mix of inputs or specific genera tors have certain quantitative relationships to Pb-B levels. Charney et al. (1983) have shown that Pb-B levels can be reduced through indoor dust abatement but only to a certain point. Milar and Mushak (1982) have shown a relationship between'"occupational11 dust brought home by lead battery plant workers and Pb-B levels in their young children. The recent study by Ryu et al. (1985) shows household contamination via secondary transport from the workplace and lead transfer to infants. Reports of the Cincinnati prospective lead studiest, concerned with childhood lead poisoning in this city, have shed considerable light on relationships among pathways for household dust, lead on the hands of children, and socioeconomic factors concerning leaded paint as the likely primary contributors (Bornschein et al., 1985; Clark et al., 1985; 1987; Que Hee et al ., 1985). Clark et al. (1987) have shown that dust lead is best correlated with lead on the hands of children and point to dust lead abatement as a key factor in reducing lead hazards in housing. Field studies are needed to provide evidence that "macro" rather than "micro" control strategies are effective means of lead abatement in areas larger than a single home or several homes. The focus of most studies to date has been specific abatement methods that are employed for individual lead paint-containing units. Mobility of lead in dust and soil prevents simple conclusions about single unit abatement to be extended to a neighborhood or even larger area. Field surveys are also needed to define blood lead-source lead relationships. Past attempts to define soil and dust lead in terms of proportional contributions of paint lead or airborne lead when both primary Inputs were operative have been unsuccessful for various reasons. The 1986 Superfund Act provides for the funding and execution of demon stration projects to address the problem of area-wide soil (and dust) lead in urban tracts. In response, in April 1987, EPA conducted an experts1 workshop on the design and scientific conduct of soil lead abatement projects. Methods of environmental and biological monitoring as well as the statistical design of IX-13 DUP040009699 units in the city had lead plumbing and that the city's water was highly corro sive, began efforts to reduce corrosivity. These efforts considerably reduced the amount of lead in tap water (see discussion in U.S. EPA, 198$a). In Chapter VI, we noted that the blood lead levels of Boston children had been related to past elevated tap water lead levels. U.S, EPA (1986b) has estimated that the treatment to reduce corrosivity costs just 25% of the value of the health benefits realized from reduced lead exposure, that is, a benefit*-torcost ratio of 4:1. The broader actions under the proposed EPA regulations are expected to have a wide impact on potential childhood lead exposure. e. Lead in Food ' Lead from food and beverages is encountered by virtually the entire U.S. child population and, as shown in Chapter VI, about 5% of the children have a lead intake high enough to result in Pb-8 increases causing risk of health impacts. Consequently, prevention measures that limit lead exposure from food are quite important. Regulating lead contamination in foods has been the responsibility of the U.S. Food and Drug Administration (FDA) for several decades and control dates from the identification of lead-containing pesticide residues on sprayed fruits. Collectively, FDA actions from the 1970s onward have targeted either control through setting total lead intake goals or efforts directed at known significant sources of lead inputs into foods. In 1979, FDA set a long-term goal of less than IDO pg/day for reducing the daily lead intake from all foods for children l to 5 years old (FR 44:(l7l) 51233-51242, 1979). This is a maximum permissible intake for any child and not a mean intake for all chil dren. To achieve this gpal within the shortest feasible time, attention focused on (1) establishing permissible lead residues in evaporated milk and evaporated skim milk; (2) setting maximum levels for lead in canned infant formulas, canned infant fruit and vegetable juices, and glass-packed infant foods; and (3) establishing action levels for other foods. Along with these activities, FDA monitors and enforces controls on food-related materials, for example, leaching from pottery glazes and food utensils. Lead can enter the food supply during production, processing, or distribu tion. U.S. EPA (1986a) has pointed out that during these activities, the lead content in food may be increased 2-fold to 12-fold over background levels. Processing is the major pathway for contamination--especially lead leached from IX-16 DUP040009700 4. lead in Drinking Water EPA is required, by the 1974 Safe Drinking Water Act (SDWA), to set drinking water standards with two levels of protection* Of interest here are the primary standards for drinking water, which define contaminant levels in terms of maximum contaminant level (MCL) of treatment requirements* MCLs are limits enforceable by law and are to be set as close as possible to maximum contaminant level goals (MCt-Gs), which are levels essentially determined by relevant toxicologic and biomedical considerations independent of feasibility. Recently Congress ordered EPA to tighten the drinking water standards for various substances, including lead. The current MCL for lead is 50 pg/1 of water. The proposed standard is stricter, 20 pg/1 (U.S. EPA, 1986b). In addition to the pending rule on drinking water lead per se, the 1986 SDWA amendments ban the use of lead solder and other lead-containing material in household plumbing whert residences are donneeted to public water supplies. The deadline for implementation of the ban is June 1988, States must enforce the ban or are subject to a loss of Federal grant funds. EPA's Office of Policy Planning and Evaluation (1986b) has carried out a detailed assessment of lead in drinking water from public water supplies. As noted in Chapter VI, about 20% of the population has tap water lead levels above the proposed MCL of 20 pg/1. Since EPA is Concerned with tap water lead levels as well as lead burdens in processed water leaving treatment facilities, the Agency must specify the "best available technologies" for preventing lead entry into drinking water. Proposed are corrosion controls that consist of treating the potable water with sodium hydroxide and Time to raise its pH and alkalinity and adding orthophosphate to aid development of a protective film inside the pipes. In addition, EPA is considering the removal of lead service connections and goosenecks (connections from the street main to house Tines) for inclusion in the "best available technologies." Corrosive drinking Water is quite common to high-density U.S, population areas, and U.S. EPA (1986b) has estimated that about 62 million Americans have such drinking water. The best U.S. case study for primary prevention of expo sure to lead in drinking water at the community level is that of Boston. In the 1970s, Boston water authorities, knowing that many of the occupied housing IX-15 1980-1985, lead in canned food was reduced 77% (NFRA, 1986) and lead in infant foods was reduced .considerably (Jellinek, 1982). Recent data, from F0A update the age-dependent, reduction found in data from the total Diet Study between 1982-1984 and 1984-1986. Table XX-6 gives total diet lead changes with the percentage decline for some age-sex categories. TABLE IX-6. AGE- AND SEX-DEPENDENT DIET LEAD INTAKES, (pg/kg/day) IN THE- UNITS) STATES AT TWO TIME PERIODS* '' Age-Sexc (Body Weight) 1982-1984 (pg/kg/day) 1984-1986 (pg/kg/day) Change (%) (pg/kg/day) 6-11 Mo. (9 Kg) 2 yr. (13 Kg) 14-16 F (54 Kg) 14-16 M (60 Kg) 25-30 F (60 Kg) 25-30 M (76 Kg) 60-65 F (64 Kg) 60-65 M (76 Kg) 1.70 1.60 0.48 0.63 0.43 0.48 0.42 0.44 1.11 1.00 0.30 0,38 0.27 0.29 0.25 0.26 -0,59 (35)= -0.60 (37) -0,18 (33) -0.25 (40) -0.16 (39) -0.19 (40) -0.17 (40) -0.18 (42) aSource: FDA Division of Toxicology, Communication of Internal Tabulations to ATSDR, April 23, 1987; based on Total Diet Study results. ^Revised Total Diet Study points, 8 collections. cLast six age-sex entries are in years. The data for the ongoing Total Diet Study are based on samples that are very small in relation to the enormous quantities of food units produced and Consumed in the United States and probably do not account adequately for variation by region and. multiplicity of processors. The types of food items selected for testing also may not reflect the variations in food Selection and consumption patterns among various segments of the U.S. population. The level of lead in food may, consequently, be smaller or greater than indicated. 2, Primary Prevention Exposure Using Combined Environmental and Biological Measures Biological factors can suppress lead uptake into the body or enhance its excretion. When these factors are nutrients that have well-established inter active relationships with lead uptake and toxicity, such nutrients can be used to reduce internal Or in vivo exposure. Such factors, when employed in a prophylactic, communitywide way, can also be viewed as an example of primary IX-18 DUP040009702 lead-soldered cans* Since World War II, the ratio of lead to tin in this soldering material has remained at 98:2* the percentage of food cans that are lead-soldered continues to decline. Table IX-5 shows the percentages from 1979 through the first quarter of 1986. . The percentage was very high in 1979--over 90%--but when the final 1986 figures are in, the percentage for that year should be about 20%. FDA (FR 44: (171) 51233-51242, 1979) has estimated that about 20% of all dietary lead is from canned foods and that about two-thirds of this is from lead soldering; there fore, about 14% of all dietary lead originates from lead seams. Recent data provided to FDA by the National Food Processors Association (NFPA) (1986) indi cate about a 77% reduction in lead from canned food during the period 1980-1985 This table does not include imported canned foods; we have no data for this contribution to lead in food. TABLE IX-5. PERCENTAGE OF LEAD-SOLDERED CANS IN ALL U.S. MANUFACTURED FOOD CANS FROM 1979-19855 Year Total Food Cans (M) Lead-soldered Cans (M) Percent of Total 1979 1980 1981 1982 1983 1984 1985. .1986 30,543 28,432 27,638 27,544 26,942 28,121 27,767 6,517 27,576 24,405 20,516 . 17,412 13,891 11,683 8,769 1,807 90.29 85.84 74.23 63.21 51.56 41.55 31.58 27.72 aSource: Can Manufacturers Institute data to U.S. FDA., M = Millions* ^First quarter, 1986* FDA activities, to a large extent, consist of establishing voluntary cooperation from domestic food manufacturers and processors, and much of the data are provided by the industry. Undoubtedly, lead in food due to leaching from leaded sources has been significantly reduced. But FDA does not monitor the lead content of imported canned foods, and these imports may have captured significant shares of the domestic market for some food items. Some changes in steps causing the lead contribution from the food processing industry were not taken until after 1981/1982. In the period IX-17 B. SECONDARY PREVENTION MEASURES FOR LEAD EXPOSURE This section assesses environmental, erivirpnmenial/friological, and extra-environmental measures, 1. Environmental Lead Control This discussion addresses screening programs and other aspects of early intervention In exposure and toxicity, and environmental hazard identification and hazard abatement, ;> a. Screening Programs and Case Finding The 1971 Lead-Based Paint Poisoning Prevention Act, as noted by Farfel (1985), did not specifically dictate health-based (secondary prevention) versus hazard-abatement (primary prevention) steps to be taken to ameliorate lead poisoning in U.S. children. While Title II of the Act authorized grant appropriations to the responsible agency to remove leaded paint on a tract basis in high-risk neighborhoods, funding for this purpose was not actually provided. The Department of Health, Education, and Welfare emphasized intervention--including medical management if necessary--for documented toxicity. The various screening programs, their history* and their quantitative aspects, were discussed in Chapter V: the focus here is on their role as secondary prevention instruments. While the screening programs were administered by the U.S, CDC (until FY 1982 when CDC control ended) about 4 million children were screened nationwide, and about 250,000 children were registered as having met toxicity risk criteria. The screening program surveyed about 30% of the high-risk children. The detection rates for positive toxicity are considerably below those found by NHANES II, for reasons noted in Chapter V. Case finding and cluster testing, followed by targeted screening, also produce much higher positive response rates (Farfel* 1985). Screening and early detection of exposure and toxicity undoubtedly have reduced the rates of severe lead poisoning. However, chronic exposure and lower grade toxicity appear more resistant to such secondary prevention approaches. The persistence of these problems is predictable, given the levels and types of unabated exposure remaining in the United States. IX-20 DUP040009704 prevention. When these factors are exploited on an ad hoc basis in children or families where lead poisoning has occurred, their use becomes more a secondary prevention measure. Chapter III discusses metabolic interactions of lead. As discussed by U.5. EPA (1986a) and Mahaffey et al. (1986), a number of nutritional factors suppress lead absorption and toxicity in test animal and human populations. However, only a few, particularly iron and calcium, can realistically be considered for preventive community medicine for high-risk populations. Results of numerous studies have shown that both calcium status and Iron status in young children are inversely related to the lead absorption level-- that is, as calcium or iron levels decrease, lead levels rise. Host of these studies are discussed in U.S. EPA (1986a). A more recent analysis of the MHANES II survey data showed a significant negative correlation between calcium status and Pb-B levels in a group of children under 11 years of age (Mahaffey et al., 1986). As Mahaffey (1982) has indicated, improving the nutritional status of children with high risk of exposure/toxicity greatly increases the effectiveness of environmental lead, abatement. But nutritional supplements only shift the lead level required for toxicity rather than eliminating lead uptake and its effects entirely. Other antagonizing nutrients may not be particularly useful or advisable in this connection. Levels of phosphorus in most diets seem high enough to suggest intake is at adequate levels in poorer children, which is borne out by the Mahaffey et al, (1986) examination of the NHANES II data for children. Vitamin 0 enhances lead uptake in the gut, but its intake is essential to health and cannot be reduced. As noted in comments on active versus passive measures in the Introduction, nutrition monitoring and maintenance are probably best done in relation to the lead antagonizing nutrients in a program of overall nutritional care, that is, the Women, Infants, and Children (WIC) nutrition program. The level of funding and other support for such programs determines their potential in reducing net lead exposure. We can, in fact, reverse the issue and say that increased nutritional impairment for those at high risk for lead poisoning will enhance exposure and toxicity risk in that population. IX-19 In St. Louis, the entire screening program cost $403,453 and Identified 1,356 cases of toxicity; that is just under $300 per poisoned child. In Baltimore, the multiple hospital admissions required for only some of the poisoned children cost about $16,000 per child in 1986 dollars. This does not account for additional essential costs for adequate management of severe toxic cases. These additional huge costs stem from medical follow-up care and treat ment, remedial education, etc. The monetized costs of the sequelae in signifir ' .1, '! 1 ':i\ ......... \ " :v / cant toxicity cases arespelled out in U.S. EPA (1985 and 1986b). The effec tiveness of screening children for lead poisoning is well demonstrated in terms of deferred or averted medical interventions, and in most settings, is quite cost-effective. in March 1987, the Comnrittee on Environmental Hazards, American Academy of Pediatrics, issued its "Statement on Childhood Lead Poisoning," It includes this statement: "...to achieve early detection of lead poisoning, the Academy recom mends that all children in the United States at risk of exposure to lead be screened for lead absorption at approximately 12 months of age,... Furthermore, the Academy recommends follow-up.,.testing of children judged to be at high risk of lead absorption." These guidelines from America's pediatric medicine community probably cannot be effectively implemented or coordinated with the current levels or existing type of program support at local. State, and Federal levels. b. Environmental Hazard Identification and Abatement for Severe Poisoning Cases When cases of toxicity were found, mass screening programs for lead poisoning routinely made efforts to find the sources, A careful examination of the information on reducing lead exposure by completely or partially removing leaded paint clearly shows that, at best, the effect is debatable. At worst, the approach may not work. In a prospective study, Chisolm et al. (1985) observed that when children return to "lead abated" structures, their Pb-B levels invariably return to unacceptable levels. This is not a case of endogenous Pb-B increase from the release of bone lead, because children heavily exposed before treatment will respond better when placed in lead paint-free housing. IX-22 DUP040009706 2, Envl ronmental/Biologi.cal Prevention Measures This approach is analogous to that described for primary prevention stra tegies that combine nutrition and environmental control. As a secondary prevention measure, however, nutritional optimization might be more debatable than when it is used on a community level with children not already showing signs of lead toxicity* A secondary nutritional approach would also require that the affected family take a more active role, and this raises the issue of compliance, funds for adequate diets, etc. 3. Extra-Environmental Prevention Measures These measures are legal sanctions to force the removal of lead from documented poisoning sites. Legal sanctions are some of the tools available for addressing demonstrated and significant health risks. Can one effectively use a legal framework to expedite the rapid and safe removal of lead hazards from children's daily environment? Conversely, can we conclude that a real handicap for such action is the absence of supporting legal tools? Finding answers to these questions in the available information is not easy, but it is useful to examine a screening program with a legal component and assess its contribution to overall abatement. In its summary of screening activities submitted to ATSOR, the City of St. Louis summarized its dealings with landlords and others who own housing or public-use facilities where lead poisoning had been found. A summary of 1985 court activity stemming from lead hazards, including the licensing of day care centers and similar institu tions, indicated e case load of 1,086, with 387 of the cases carried over from 1984. From this cumulative docket, 154 defendants were fined $2,447, an average of $16. Minor fines appeared to be the only measure at the city's disposal, because the 1984 count was virtually identical to 198.5'$ and the average fine for 1984 was the same as for 1985. We cannot say whether minor fines as legal sanctions influenced the city's lead toxicity rate as identified from screening. In the most recent data, this rate was 11%--a rate that has remained about the same since 1978. This case study does suggest, however, that the persisting high lead toxicity rate has not resulted in more effective legal measures. IX-24 DUP040009708 Ample information has accumulated to show that leaded paint removal is hazardous to the workers doing the removal and that lead from the paint con tinues to be hazardous to the occupants because residual material has been moved to other areas that children contact. A major difficulty is the relative mobility of powdering lead paint, which enters cracks and crevices settles on contact surfaces, and readily sticks to children's hands. As Charney et al. (1983) noted, response to the dust problem may well be as effective as removing the paint film* The problem of continued exposure risk, even during or after leaded paint abatement, can be illustrated jo the recent study by Rey-Alvarez and MenkeHargrove (1987). Rey-Alvarez and Menke-Hargrove examined a total of 13 lead* polsopqd children whose exposure had been exacerbated in varying ways when leaded paint was being or dad been removed. In the case of a child remaining in a unit where lead paint was being removed, the child's Pb-B abruptly increased from an average of about 45 pg/dl to 130 pg/dl at the end of the paint removal period. In 12 other children, Pb-B levels that were already elevated increased to higher levels after lead abatement of the unit's interior surfaces. The erythrocyte protoporphyrin levels also greatly increased, Farfel and Chisolm (1987) also document that traditional paint removal increases household dust and child Pb-B levels. The Rey-Alvarez and MenkeHargrove (1987) and Farfel and Chisolm (1987) data augment the experiences of other investigators and make it clear that lead exposure during and after paint lead removal can be only marginally lowered and may actually increase. Chisolm (198$) has drawn attention to the need for some fresh approaches to the problem of removing lead from occupied housing. One potentially promis ing technique is a "wet" method for removing leaded paint from surfaces, which eliminates the creation of lead dust, but it requires extensive field testing. The key to removal is retention add control oyer the material being removed. Extensive work in this area is required to identify safe and effective methods. Finally, a hidden assumption underlies the efforts to remove leaded paint from the homes of children found to have lead poisoning; residential stability--that the child will remain in the cleaned-up home. In reality, there is high residential mobility among poor, inner-city residents. The long-term effectiveness of unsystematic "spot" abatement is questionable, perhaps even for the individual children for whom the effort has been made. IX-23 DUP040009709 determined by the toxicity and other characteristics of the wastes and whether the release has affected or will affect people. The HRS is not an assessment of the risks found at a facility. Such an assessment occurs only after a great deal of additional data have been gathered and is used to help determine the type and degree of cleanup necessary to reduce the risk to human health to an acceptable level. A. NPL SITES--PROPOSED AND FINAL To be listed on the NPL, a site must score at least 28.5 out of a possible - . . . i* score of TOO under the HRS in effect September 30, 1987. (EPA is now revising the HRS; see discussion later in this chapter.) Of the 957 proposed and final NPL sites as of September 30, 1987, 307 have lead as an identified contaminant, and 174 have an observed release of lead to air, to surface water, or to groundwater. An observed release is documented by monitoring data showing such a release from the site. The sites with only an identified contaminant had no data showing release of the contaminant from the site. ATI proposed and final NP;L sites with an observed release of lead are listed (with their HRS scores) in Appendix F. Exposure of Children to Lead at NPL Sites EPA reviewed site files to obtain data regarding the exposure of children at each NPL site with an observed release of lead. In only a few cases was the Agency able to document exposure of children to lead from the site, since ho records are kept that separate children from the general population exposed to releases from a site. In some cases, however, studies had been conducted around sites that showed that children were exposed to lead from the sites. These are documented below. The Interstate Lead Company, an NPL site in Leeds, AL (HRS score 42.86), is a battery recycling and secondary lead smelting operation. Results of a March 1984 study of lead contamination conducted by the Jefferson County Department of Health and Bureau of Communicable Diseases, showed that children under 10 years of age living less than one-half mile from the lead plant had higher blood lead levels than children the same age living farther from the plant. Blood lead levels of all children ranged from 6 to 29 pg/dl. X-2 DUP040009710 X. A REVIEW OF ENVIRONMENTAL RELEASES OF LEAD AS EVALUATED UNDER SUPERFUND Section 118(f)(2) of the Superfund Amendments and Reauthorization Act (SARA) of 1986 requires this report tp "score and evaluate specific sites at which children are known to be exposed to environmental sources of lead due to releases, utilizing the Hazard Ranking System of the National Priorities List." EPA has carried out this requirement in two ways: (1) by identifying proposed and final sites on the National Priorities List (NPL) that have been numeric cally scored under the Hazard Ranking System (HRS) and at which lead has been released into ground or surface waters or air, highlighting those sites where children are known to have been exposed to lead; and (2) by gathering data at an urban area in Boston where children are known to be exposed to lead in soil, and scoring one residence as a site under the HRS. The HRS was designed to respond to section .105(a)(8)(A) of the Comprehen sive Environmental Response, Compensation and Liability Act of 1980 (CERCLA). This section requires that the National Contingency Plan (NCP) include "criteria for determining priorities among releases or threatened releases throughout the United States for the purpose of taking remedial action,,.,." Section 105(a)(8)(B) requires that the criteria be used to prepare a list of national priorities for sites with known or threatened releases of toxic substances throughout the United States, This use of the HRS to form the NPL is a means of directing EPA response resources to those facilities believed to present the greatest magnitude of potential harm to human health and the environment. The HRS is a means of comparing one site against others based on the estimated relative threat to human health and the environment* Relative threat is determined by assessing the likelihood of release or migration of waste contaminants from a facility, along with the consequences of such a release, such as effects on people. Migration of contaminants from a site occur through air, surface water, and groundwater* Consequences of such a release are X-l DUPQ40009711 The East Helena, MT, site (HRS score 61,65) is a primary lead and zinc smelter where 8.4 square miles of land have been contaminated, with lead in soil measuring more than 1,000 ppm. In a random sample of 90 children living near the smelter, blood lead levels of 6 to 25 pg/dl were detected. In 1975 and 1978, cattle reportedly died from lead poisoning. At the NL Industries/Taracorp Lead Smelter, an NPJ, site in Illinois (HRS score 38,11), the Illinois EPA measured high lead levels in the soil of residential areas near the smelter. Two soil samples exceeded 5,000 ppm lead. The Illinois EPA recommended that small children living nearby be restricted from playing in the dirt, from eating outside, and from placing dirt or dirty objects in their mouths. The Sharon Steel Smelter, in Utah, has been proposed for the NPL (HRS score 73,49). It is an inactive smelter with 10 million tons of tailings piled on the site. People have taken some of the waste from these piles to use in sandboxes and gardens. Analyse? by the State of Utah indicate elevated levels of lead and other heavy metals in edible portions of food grown on soil to which the waste from this site has been added. At the Harbor Island Battery Recycling: site in Washington State (HRS score 34,60)* elevated levels of lead have bedn reported in workers and their chil dren. At the Brown's Battery Recycling site in Pennsylvania (HRS score 37.34), the Pennsylvania Department of Health measured elevated blood lead levels in four children. One child received treatment to reduce his body burden of lead. Soil from three residences adjacent to the primary disposal area had lead levels ranging from 1,120 to 84,200 ppm. At the Bunker Hill Mining and Metallurgical site (HRS score 54.76), a lead smelter in Idaho, the Idaho Department of Health and Welfare found an epidemic proportion of children (98%) living within 2 miles of the smelter who had blood lead levels exceeding 40 pg/dl. The Lackawanna Refuse site in Pennsylvania (HRS score 36.57) is a former strip mining site. It is near a residential area of 9,500 people, and local children use the site as a recreational area. EPA and the Pennsylvania Depart ment of Environmental Resources found concentrations of 12,000 ppm lead in the waste contained in the thousands of drums found at the site. As can be seen from the descriptions of the foregoing cases, the sites on the National Priority List with observed releases of lead consist of sites X-3 HRS Scoring at the Boston Urban Site Three pathways in which a contaminant can migrate from a site (the princi* pal criteria for placing a site on the NPL) were evaluated. These include the groundwater pathway in which a contaminant leaches through the soil and into the groundwater, the surface water pathway in which a contaminant is washed into a stream or pond or other surface water, and the air pathway in which a' contaminant is volatilized, or otherwise migrates from the site into the air. Each pathway is scored by one of two methods, an observed release, where quanti tative evidence exists to show that a contaminant has migrated from the site, . or in cases where no quantitative data exist to document an observed release, the potential for release is scored. Groundwater Pathway, The concern for contaminant migration to groundwater is a concern for drinking water, specifically the health concern for the exposed population drinking water from a contaminated aquifer. In this case, no drinking water aquifer is near the site, and therefore no chance that lead could migrate from the site and contaminate drinking water. In any case, lead tends not to migrate through soil, but rather tends to remain in the topmost centimeter. Since no observed release exists, the potential for lead migration to groundwater must be scored. Scoring a potential release consists of two parts; route characteristics and containment. If all sections of these two parts are assigned maximum scores, the potential contamination score could equal the score for an observed release. In most instances, the potential for release is assigned a lower score than an actual release. Route characteristics consist of four physical characteristics of the site and the waste that would indicate a potential for contaminant migration to groundwater. These are: depth to the aquifer of concern, net precipitation, permeability of the unSaturated zone (impediment to migration), and physical state of the waste. Well logs for the Boston study area indicate that depth to water is usually less than 20 feet, resulting in a score of 6, the highest score for that category. The net annual precipitation (rainfall minus evapora tion) for the area is 22 inches, resulting in the highest score of 3, The soil in the area is glacial deposit, which is moderately permeable, allowing a score of 2 (of a possible 3). The physical state of the waste is particulate form, but in a powder or fine dust, allowing a score of 2 (of a possible 3). The X-6 DUP040009714 TABLE X-l. MOST COMMON ACTIVITIES ASSOCIATED WITH LEAD WASTE AT NPL SITES WITH LEAD RELEASE Activity of NPL Site With Observed Lead Release Number Rank of Sites Rank All NPL Sites Number of Sites: Percentage With Lead Release Landfill 1 75 commercial/ industrial 2 349 21 Surface impoundments 2 66 1 350 19 Containers/drums 3 49 3 261 19 Laridfil 1, municipal 4 35 4 158 22 Waste piles 5 27 10 89 30 Spill 6 21 6 139 15 Other manufacturing/ industrial 7 18 5 142 13 Chemical process/ manufacturing 8 18 7 104 17 Battery recycling 9 15 24 17 88 Tank, above ID 14 ground 9 94 15 Leaking 11 10 containers 8 95 11 Ore processing, refining, smelting 12 9 19 29 3! aThe release of lead is not necessarily attributed to the specific activity indicated. Sites often have mere than one activity and EPA reporting requirements do not identify the activity to which the release of a specific substance is attributable. These activities are present at 162 of the 167 sites with an observed release of lead. X-5 DUP040009715 approximately 1,500 feet from one site. Although the slope was less than 1%, a value of 1 was assigned for that factor because the area is highly urbanized, and there are probable paths for surface water flow, such as through storm Sewers. The 1-year, 24-hour highest rainfall for the area is approximately 2.5 inches, resulting in a score of 2. The distance to the pond is approxi mately 1,500 feet, also resulting in a score of 2, The physica! state of the waste, namely particulate, is fairly easily transported by rainfall to surface water; therefore the score of 2 was assigned; The route characteristics score is 9 (of a possible 15), which multiplied by the containment score of 3 (of a possible 3) equals 27 (of a possible 45). Waste characteristics would be the same as those scored for groundwater migratidn, Sd the sdore of 19 is the eame as that for the groundwater pathway. The category for potential impact on people of the environment consists of three factors: the use of the water, distance to a sensitive environment, and population served by drinking water intakes downstream from the site. The use of the pond, since it is in a city park, is considered to be recreational, and therefore a value of 2 was assigned. There are no sensitive environments or drinking water intakes near the site; therefore a score of 0 was assigned for each of these factors. The total category score is 4.78. Air Pathway. The air route for migration of a contaminant from a site can only be scored for an observed release. To document an observed release, it must be shown that lead is migrating by air from the site or has done so in the past. To document ah observed release, alternative sources for the lead must be screened out, which means that background levels must be determined so that the lead migrating from the site can be attributed to the site (e.,g., lead-based paint). Lead is ubiquitous to urban areas, being released from automobile emissions and from various industries. Most of the lead released settles on soil or pavement. Separating lead attributable to house paint from lead attributable to other source? requires very sophisticated sampling and analytical techniques. If the lead in soil were shown to be attributable to leaded paint, the lead must also be shown to have migrated through the air. Thus, other migra tion routes such as physical transfer by the daily activities of residents (e.g., transfer of house dust to soil or removal of paint chips) or transfer by rainfall must be ruled out. Finally, an observed release must be monitored at the breathing zone and show levels significantly above background levels. The X-8 DUP040009716 total score for route characteristics for groundwater contamination is 13 (of a possible 15). Containment refers to any means (such as grass or ground coyer in this case) that would inhibit the migration of the contaminant from the site. Since lead remains in the topmost centimeter of soil, and at the two houses selected for ranking no ground cover was observed, the maximum score of 3 was assigned, meaning no containment was observed. The score for potential lead migration to groundwater received a score of 39, 6 points below the maximum score of 4$ for an observed release. The HRS next evaluates the consequences of such a release in terms of toxicity, persistence and amount of the waste* and the possibility that people might use a potentially contaminated aquifer for drinking.water. A waste characteristics score of 19 ** out of a possible 26 -- was ^ obtained for the site since lead's score of toxicity is set at 1$, and the quantity present was scored as 1. The quantity of lead deposited at the site is unknown, but in any case would be a small amount compared with, e.g., waste deposit quantities at dumpsites. In scoring the possibility that people might use a potentially contaminated well or aquifer for drinking water, the HRS scores the use of the nearest aquifer of concern within a 3-mile radius of the site, the distance to the nearest well that draws water from the aquifer of concern, and the number of people drinking water from welis within a 3-mile radius of the site. In this case, there is no drinking water well within a 3-mile radius of either site, but there are industrial facilities with wells for industrial purposes within the 3-mile radius. For this reason* a value of 1 (rather than 0) has been assigned. However, no value .other than 0 could be assigned as distance to aquifer of concern, and number of people drinking water from wells within a 3-mile radius. This category score is 3 (of a possible 49). Surface Water Pathway. Scoring for migration of contaminants from a site via the surface water pathway closely follows that of the groundwater pathway. Where no observed release can be documented, as here, the potential release is scored using route characteristics and containment. Route characteristics for surface water migration include facility slope and intervening terrain to the nearest downhill surface water, rainfall, the distance to the nearest surface water, and the physical state of the waste. In this case, the only surface water near either site is a pond on a golf course, X-7 DUP040009717 fire or explosion threat to the public or to sensitive environments, or a fire and explosion threat has been demonstrated by observation at the site. Such a threat could result in consideration for a removal action at a site.. Since neither of these events is relevant to the threat from this urban site, no evaluation of the fire and explosion mode was done. e< REVISION OF THE HAZARD RANKING SYSTEM ./ The Superfund Amendments and Reauthorization Act specifically directed EPA to modify the HRS so that "to the maximum degree feasible, it accurately' assesses the relative degree of risk to human health and the environment posed by sites." EPA was specifically directed to assess human health risks associ ated with actual and potential surface water contamination, specifically considering recreational use of the water, and the migration of a contaminant to downstream sources of drinking water; damages from an actual or a threatened release to natural resources that may affect the human food chain; actual or potential ambient air contamination; and those wastes described in Section 3001 of the Resource Conservation and Recovery Act (e.g., flyash, bottom ash, slag waste, and flue gas emission control waste). EPA was also directed to give high priority to facilities where a release has resulted in closure of drinking water wells or has contaminated a principal drinking water supply. In an Advance Notice of Intent to Revise the HRS, published April 9, 1987, EPA noted that the direct contact mode has b.een one of the most significant factors in selecting a remedy when cleaning up hazardous waste sites where direct contact with the site and the contaminants were factors. The Agency intends to include a direct contact factor in its revised HRS, for purposes of placing sites on the NPL, and solicited comments on appropriate methods to do so, EPA is addressing the concerns listed in SARA in its update of the Hazard Ranking System, The choice of data and of models to evaluate the data for each pathway has been reviewed by various offices within the Agency, and by the Agency's Science Advisory Board. An updated version of the HRS is expected to be proposed for comment in the summer of 1988. Comments will be considered and a final update of the HR$ will be published. X-10 DUPO40009718 EPA considered methods to obtain such data, but would have had to mount a research project without any assurance of obtaining usable data- the Agency decided to treat this site like any other site to be scored under the HRS, thereby foregoing the research monitoring project. The site score for the air pathway was 0. Site Migration Scoring. The Site Migration Score is the principal basis for proposing that a site be included on the NPL. It is a composite of the migration scores calculated for each of the three migration pathways- It may be defined as the square root of the sum of the squares of each pathway score divided by 1.73. Sites with a migration score of 28.5 or higher qualify for inclusion on the NPL. The highest Site Migration 5core for the two actual Boston urban lead sites was 3.56. Additional Modes of Potential Harm. Two additional modes of potential harm to people or the environment from a site are also scored under the HRS, but are not used for the purpose of placing a site on the NPl, These modes are direct contact with contaminants from a site and threat of fire or explosion from a site. These scores may be used for purposes of removal actions or for enforcement actions against a responsible party, A site need not be listed on the NPL for EPA to take either removal or enforcement action to protect people or the environment. Direct Contact Mode. A site may be scored on the basis of an observed incident or on the potential for an incident, using factors of accessibility and containment- In the case of the Boston urban sites, the score was based on an observed incident, namely one documented child with an elevated blood lead level- The score is 45- The waste toxicity was scored at the highest value, 15, for lead- Exposed population within a 1-mile radius is nearly 12,000 people according to U.S. Census data, and this resulted in a score of 4, The distance to a critical habitat is considerably more than one mile, resulting in a score of 0- For the direct contact mode, this site would score 50, a level at which the Agency would reevaluate the site for potential removal action. Fire and Explosion Mode. The fire and explosion mode is evaluated when either a state or local fire marshal has certified that the site presents a significant X-9 DUP040009719 0. SUMMARY As pointed out in this chapter, there is no question that children are being exposed to lead at sites that are already on the National Priority List for Superfund remedial action. These sites were placed on the NPL according ,, to their HRS score, which showed migration of lead and other contaminants from the sites, and in some cases actual exposure of children to the lead and other contaminants from the site. The scoring of the Boston urban lead site under the HRS pointed out the ^ differences of this area from the usual sites scored under the HRS. The Boston site was heavily residential, rather than an abandoned dumping area. It had only one known contaminant rather than an unknown mixture, so that it needed no Complex assessment or site inspection. It had no hazard from migration of the contaminant, but rather from the nonmigration of the lead, which made it available to children. The only mode by which this site could have scored high enough to be placed on the NPL was by the direct contact route. The air route could have contributed to the score if an experimental monitoring project had been con ducted and if all conditions had been ideal. This includes enough wind so that the soil containing lead had been blown off site, into the breathing zone of children, and recorded by the monitor. The revised HRS to be proposed in 1988 is to contain a revised direct contact mode for use in listing NPL sites. Under the new HRS, it is possi ble that an urban site having leaded paint contamination would score above the HRS cutoff score based on direct contact alone. The proposed HRS will also Include a potential air pathway, which, depending On its characteristics, may be more favorable to this sort of site than is the present observed air pathway. This factor may also increase the HRS score of an urban leadcontaminated site. When the revised HRS is finally available, EPA will be able to determine how such urban lead-contaminated sites will score relative to other sites scored under the system. During the interim, EPA will be collecting data through the pilot projects under Section 111 of SARA to determine the impact of lead-contaminated soil removal on children's blood lead levels. X-ll DUP040009720 do so in ways that assured a satisfactory level of certainty for the numbers. Vte therefore provided national-level estimates. There is surprisingly little information on the actual numbers of young children with a record of being exposed to a source of lead sufficient to raise the Pb-B levels to either some measured amount or to some toxicity level. Information that is available is diffuse in terms of the levels of exposure, the number of years in the childhood age span, and other related measures. In some cases, exposure is defined according to the number of children potentially at increased risk because of their proximity to lead-emitting sources. In other cases, exposure is estimated on the basis of elevated;;Pb-B levels. Pb-B levels as risk thresholds are defined differently among studies. However, even potential exposure of children due to contact with a lead source presents a higher risk situation than does the absence of such sources. Better enumeration and screening for Pb-B levels are required in communi ties contiguous to stationary lead operations, e.g., primary and secondary smelters. A tjiajor problem with estimating the effects of lead in dust and soil as a source for childhood exposure is that there is simultaneous direct exposure to lead from paint and air sources, the primary contributors to this pathway. Better data are needed on the relationships between airborne lead and lead from dust or soil, especially on changing airborne levels. For example, we could not distinguish between children exposed to the two media and encountered over estimating and multimedia-uptake problems. On the other hand* some sizable fraction of these children have other source exposures. More specific information is required on the distribution of lead concen trations in the tap water qf households with young children, U.S. EPA (1986b) has estimated that 20% of households have drinking water above the proposed standard for lead. Assessing actual lead levels in various tap water sources* beyond the projected water-based Pb-B changes given in Chapter VI, would still be helpful. Information on dietary lead intakes by infants and toddlers needs to be updated. Information is also needed on the intake distribution among children. The model of food consumption by Beloian described in Chapter IX is relevant to earlier rather than more recent food lead levels. The FDA has provided recent in-house estimations of dietary lead intakes and changes therein. Evaluating the efficacy of remaining further actions and future assessment of this exposure route is needed since we will reach the limits to further food lead controls not too far in the future. XI-2 DUP040009721 ' XL LEAD EXPOSURE AND TOXICITY IN CHILDREN AND OTHER RELATED GROUPS IN THE UNITED STATES: INFORMATION GAPS, RESEARCH NEEDS., AND REPORT RECOMMENDATIONS In the preparation of this report to Congress, exposure and health risk problems were Identified that require further analysis because of significant gaps In Information, These gaps are identified as are research needs that must be addressed in order to fill the gaps. The current status of the lead problem and the underlying data base prompted the recommendations presented, A, INFORMATION GAPS As noted early in the report, comprehensive, current, and accurate data on the numbers of children and other groups exposed to lead at some level of con cern, by location or source, were not readily available. Since these data did not always exist in the exact form required, we often estimated the numbers, using the statistical techniques that seemed most precise, to be reasonably responsive to the letter and spirit of Section 118(f) of SARA, Part of this gap in information is being addressed. The National Center for Health Statistics is preparing to carry out the third National Health and Nutrition Examination Survey (NHANES HI); information of the type presented in the second survey, with respect to Pb-B and EP levels, will be updated and future Pb-B levels will be collected in ways more useful for various public health purposes. This survey will be executed and analyzed in the period 1988-1994, The 1990 Census will also provide enumerations of children for the different categories for the year 1990. Such data will be more current for such factors as the effects of economic dislocations occurring that are structural rather than cyclical in nature, e. g., shifts from well-paid indus trial jobs to services jobs for certain segments of the population. Those data collections will occur well into the future, however, and the estimates in this report will have to suffice as reasonable interim assessments. We tried several approaches to identify and rank children with elevated Pb-B levels by regional or other division of geographic area, but could hot XI-1 DUP040009722 B. RESEARCH NEEDS A minimum inventory of research needs In areas covered by this report includes; (1) Continuing and regionally comprehensive studies of quantitative relation ships between exposed populations and both their geographic distribution and various lead sources are needed. These include the high-lead sources as well as those provisionally viewed as background or low-level. As part of this effort, data collected by U.S. Census-taking methods shoul.d include elements relating to environmental exposure to toxicants. (2) As a follow-up to (1), further examination is needed of body lead-source lead relationships to include dust/soil versus blood lead and paint lead versus blood lead. (3) Continued development of quantitative biokinetlc/aggregate uptake models is necessary for reliable prediction of body lead burdens which may reduce the need for expensive population surveys. (4) Both the number and scope of prospective studies of lead exposure and toxicity in U.S. populations should be expanded to build on several ongoing U.S. efforts. Present programs offer valuable public health and scientific information on in utero and neonatal lead contact and its consequences. (5) Cautious examination of the use of improved Chelation therapy modalities is required, with emphasis on Specificity for lead and minimal side effects. (6) Further research is needed on the relative strengths and shortcomings of biological indicators of systemic exposure. Of particular importance here are in vivo measures of lead accumulation in the mineral tissue of young children as a means of providing a biological record of exposure during periods of maximum vulnerability. Other key areas in lead metabolism deal with uterine lead uptake and deposition versus Pb-B values during pregnancy and such relationships as factors determining whether a fetus sustains toxic injury or not. (7) In the area of lead exposure abatement, research on several fronts is required: XI-4 DUP040009723 Although much information has been presented on the adverse lead effects in young chi ldren and other risk groups * gaps remai n in our data base. For example, there are questions as to which biological indicator is appropriate for use at which time frame of child development. It is also important to knovr which of the early effects of lead have the most useful predictive value for later outcomes and which toxic responses will persist, both into later childhood and in later decades. Some of' these questions may be answered through the prospective studies under way in the United States and elsewhere. The area of lead exposure abatement approaches and strategies is plagued with both qualitative and quantitative unknowns. Information is needed on the full range of lead paint/dust/soil removal options in terms of their technology and costs. In particular, field studies are needed on the relative efficacy of lead removal protocols for large abatement efforts versus small efforts with individual homes or contiguous tracts of housing. As part of recent legislation (SARA, 1986), EPA is now sotting up and will be evaluating results from several soil lead abatement demonstration projects in the United States. Present methods of lead removal from homes and other sites and its disposal are relatively crude. Evidence that the methods appear to endanger abatement workers and occupants alike was presented in the report. Also needed are better methods of preventing dispersal of removed lead from one site to other sites. Chisolm (1986) has suggested wet chemical methods using certain paint surface removal agents, and nonthermal, nondust approaches may be the best ways tp proceed, so long as these alternatives are safe and economical. Knowledge is also lacking about the support approaches for any assault on lead exposure via extra-environmental means. These approaches include main taining optimal nutrition in risk populations through community-level programs and effective legal infrastructures to enforce compliance with abatement mea sures and timetables. A good overview also is lacking on how changes in screening program organization have affected the scope and effectiveness of lead screening programs in high-risk areas. Because the societal and monetary cost'-effectiveness of screening is documented, it is desirable to know the level of undetected toxicity among screened target populations. XI-3 DUP040009724 coordinated to be effective. In addition, such an attack must incorporate well"defined goals so that its progress can be measured. For example, the lead exposure of children and fetuses must be monitored and assessed systematically if efforts to reduce their exposure are to succeed, A comprehensive attack on the U.S, lead problem should not preclude focused efforts by Federal, state, or local agencies with existing statutory authorities to deal with different facets of the same problem. Indeed, all relevant agencies should continue to respond to this important public health problem, but do so with an awareness of how their separate actions relate to the goals of a comprehensive attack,s The following specific measures are recommended to support the general objective of eliminating childhood lead poisoning. 1, Lead in the Environment of Children (a) We recommend that efforts be implemented to reduce lead levels in sources that remain major causes of childhood lead toxicity. (1) Leaded paint continues to cause most of the severe lead poisoning in U.S. children. It has the highest concentration of lead per unit of weight and is the most widespread source, being found in approximately 21 million pre-1940 homes, (2) Oust and soil lead, derived from flaking, weathering, and chalk ing paint plus airborne lead fallout over the years, is the second major source of potential childhood lead exposure, (3) Drinking water lead is of intermediate but highly significant concern as an exposure source for both children and the fetuses of pregnant women. Food lead also contributes to exposure of children and the fetuses, (4) Lead in drinking water is a controllable exposure source and state and local Agencies should be encouraged to enforce strictly the Federal ban on the use of leaded solder and plumb ing materials. Stronger efforts should also be made to reduce exposure to lead-based paint and dust/soil lead around homes, schools, and play areas. (b) We recommend that efforts to reduce lead in the environment be accom panied by scientific assessments of the amounts in each of these sources through strengthening of existing programs that currently attempt such assessment. The largest information gap exists in determining which XI-6 DUP040009725 '4KK. (a) Field studies on the efficacy of broader lead removal from child environments, e.g., at a tract or neighborhood level or larger. Such efforts would include before-and-after evaluation of Pb-B levels, done with careful statistical and quality control/ quality assurance protocols. In response to SARA, EPA is now addressing this problem systematically via three demonstration projects. (b) Field studies of the type detailed above with designs stratified to permit assessment of how such procedures relate to primary contributors, for example, lead paint versus urban air fallout of lead. Here, also, the EPA demonstration projects will be helpful, if sub-studies are made of these variables. (c) Further development of field methods is necessary to test lead in various exposure media. Of particular importance are improved in situ methods for lead in painted surfaces, (d) Assessment of the actual physical removal technology for removal of leaded paint , dust, and the like. A related examination of practical disposal plans is also necessary. As noted earlier, leaded paint consists of an aggregate burden of millions of tons, while other inputs also add up to millions of tons. Therefore, disposal is not inconsequential to the lead abatement problem. Moving the lead may also inadvertently shift exposure to another population. A draft report for a model site in Boston (Appendix E), discusses various scenarios and associated problems. (e) Further examination of the efficacy of lead screening programs for high-risk populations both for their scope and effectiveness and for the relationship between public financial support of screening and the ability to identify children at risk is needed. (f) Assessment of the relative costs of effective, if expensive, alternatives to the piecemeal abatement, the piecemeal enforce ment, and the piecemeal follow-up for reexposure that appears to be the present status of remedial actions. Is it less expen sive, in human and resource terms, to consider such measures as relocation? (g) Research that explores the feasibility of better biochemical screening measures beyond the use of erythrocyte protoporphyrin (EP) since this measure is not reliable and yields too many false negatives. Failure to detect positive cases makes such research urgent. C. RECOMMENDATIONS In view of the multiple sources of lead exposure, an attack on the pro blem of childhood lead poisoning in the United States must be integrated and XI-5 DUP040009726 (4) Lead pollution is a health problem that involves almost all seg ments of U.S, society. Extra-environmental or legal measures should be explored to reduce lead levels in the environment by both public and private sectors,. 2. Lead in the Bodies of Children (a) Children are being exposed to and poisoned by lead while environmental lead reduction is under way. Screening programs with sufficient funding to make a real and measurable impact are urgently needed. (b) There is a need to maintain screening programs extant in some states that currently identify children at risk from lead exposure at or above blood* lead levels of 25 pg/dl. Since current EP tests, used as the initial screen, cannot accurately identify children with blood lead levels below 25 pg/dl, screening tests that will identify children with lower bloodlead levels must be developed* (c) The 1987 statement of the American Academy of Pediatrics calling for lead screening of all, high risk children should be supported by assistance in implementation. (d) Use of in vivo cumulative lead screening methods is recommended as soon as available. A quick, accurate, noninvasive screening test would be bet ter accepted by parents, resulting in many more children being screened. (e) We recommend that screening be extended to all high-risk pregnant women, with particular emphasis on urban teenaged pregnant women, and that prenatal medical care providers be involved in this effort. (f) We recommend determination of the prophylactic role of nutrition in ameliorating systemic lead toxicity. (g) Further use should be made of metabolic models already developed and research to refine them should be done. This will enable their use to predict total body burden contributions from varying environmental sources of known lead levels. (h) Long-term prospective studies of lead's effects during child growth and development should continue to be supported through appropriate support mechanisms, beginning with the relationship of maternal lead burden to in uterp toxicity and including children with neurological disabilities and genetic disorders, such as sickle cell anemia. XI-8 DUP040009727 (1) Natlonwide assessments of lead toxicity status in U.S. children on a con tinuing basis are recommended. Efforts such as the planned NHANES III survey should be supported to maximize the data collected about lead expo sure levels. Support as well should be provided for more geographically focused surveys, e-g. bn the level of Metropolitan Statistical Areas (MSAs). Xt-9 DUP040009729 Bander, L. K-; Morgan, K, j.; Zabik, M, E. (1983) Dietary lead intake of preschool children. Am. 0, Public Health 73: 789-794- Barltrop, D. (1969) Transfer of lead to the human foetus* In: Barltrop, D.; Burland, W. L., eds. Mineral metabolism in pediatrics, Philadelphia, PA: Davis Co.; pp. 135-151. Barltrop, D. (1972) Children and enyifomental lead* In: Hepple, P., ed. Lead in the environment: proceedings of a conference. London, United Kingdom: Institute of Petroleum; pp. 52-60. ' Barry, P. 5, I. (1975) A comparison of concentrations of lead in human tissues. Br. J, jnd. Med. 32: 119-139, Barry, P, S, I, (1981) Concentrations of lead in the tissues of children. Br. J. Ind. Med. 38: 61-71. Bayley, N, (1969) Bayley scales of infant development. New York, NY: Psychological Corp. Bellinger, 0, C,; Needleman, H. L.; Leviton, A.; Waternaux, C,; Rabinowitz, M. B.; Nichols, M. L. (1984) Early sensory-motor development and prenatal exposure to lead, Neurpbehav. Toxicol, Teratol. 6: 387-402. Bellinger, D. C.; Leviton, A. ; Waternaux, C,; Needleman, H, L.; Rabinowitz, M, 8. (1985) A longitudinal study of the developmental toxicity of lowlevel lead exposure in the prenatal and early postnatal periods. In: J. D. Lekkas, ed:. International Conference: heavy metals in the environ ment, v. 1; September; Athens, Greece, Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 32-34. Bellinger, 0. C.; Leviton, A,; Needleman, H, L.; Waternaux, C.; Rabinowitz, M, B. (1986) Low-level lead exposure and infant development in the first year. Neurobehav. Toxicoi, Teratol. 8: 151-161. Bellinger, D.; Leviton, A, ; Waternaux, C.; Needleman, H,; Rabinowitz, M. (1987a) Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development. N. Engl, J. Med. 316: 1037-1043. Bellinger, 0.; SIonian, J.; Leviton, A.; Waternaux, C.; Needleman, H,; Rabinowitz, M, (1987b) Low-level lead exposure and child development: assessment at age 5 of a cohort followed from birth. In: Lindberg, S, E.; Hutchinson, T. C., eds. International conference: heavy metals in the environment, v. 1; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 49-53, Beloian, A> (1982) Use of a food consumption model to estimate human contami nant intake. Environ, Monit, Assess. 2: 115-127. Beloian, A. (1985) Model system for use of dietary survey data to determine lead exposure from food. In: K. R. Mahaffey, Dietary and environmental lead: human health effects. Amsterdam, The Netherlands: Elsevier; pp. 109-155. R-2 DUP040009730 REFERENCES Alexander, F:. W.; Delves, H. T, (1981) Blood lead levels during pregnancy. Int. Arch. Occup. Environ. Health 48: 35-39. Alexander, F. W.; Delves, H. T.; Clayton, B. E. (1973) The uptake and excretion by children of lead and other contaminants. In: Barth, 0.; Berlin, A.; Engel , R.; Recht, P,; Sweets, J., eds. Environmental health aspects of lead: proceedings, international symposium; October 1972; Amsterdam, The Netherlands. Luxembourg: Commission of the European Communities; pp. 319-331, American Academy of Pediatrics. (1987) Statement on childhood lead poisoning. Committee on environmental hazards/committee on accident and poison prevention. Pediatrics. 79: 457-462. Angle, C. R,; Marcus, A, ; Cheng, I.-H.; Mclntire, M. S. (1984) Omaha childhood blood lead and environmental lead: a linear total exposure model. Environ. Res, 35: 160-170. Annest, J. L,; Mahaffey, K. R. (1984) Blood lead levels for persons ages 6 months-74 years, United States, 1976-80. Washington, DC: U.S. Department of Health and Human Services; DHHS publication no. (PHS) 84-1683. (National health and nutrition examination survey series 11, no. 233.) Annest, J. JL; Pirkle, J. L.; Makric, 0.; Neese, J. W.; Bayse, 0. 0.; Kovac, M, G. (1983) Chronological trend in blood lead levels between 1976 and 1980. H. Engl. 0. Med- 308: 1373-1377. Araki, $.; Ushio, K. (1982) Assessment of the body burden of chelatable lead: a model and its application to lead workers, Br. J, Ind, Med, 39: 157-160. Arizona Department of Health Services. (1976) Lead-based paint report of findings to the State Legislature, December 20. Baghurst, P. A.; Robertson, E, F.; McMichael, A, J. ; Vimpani, G. V.; Wigg, N, R.; Roberts, R. R. (19S7) The Port Pirie cohort study: lead effects on pregnancy outcome and early childhood development. Neurotoxicology 8: 395-402. Baker, E. L., Or,; Falland, 0. S,; Taylor, T. A.; Frank, M.; Peterson, W.; Lcvejoy, G.; Cox, 0,; Housworth, J.; Labdrigan, P. j, (1977) Lead poison ing in children of lead workers: house contamination with industrial dust. N. Engl. J. Med, 296; 260-261. Baltimore City Health Department. (1971) Chronology of lead poisoning control: Baltimore, 1931-1971. Baltimore Health News 48: 34-40. R-l DUP040009731 Burchfiel, J, L.; Ouffy, F. H.; Bartels, P. H.; Needleman, H, L, (1980) The combined discrimination power of quantitative electroencephalography and neuropsychologic measures in evaluating centra) nervous system effects of lead at low levels. In: H. L. Needleman, ed, Low level lead exposure: the clinical implications of current research. New York, NY: Raven Press; pp. 75-89. Byers, R. K.; Lord, E. E, (1943) Late effects of lead poisoning on mental development. Am. J. Ois, Child. 66: 471. Centers for Disease Control. (1978) Preventing lead poisoning in young cfnldren. J. Pediatr. (St. Louis) 93: 769-720. Centers for Disease Control. (1982) Lead poisoning. Morbid. Mortal. Rep. 30: 112-113. Centers for Disease Control. (1983) Abortion surveillance, 1979-1980. issued May 1983. (Tables 3, 6, 7, and 8). Centers for Disease Control, (1985) Preventing lead poisoning in young children: a statement by the Centers for Disease Control, January, 1985, Atlanta, GA: U.S. Department of Health and Human Services; no. 99-2230. Centers for Disease Control. (1986a) East Helena, Montana, child lead study, Summer, 1983; final report, July, 1986, Centers, for Disease Control. (1986b), Final report: Kellogg revisited-1983, Childhood blood lead and environmental status report. Panhandle District Health Department, Idaho Department of Health and Welfare, Center for Environmental Health/Centar for Disease Control, Public Health Service, United States Environmental Protection Agency, July, 1986, Centers for Disease Control. (1986c) Abortion statistics, U.S. 1982-1983 [Prerelease to state health agencies, 1986), Center for Health Promotion and Education. Chamberlain, A. C, (1983) Effect of airborne lead on blood lead. Atmos, Environ, 17: 677-692. Chamberlain, A, C.; Heard, M, J.; Little, P.; Newton, 0,; Wells, A. C,; Wiffen, R, D, (1978) Investigations into lead from motor vehicles. Harwell, United Kingdom: United Kingdom Atomic Energy Authority; report no. AERE-R9198. Charney, E.Sayre, J. ; Coulter, M. (1980) Increased lead absorption in inner city children: where does the lead come from? Pediatrics 65: 226-231, Charney, E.; Kessler, fl,; Farfel, M.; Jackson, D. (1983) Childhood lead poison ing: a Controlled trial of the effect of dust-control measures on blood lead levels. N. Engl, J. Med, 309: 1089-1093, R-4 DUP040009732 Beni gnus, V, A.; Otto, 0. A.; Muller, K, E,; Seiple, K. j, (1981) Effects of age and body burden of lead on CNS function In young children. II. EEG spectra. Electroencephalogr. Clin. Neurophysiol. 52: 240-248. Billick, I.j Gray, V. (1978) Lead-based paint-poisoning research, review and evaluation, 1971-1977. Washington, DC:U.S. Department of Housing and Urban Development; HUD RP-809. Blackfan, K. D. (1917) Lead poisoning in children with especial reference to lead as a Cause of convulsions. Am. J, Med. Sci. 153: 877-887. Blake, l(, C. H. (1976) Absorption of 2<*3Pb from gastrointestinal tract of man. Environ. Res. 11: 1-4. Blake, K. C. H, (1980:) Radioactive lead studies in the human [dissertation], Capetown, South Africa: University of Capetown. Bornschein, R, L,; Rabinowitz, M. B., eds. (1985) The second international conference on prospective studies of lead; April 1984; Cincinnati, OH. Environ, Res, 38(1). Bornschein, R. L.; Succop, P,; Dietrich, K. N,; Clark, C- S.; Que Hee, S.; Hammond, P. 8, (1985) The influence of social and environmental factors on dust lead, hand lead and blood lead levels in young children. Environ. Res. 88: 108-118. Bornschein, R, L.; Succop, P, A. ; Dietrich, K. N,; Krafft, K,; Grote, J.; Mitchell, T.; Berger, 0.; Hammond, P. B, (1987a) Pre-natal lead exposure and pregnancy outcomes in the Cincinnati lead study. In: Lindberg, S. E.; Hutchinson, T. C., eds. International conference: heavy metals in the environment, v. 1; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd,; pp. 156-158. Bornschein, R. L.; Succop, P. A. ; Krafft, K. M.; Clark, C. 5. ; Peace, B.; Hammond, P. B. (1987b) Exterior surface dust lead, interior house dust lead and childhood lead exposure in an urban environment. In: Hemphill, D. D,, ed. Trace substances in environmental health - XX: proceedings of University of Missouri's 20th annual conference; June 1986; Columbia, M0. Columbia, M0: University of Missouri; pp. 322-332. Bornschein, R. L.; Grote, J.; Mitchell, T.; Succop, P,; Shukla, R. (1987c) Effects of prenatal and postnatal lead exposure on fetal maturation and postnatal growth. In: Smith, M.; Grant, L. 0.; Sors, A., eds. Lead expo sure and child development: an international assessment. Lancaster, United Kingdom: MTP Press; in press. Brunekreef, B. D. (1984) The relationship between air lead and blood lead in children: a critical review. Sci. Total Environ, 38: 79-123, Brunekreef, B, 0. ; Noy, D.; Biersteker, K,; Boleij, J. (1983) Blood lead levels of Dutch city children and their relationship to lead in the environment. 8. Air Pol Jut. Control Assoc, 33: 872-876, R-3 DUP040009733 Chisolm, J. 0., Jr. (1981) Dose-effect relationship for lead in young children: evidence in children for interactions among lead, zinc and iron. In: Lyriam, D. R.; Piantanida, L. G.; Cole, J. F., eds. Environmental lead: proceedings of the second international symposium on environmental lead research; December, 1978; Cincinnati, Ohio, New York, NY: Academic Press; pp. 1-7. (Ecotoxicology and environmental quality series). Chisolm, J. J., Jr. (1986) Removal of lead paint from old housing: the need for a new approach. Am. J. Public Health 76: 236-237. Chisolm, J. J., Jr.; Barltrop, D. (1979) Recognition and management of children with increased lead absorption. Arch. Dis. Child. 54: 249-262, Chisolm, J. J., Jr.; Hell its, E. D.; Quaskey, S. A. (1985) The relationship between the level pf lead absorption in children and the age, type and condition of housing. Environ. Res. 38: 31-45. Christoffersson, J. 0.; Schutz, A.; Ahlgren, L.; Haeger-Aronsen, B.; Mattsson, S.Skerfvig, 5. (1984) Lead in, finger-bone analyzed in vivo in active and retired lead workers. Am. J. Ind. Med. 6: 447-457, Ciriello, P. L.; Goldberg, T. (1987) Draft report: lead-contaminated soil cleanup. Boston, MA: U.S. Environmental Protection Agency, Region I, March 27, 1987. (Appears in this report as Appendix E), City of Dallas Department of Health. (1985) Blood lead screening program: East Oak Cliff and West Dallas. Final report: Fall, City of Chicago, IL. (1985) Department of Health lead screening statistics: 1985 report. Clark, C. S.; Bornschein, R. L. ; Succop, P. ; Que Hee, S. S,; Hammond, P. B,; Peace, B. (1985) Condition and type of housing as an indicator of poten tial environmental lead exposure and pediatric blood lead levels. Environ, Res. 38: 46-53. Clark, C. S.; Bornschein, R, L.; Succop, P.; Hammond, P, B,; Peace, B.; Krafft, K.; Dietrich, K. (1987) Pathways to elevated blood lead and their impor tance in control strategy development. In: Lindberg, S. E.; Hutchinson, T. C., eds. International conference: heavy metals in the environment, v, 1; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 159-161, Caere, J, C,; Ter Haar, G. L. (1977) Lead levels in tissues from rats fed soils containing lead. Arch, Environ. Contam. Toxicol. 6: 111-119. Davis, J. ML; Svendsgaard, D. J. (1987) Low-level lead exposure and child development. Nature (London) 329: 297-300. de la Burde, B.; Choate, M. S,, Jr. (1972) Does asymptomatic lead exposure in children have latent sequelae? J. Pediatr. 87: 1088-1091, de "la Burde * B.; Choate, M, S,, Jr, (1975) Early asymptomatic l ead exposure and development at school age. J. Pediatr. 87: 638-642. 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L (1904) A plea for painted railings and painted walls of rooms as the source of lead poisoning among Queensland children. Australia Med. Gazette 23: 149-153, Gibson, J. L.; Love, W.; Hardine, D.; Bancroft, P.; Turner, A. J. (1892) Note on lead poisoning as observed among children in Brisbane. In: Huxtable, L. R., ed. Trans. 3rd Intercolonial Medical Congress of Australasia; September. Sydney, Australia: Charles Potter; pp. 76-83. Gilsinn, J. (1972). Estimate of the nature and extent of lead paint poisoning in the United States. Washington, DC: National Bureau of Standards( NBS technical note 764. Grant,, L. D.; Davis, J. M. (1987) Effect of low-level lead exposure on pediatric neurobehavioral and physical development; current findings and, future directions. In: Smith, M.; Grant, L. 0.; Sors, A,, eds. Lead exposure and child development: an international assessment- Lancaster, United Kingdom: MTP Press; in press. Graziano, J.; Popovac, M.; Murphy* A.; Mehmeti, A.; Kline, J.; Ahmedi, G.; Shrout, P.; Zvicer, Z.; Wasserman, G.; Gashi, E,; Stein, B,; Rajovic, B. :; Belmong, L.; Colakovic, B.; Bozovic, R,; Haxhiu, R.; Radovic, L.; Vlaskovic, R.; Loiacano, N. (1987) Environmental lead, reproduction and infant development. In: Smith, M.; Grant, L, D-; Sors, A., eds. lead exposure and child development: an international assessment. Lancaster, United Kingdom: MTP Press; in press. Griffin, T. B.; Coulston, F.; Goldberg, L.; Wills, H.; Russell, J. C.; Knelson, J. H. (1975) Clinical studies on men continuously exposed to airborne particulate lead: In: Griffin, T, B,; Knelson, J. H., eds. Lead. v. 2, supplement. Stuttgart, West Germany: Georg Thieme Publishers; pp. 221-240. Gross, $. 8. (1981) Human oral and inhalation exposures to lead: summary of Kehoe balance experiments. J. ToxiCol. Environ. Health 8: 333-377. Hamilton, A. ; Rbznikoff, P.; Burnham, G. M. (1925) Tetraethyl lead. JAMA J. Am. Med, Assoc, 84: 1481-1486. Hammond, P, B, (1973) the effects of D-penici11amine on the tissue distribution and excretion of lead. Toxicol. Appl, Pharmacol, 26: 241-246. Harley, N, H.; Kneip, T. H. (1985) An integrated metabolic model for lead in humans of all ages: final report. New York, NY: New York University School of Medicine; EPA contract no. B44899. Harvard School of Public Health Community Health Improvement Program. (1981) Casas Sin Plomo: final report. Cambridge, MA: Harvard University. Harvey, P. G.; Hamlin, M. W.; Kumar, R.; Delves, H. T. (1984) Blood lead, behavior and intelligence test performance in pre-school children. Sci. total Environ. 40: 45-60. 8-8 DUP040009736 % Ernhart, C. B.; Morrow-Tlucak, M.; Marler, M. R.; Wolf, A, W, (1987a) Low level lead exposure In the prenatal and early preschool periods: early preschool development. Neurotoxicol. Teratol. 9: 259-270. Ernhart, C. B.; Brittenham, G.; Harler, M. R.; Sokol, R. J. (1987b) Lead related birth defects: some methodological issues. In: Smith, M.; Grant, L. D.; Sors, A., eds. Lead exposure and child development: an international assessment. Lancaster, United Kingdom: HTP Press; in press. / Everson, J.; Patterson, C. C. (1980) "Ultra-clean" isotope dilution/mass spectrometric analyses for lead in human blood plasma indicate that most reported values are artificially high. Clin. Chem. 26: 1603-1607. Facchetti, S. (1985) Isotope lead experiment--an update. Presented at: Lead environmental health: the current issues; April/May; Durham, NO; Duke University. Facchetti , S. Geiss, F. (1982) Isotopic lead experiment: status report. Luxembourg: Commission of the European Communities; publication no. EUR 8352EN. Farfel, M. R. (1985) Reducing lead exposure in children. Annu. Rev. Public Health 6: 333-360. Farfel, M. R.; Chisolm, J. J., Jr. (1987) Comparison of traditional and alter native residential lead paint removal methods. In: Lindberg, S. E.; Hutchinson, T. C,, eds. International conference: heavy metals in the environment, v, 2; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd,; pp. 212-214. Flanagan, P, R.; Chamberlain, M. J.; VaTberg, L. S. (1982) The relationship between iron and lead absorption in humans. An, J, Clin. Nutr. 36: 823-829. Friberg, L, T, (1985) Yant memorial lecture. The rationale of biological monitoring of chemicals--with special reference to metals. Am, Ind, Hyg. Assoc. J. 46: 633-642. Friberg, L, T.; Vahter, M. (1983) Assessment of exposure to lead and cadmium through biological monitoring: results of a UNEP/WHO global study. Environ. Res, 36: 95-128. Fulton, M.; Thomson, G.; Hunter, R.; Raab, G.; Laxen, D.; Hepburn, W, (1987) Influence of blood lead on the ability and attainment of children in Edinburgh. Lancet (1): 1221-1225. Galke, W. A. ; Hammer, D. I. ; Keil, J- E-, Lawrence, S. W. (1975) Environmental determinants of lead burdens in children. In: Hutchinson, T. C.; Lestein, S,; Page, A. L.; Van Loon, F.; Davey, T. eds. International conference on heavy metals in the environment, v, 3; October; Toronto, Ontario, Canada; pp. 53-74, GCA Corporation. (1985) Estimated numbers of children residing near lead point sources. Research Triangle Park, NC: Office of Air Quality Planning and Standards, Ambient Standards Branch; contract no. 68-02-3804. R-7 DUP040009737 Klein, H.; Namer, R.; Harper, E.; Corbin, R. (1970) Earthenware containers as a source of fatal lead poisoning. N. Engl, J. Med. 283: 669-672. Kneip, T. J.; Mall on, R. P.; Harley, N, H. (1983) Biokinetic modeling for mammalian lead metabolism. Neuretaxicnlogy 4: 189-192. Kitok, D.; Kotok, R.; Heriot, T. (1977) Cognitive evaluation of children with elevated blood lead levels. Am. J. Dis. Child. 131: 791-793. Lansdown, R.; Yule, W.; Urbanowicz, M. -A.; Hunter, J. (1986) The relationship between blood-lead concentrations, intelligence, attainment and behaviour in a school population: the second London study. Int. Arch. Occup. Environ. Health 57: 225-235. Lauwers, M. C. ; Hauspie, R. C.; Susanne, C.; Verheyden, J. (1986) Comparison;of biometric data of children with high and low levels of lead in the blood. Am. J. Phys. Anthropol. 69: 107-116. Lerman, 0. L. (1986) How well can alternate policies reduce rural substandard housing? Washington, DC: U.S. Department of Agriculture, Economic Research Service; Rural Development Research Service report no. 67. j Levin, R, (1987) Lead in U,S. public drinking water: the benefits of reducing that exposure. In: Lindberg, S. E.; Hutchinson, T. C., eds. International conference: heavy metals in the environment, v, 2; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 215-217. Lin-Fu, J. S. (1982a) Children and lead: new findings and concerns. N, Engl. J. Med. 307: 615. Lin-Fu, J. S. (1982b) The evolution of childhood lead poisoning as a public health program. In: Chisolm, J. J. , Jr. ; O'Hara, D. M., eds. Lead absorp tion in children: management, clinical and environmental aspects. Baltimore, MO: Urban and Schwartzenberg; pp. 1-10. -.Lin-Fu, J. S, (1985a) Undue lead absorption in children: scope of the problem-- the nation and New England: proceedings of symposium on clinical manage ment of children with undue lead absorption; Apri1; Worcester, MA, Worcester, MA: New England Consortium of Childhood Lead Paint Poisoning Programs. Lin-Fu, J, S. (1985b) Childhood lead poisoning: the national perspective: symposium for health care providers--childhood lead poisoning: is it still a problem? Cincinnati, OH; Children's Hospital Research Foundation. Lin-Fu, J. S, (1987) Review of second draft of AtSDR Report to Congress. Memorandum: Bureau of Health Care Delivery and Assistance, HHS, to Agency for Toxic Substances and Disease Registry. April 8, 1987. Llppmann, M. (1986) [Letter regarding review of Air Quality Criteria for Lead], Washington, D.C,: U.S. Environmental Protection Agency, Clean Air Scien tific Committee; August 29. R-10 DUP040009738 Hatxakis, A.; Kokkevi, A.; Katsouvanni, K,; Maravelias, K.; Salaminios, F.; Kalandidi, A. ; Koutselinis, A,; Stefants, K.; Trichopoulos, D. (1987) lead exposure and children's cognitive functions and behavior. In: Lindberg, S. E.; Hutchinson, T, C., eds. International conference: heavy metals in the environment, v. 1; September; New Orleans, LA, Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 204-209. Heard, M. J.; Chamberlain, A. C. (1982) Effect of minerals and food on uptake of lead from the gastrointestinal tract in humans. Hum. Toxicol. 1: 411-415,.' Heard M. J.; Chamberlain, A. C. (1983) Uptake of lead by humans and effects of minerals and food. Sci. Total Environ. 30: 245-253. Hofmann, W.; Steinhausler, H.; Pohl, E. (1979) Dose calculation for the respira tory tract from inhaled natural radioactive nuclides as a function of age. I. Compartmental deposition, retention and resulting dose. Health Phys. 37: 517-532. Hryhorczuk, D. 0.; Rabinowitz, M. B.; Hessl, 5, M,; Hoffman, D.; Hogan, M. M.;, Mallin, K.; French, H.; Arris, P.; Berman, E. (1985) Elimination kinetics of blood lead in workers with chronic lead intoxication. Am. J. Ind. Med, 8: 33-42. Hunter, J.; Urbanowicz, M. A.; Yule, W,; Lansdown, R. (1985) Automated testing of reaction time and its associatiori with lead in children, Int. Arch. Occup. Environ, Health 57: 27-34, dames, A. C, (1978) Lung deposition of sub-micron aerosols calculated as a function of age and breathing rate. In: National Radiological Protection' Board annual research and development report, Harwell, United Kingdom: National Radiological Protection Board, Atomic Energy Research Establishment; pp. 71-75. Jelinek, , F. (1982) Levels in lead in the United States food supply. J. Assoc. Off. Anal. Cheffl, 65: 942_946. Johnson, J,; Paul, R. (1986) Estimation of daily lead uptake in children and resulting end-of-month blood lead levels. Research Triangle Park, NO: U.S. Environmental Protection Agency, Office of Air Quality Planning and Standards; contract no. 68-02-4309. Johnson, N. E.; Tenuta, K. (1979) Diets and lead blood levels of children who practice pica. Environ. Res. 18: 369-376. Kang, H. K.; Infante, P. F.; Carra, J. 5, (1983) Determination of blood-lead elimination patterns of primary lead smelter workers. J. Toxicol. Environ. Health 11: 199-210. Kjellstrom, T, (1985) In: Friberg, L. ; Elinder, C, G,; Kjellstrom, T.; Nordberg, G. S., eds. Critical organs, critical concentrations and whole-body dose-response relationships, in cadimum and health. A toxicological and epidemiological appraisal: v. 2. Boca Raton, FL: CRC Press, R-9 DUP040009739 8z/600ovodna Z-IX saansodxs [BuoiqBdnaao apnpui ^[[Bpadsa ppoqs qoiqM `sadjnos ajnsodxa pea[ "quBptJiuSp qsoui Jiaqq aonpaj 35q ssasse oqj. uoLquaqqe asop spaau uoiqBpdod >|6M6 sj.qj. -7q 78 8m 's*n quEuBajd jo* iioLqjodoad auios 9M spAdf aixoq ^[[Biquaqod qe sjn33o snqaj SuidopAap aqq jo aan'sodxa OJaqn ui qsqqBuojqs si aPuaptAa am () pauapLSUOD aq qsniu [Bsodsip ej.ES `aqsiupp `quauiuoj.LAua s.pjtqo [ :8 ;6 6 paAouiaj si [M<= j'b quiad papea\ uaqw `ajduiExa 6 >6 :papioAB si jaqqous oq mntpaui 6 ? aojnos euo @8 A6 6 uia[qojd aqq jo 6uLqjiqs ssapinaj pin. os squautqjEduiod jaqqo uo sqoEduu jo suuaq ui paqEn[q ^ q aq qsnui quauiqjEduioo pquauiuojLAua ACq E8 suoiqanpaj peaj pauue[(j j.uEj.nn.od quaqsjsjad pue snoqpb.iqn q qqoq FM peaq (g) *(os[E suoiqspuauiiuoaaa jo z uoiqoas aas) suoipB qons jo fouapijja pus ' ssauaA.iqaajja uuaqlBuo[ aqq jo quauissassE Aq paiiipduiaooE aq squauiuojLAua spajptiqo ui uoiqonpaJ aijpads-aajnos qe sqduiaqqs [[E qEqq puauruiooaj aft (I) saiqifpEj qqns ui qsnp puE [tos ui pus `aaqEM 6upfuj.jp ui -quiEd gi pE3[ aqq ^pBpo.tqjEd ` -oqa ` suaqjEfuapupf ` sa laasunu `sjaquap ajEp Asp `spoqss GM psaj jo asuasajd aqq BututuiBxa uo sisEqduia puauwiopaj afl 'HI8 q I8 q 6quauiuojiAua s,p[iq3 aqq jo sqaed [[q JM UQLqEuLuiEquoo pE3[ jo quaqxa aqq X[[nj aujuiExa oq paau aqj (a) 'pauiuiJdqap aq K[ q saqEJ Aqp.ixoq psa[ ui saduajajjtp 3iqdEj6oa6 qEqq os uuojiun apEut pusA[[EUdLqEU pafidHiod aq ppoqs sioBjSoad Buiuaajas :8 ;6 6 sqEQ -spuajq Kjiquaoi. oq pus uo.LqEuiiaEquoo psaf BuLULEutaj jo quaqxa aqq ssassE oq papuatu -UI0D3J pug paapbaj 3Lq sisEq [Euotqeu q u o Bqsp psai [EquauiuojtAua jo uoiqBuiuiassip pus `uotqBqajdjaqui `uoiqoajpo aqq ui squdiaaAOjdaii 6 MCq N (p) saoBjuns paquiEd ui pE3[ jo Buiqsaq pfaij nqis uT 6 O6 paupbau sue sanbjuqaaq aspaad pus aAiqiSuas aaow 'pEa[ ajjpads aDanos jo Buijoqiuoui [equauiuojLAua aoj [Biquassa si saL6o[0poqqaia aAiqiSuas puB aspaud jo asp (3) EqBp paqoaffoo /C[[B3iqBiuaqsKs jo /CqpnEd E P8 Q6 6 aajjns suiBJBoad 6u.LJpqj.uoui jaqBjUi -sajnsBatu uoiqudAjaqui qjoddns oq uoiqB[ndod aqq jo BqBjqs xsu q6xq aqq uo uoiqBiBJojuj. quapijjns ^ PLSiA qou op 3[qB[iBAB saajnosaj aqq qqL paq3a[[oo AjquajJno aqBp ' 9m 'Pqu3ui3[ddns aq qsnui `Apnqs qaLQ [6qoi s.VQd aqq SB qohs `suiejBojd . papaau yCpupBun RM jaqBM puB pooj S8 T6 6 sajnsodxa pBa[ jo Buijoqiuoui OLqBiuaqsAs *siSBq BajB-ja[[Bius Jo [BUOiSaj B uo psaj qsnp/Lps jo suop -nqLjqstp UM uoLqBuuojuj 6 V6 sqsixa deB uoiqBuuojuL jEjiuiis v 'SLOAat snopjBzBq qe quisd papBdf suisquoa `Buisnoq oijqnd Butpnpui. `BuLsnoq Miller, T. R.; Toulmin, L. (1987) Economic analyses of lead paint regulations governing HUD-assisted and FHA insured housing: final report. Washington, DC: U.S. Department of Housing and Urban Development; Urban institute Project 3673-01. Moore, M. R.; Meredith, P. A.; Watson, W. S.; Sumner, D. J.; Taylor, M. K.; Goldberg, A. (1980) The percutaneous absorption of lead-203 in humans from cosmetic preparations containing lead acetate, as assessed by whole-body counting and other techniques. Food Cosmet. Toxicol. 18: 399-405. / Moore, M. R.; Goldberg, A.; Pocock, 5. J.; Meredith, P. A.; Stewart, I. M,; Macanespie, H.; Lees, R.; Low, A. (1982) Some studies of maternal and infant lead exposure in Glasgow. Scott. Med. 27: 113-122. Moore, M. R.; Bushnell, I. W. R.; Goldberg, A. (1987) A prospective study'Of the results of changes in environmental lead exposure in children in Glasgow. In: Smith, M.; Grant, L. D.; Sors, A., eds. Lead exposure and child development: an international assessment, Lancaster, United Kingdom: MTP Press; in press. Morrow, P, E.; Beiter, H.; Amato, F.; Gibb, F. R. (1980) Pulmonary retention of lead: an experimental study in man. Environ. Res, 21: 373-384. Morse, D. L.; Watson, W. N.; Housworth, J.; Witherell, L. E.; Landrigan, P. J. (1979) Exposure of children to lead in drinking water. Am. J. Public Health 69: 711-712. Mushak, P, (1987) Biological monitoring of lead exposure in children: overview of selecied bipkinetic and toxicologicai issues. In: Smith, M,; Grant, L. D.; Sors, A., eds. Lead exposure and child development: an inter national assessment. Lancaster, United Kingdom: MTP Press; in press. Mushak, P..; Schroeder, C. (1981) Multiple media pollutant exposures and their regulation, Washington, DC: National Commission on Air Quality; contract no. 23 AQ 6981. National Food Processors Association. (1986) Retail market survey data for lead in canned foods. Washington, DC: August 7. National Research Counci1. (1972) Airborne lead in perspective. Washington, DC: Committee on Medical and Biologic Effects of Atmospheric Pollutants. National Research Council. (1976) Recommendations for the prevention of lead poisoning in children. Washington, DC: National Academy of Sciences. National Research Council. (1980) Lead in the human environment. Washington, DC: National Academy of Sciences. National Research Counci1. (1987) Risking the future. Adolescent sexuality, pregnancy, and childbearing: y, 1. Cheryl B. Hayes, ed, Washington, DC: National Academy Press. Needlemart, H. L,, ed. (1980) low level lead exposure: clinical implications of current research. New York, NY: Raven Press. R-12 DUP040009740 Mahaffey, K. R. (1982) Role of nutrition in prevention of pediatric lead toxicity. In: Chisolm, J. J., Jr.; O'Hara, 0. M, eds. Lead absorption in children: management, clincial and environmental aspects. Baltimore, MO; Urban and Schwartzenberg; pp. 63-78. Mahaffey, K. R.; Annest, J. L. (1986) Association of erythrocyte protoporphyrin with blood lead level and iron status in the second National Heath and Nutrition Examination Survey, 1976-1980. Environ. Res. 41: 327-338. Mahaffey, K. R.; Michaelson, I. A. (1980) The interaction between lead and nutrition. In: Needleman, H. L., ed. Low level lead exposure: the clinical implications of current research. New York, NY: Raven Press; pp. 159-200. Mahaffey, K. R.; Treloar, S.; Banks, T. A. (1976) Differences in dietary intake of calcium, phosphorus and iron of children having normal and elevated blood lead concentrations. J. Nutr. 106(7):xxx. Mahaffey, K. R.; Annest, J. L.; Roberts, J.; Murphy, R. S. (1982) National estimates of blood lead levels: United States 1976-1980: association with selected demographic and socioeconomic factors. N. Engl. 0. Med. 307: 573-579. Mahaffey, K. R. ; Gartside, P. S.; Glueck, C. J. (1986) Blood lead levels and dietary calcium intake in 1- to 11-year old children: the Second National Health and Nutrition Examination Survey, 1976-1980. Pediatrics 78: 257-262. Manton, W. I. (1985) Total contribution of airborne lead to blood lead. Br. J. Jnd. Med. 42: 168-172. Markowitz, M. E.; Rosen, J. F. (1981) Zinc (Zn) and Copper (Cu) metabolism in CaNa2 EDTA-treated children with plumbism, Pediatr. Res. 15: 635, McBride, W. G.; Black, B. P.; English, B. J. (1982) Blood lead levels and behavior of 400 pre-school children. Med. J. Aust. 2: 26-29. McBride, W. G.; Cooney, G. C.; Bell, A. (1987) Blood lead levels in Sydney urban children. In: Lindberg, $. E.; Hutchinson, T. C., eds. International conference: heavy metals in the! environment, v. 1; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 153-155. McKhann, C. F. (1926) Lead poisoning in children. Am. J. Dis, Child. 2: 386-392. McM'ichaelA. J.; Vimpani, G. V.; Robertson, E. F.; Baghurst, P. A.; Clark, P, JD. (1986) The Pont Pirie cohort study: maternal blood lead and pregnancy outcome. J. Epidemiol, Commun. Health 40: 18-25. Mie'lke, H.; Blake, B.; Burroughs, S.; Hassinger, N. (1984) Urban lead levels in Minneapolis: the case of the Hmong children. Environ. Res. 34: 64-76. Milar, C. R.; Mushak, P. (1982) Lead-contaminated house dust: hazard, measure ment and decontamination. In: Chisolm, J. J., Jr.; O'Hara, D. M., eds. Lead absorption in children: management, clinical and environmental aspects, Baltimore, MD: Urban and Schwartzenberg; pp. 143-152. R-ll DUP040009741 Patterson, C. C. (1965) Contaminated and natural lead environments of man. Arch, Environ, Health 11: 344-360. Pennington, J. A, T. (1983) Revision of the total diet study food list and diets. J. Am. Diet. Assoc. 82: 166-173. Perino, J.; Ernhart, C. B. (1974) The relation of subclinical lead level to cognitive and sensory-motor impairment in black pre-schoolers. J. Learn, Dis. 7: 616-620. y Perlstein, M. A.; Attala, R. (1966) Neurologic sequelae of plumbism in chil dren. Clin. Pediatr. 5: 212-398, Piomelli, S.; Corash, L.; Corash, M. B.; Seamon, C..; Mushak, P.; Glover, B.; Padgett, R. (1980) Blood lead concentrations in a remote Himalayan popula tion. Science (Washington, DC) 210: 1135-1137. Piomelli, S.; Seaman, C.; Zullow, 0.; Curran, A; Davidow, B. (1982) Threshold for lead damage to heme synthesis in urban children. Proc. Natl. Acad. Sci. U. S. A. 79: 3335-3339. Piomelli* S.; Rosen, J. F.; Chisolm, J, J., Jr.; Graef, J, W. (1984) Management of childhood lead poisoning, J. Pediatr. 105: 523-531. Pocock, S, J,; Ashby, 0,; Smith, M. A. (1987) Lead exposure and children's intellectual performance. Int. J, Epidemiol. 16: 57-67. Pope, A. (1986) Exposure of children to lead-based paints. Research Triangle Park, NC: U.S. Environmental Protection Agency, Strategies and Air Stan dards Division; EPA contract no, 68-02-4329, Public Health Foundation. (1986) Special report: State Health Agency lead poisoning prevention activities, 1983. Washington, DC: Public Health Foundation, Que Hee, S. S.; Peace, 6.; Clark, C, S.; Boyle, J, R.; Bornschein, R. L.; Hammond, P, B, (|l985) Evolution of efficient methods to sample lead sources, such as house dust and hand dust, in the homes of children. Environ. Res. 38: 77-95. Rabinowitz, M. 6.; Needleman, H. L. (1982) Temporal trends in the lead concen trations of umbilical cord blood. Science (Washington, DC) 216: 1429-1431. Rabinowitz, M. B,; Wetheri11, 6, W.; Kopple, J, 0. (1976) Kinetic analysis of lead metabolism in healthy humans. J. Clin, Invest. 58: 260-270. Rabinowitz, M. B.; Wetheri 11, G. W.; Kopple, J. 0. (1977) Magnitude of lead intake from respiration by normal man. J. Lab. Clin. Med. 90: 238-248. Rabinowitz, M. B.; Kopple, J. 0.; Wetherill, G, W. (1980) Effect of food intake and fasting on gastrointestinal lead absorption in humans. Am, 3, Clin. Nutr. 33: 1784-1788. R-14 D U P040009742 Needleman, H. L. (1987) Low level lead exposure end children's intelligence: a quantitative and critical review of modern studies. In: Lindberg, S. E.; Hutchinson, T. C., ed$. International conference: heavy metals in the environment, v. 1; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 1-8. Needleman, H. L.; Bellinger, 0. C. (1987) Type II fallacies in the study of childhood exposure to lead at low dose: a critical and quantitative review. In: Smith, M.; Grant, L. D.; Sors, A., eds. Lead exposure and child development: an international assessment. Lancaster, United Kingdom: MTP Press; in press. Needleman, H. L.; Shapiro, I. M. (1974) Dentine lead levels in asymptomatic Philadelphia school children: subclinical exposure in high and low risk groups. EHP Environ. Health Perspect. 7: 27-31. Needleman, H. L.; Gunnoe, C.; Leviton, A.; Reed, R.; Peresie, H.; Maher, C.; Barrett, P. (1979) Deficits in psychologic and classroom performance of children with elevated dentine lead levels. N. Engl. J, Med. 300: 689-695. Needleman, H. L.; Leviton, A.; Bellinger, D. (1982) Lead-associated intellectu al deficit [letter]. N. Engl. J. Med. 306: 367. Needleman, H. L.; Rabinowitz, M.; Leviton, A.; Linn, S.; Schoenbaum, E, (1984) The relationship between prenatal exposure to lead and congenital anoma lies. JAMA J. Am. Med. Assoc. 251: 2956-2959. New York City, NY. (1982) Administrative Code 26-12.08, January, 1982. New York City Department of Health. (1985) Bureau of Lead Poisoning Control: annual report. 0`Flaherty, E. J.; Hammond, P, B.; Lerner, 5. I. (1982) Dependence of apparent blood lead half-life on the length of previous lead exposure in humans. Fuhdam. Appl. Toxicol. 2: 49-54. \ O'Hara, 0. M. (1982) Social factors in the recurrence of increased lead absorp tion. In: Chisolm, J, J., Jr,; O'Hara, D. M., eds. Lead absorption in children. Management, clinical and environmental aspects. Baltimore, MD: Urban and Schwartzenberg; pp. 89-101, Otto, D. A.; Benignus, V. A.; Muller, K. .; Barton, C. N. (1981) Effects of age and body lead burden on CMS function in young children, I. Slow cortical potentials in young children. ElectrOencephalogr, Clin. Neurophysiol. 52: 229-239. Otto, D. A.; Benignus, V, A,; Muller, K. E.; Barton, C.; Seiple, K.; Prah, J.; Schroeder, S. R. (1982) Effects of low to moderate lead exposure on slow cortical potentials in young children: two year follow-up study. Neurobehav. Toxicol, Teratol. 4: 733-737. Otto, D, A.; Robinson, G.; Baumann, S.; Schroeder, S, R.; Mushak, P.; Kleinbaum, 0.; Bpone, L, (1985) Five-year follow-up study of children with low-tomoderate lead absorption: electrophysiological evaluation. Environ. Res. 38: 168-186, R-13 DUP040009743 Ryu, J. E.; Ziegler, E. E.; Nelson, $, E.; Fomen S. J. (1985) Dietary and environmental exposure to lead and blood during early infancy. In: Mahaffey, K. R, ed, Dietary and environmental leads human health effects, Amsterdam, the Netherlands: Elsevier Press; pp. 187-209. Saenger, P.; Rosen, J. F.; Markowitz, M. E. (1982) Diagnostic significance of edetate disodium calcium testing in children with increased lead absorp tion. Am. J. Dis. Child. 136: 312-315. Saernger, P.; Markowitz, M, E; Rosen, J. F. (1984) Depressed excretion of6Beta-hydroxycortisol in lead-toxic children. J. Clin. Endocrinol. Metab. 58: 363-367. Schier, D.; Hall, W. (1977) Analysis of housing data collected in a lead-based paint survey in Pittsburgh, Pa. Part I. Washington, DC: National Bureau of Standards; report no. NBSIR 77-1250. Schneider, D, J.; lavenhar, M. A, (1986) lead poisoning: more than a medical problem. Am, J. Public Health 76: 242*244, Schroeder, S. R.; Hawk, ft- (1987) Child-caregiver environmental factors related to lead exposure and IQ. In: Schroeder, 5, R., ed. Toxic substances and mental retardation: neurobebavioral toxicology and teratology. Washington, DC: American Association on Mental Deficiency; (Begab, M. J., ed, Monographs of the American Association on Mental Deficiency: no. 8); pp. 97-137. Schroeder, S. R.; Hawk, B.Otto, D. A,; Mushak, P.; Hicks, R. E. (1985) Separating the effect of lead and social factors on IQ. Environ. Res. 38: 144-154. Schwartz, J,; Otto, D. A. (1987) Blood lead, hearing thresholds, and neurobehavidral development in children and youth. Arch. Environ. Health. 42: 153-160. Schwartz, J.; Pitcher, H.; Levin, ft.; Ostro, B.; Nichols, A. L. (1985) Costs and benefits of reducing lead in gasoline: final regulatory impact analy sis. Washington, DC: U. S. Environmental Protection Agency, Office of Policy, Planning and Evaluation; EPA report no. EPA-230/05-85-006, Schwartz, J.; Angle, C.; Pitcher, H. (1986) Relationship between childhood blood lead levels and stature. Pediatrics 77: 281-288. Shukla, R.; Bornschein, Ri l.; Dietrich, X. N. ; Mitchell, T. ; Grote, J.; Berger, 0,; Hammond, P. B.; Succop, P. A. (1987) Effects of fetal and early postnatal lead exposure on child's growth in stature - the Cincinnati lead study. In: Lindberg, S. E.; Hutchinson, T, C., eds. International conference: heavy metals in the environment, v. 1; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 210-212. Silbergeld, E. K. (1983a) Localization of metals: issues of importance to neurotoxicology of lead. Neurotoxicology 4: 193-200. R-16 DU P040009744 Rabinowitz, H.; Leviton. A.; Bellinger, 0- C. (1985) Home refinishing: lead paint and infant blood lead levels. Am. 0, Public Health 75: 403-404, Rey-Alvarez, S.; Menke-Hargrove, T. (1987) Oeleading dilemma: pitfall in the management of childhood lead poisoning. Pediatrics 79: 214-217. Robinson, G. S.; Baumann, S.; Kleinbaum, D.; Barton, C.; Schroeder, 5, R.; Mushak, P.; Otto, D. A. (1985) Effects of low to moderate lead exposure on brainstem auditory evoked potentials in children. Copenhagen, Denmark: WHO. Regional Office for Europe; pp. 177-182. (Environmental health document S'), Robinson, G. S.; Keith, R. W.; Bornschein, R. L.; Otto, 0. A. (1987) Effects of environmental lead exposure on the developing auditory system as indexed by the brainstem auditory evoked potential and pure tone hearing evalua tions in young children. In: Lindberg, S. E.; Hutchinson, T. C., eds. International conference: heavy metals in the environment, v. 1; Septem ber; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 223-225. Reels, H. A.; Buchet, J.-P.; Lauwerys, R. R.; Bruaux, P,; Claeys-Thoreau, F,; Lafontaine, A.; Verduyn, G. (1980) Exposure id lead by the oral and the pulmonary routes of children living in the vicinity of a primary lead smelter. Environ, Res, 22: 81-94. Rosen, 0. F. (1983) The metabolism in isolated bone cell populations: interac tions between lead and calcidm. Toxicol. Appl. Pharmacol. 71: 101-112, Rosen, J, f. (1985) Metabolic and cellular effects of lead: a guide to low level lead toxicity in children. In: Mahaffey, K. R., ed. Dietary and environmental lead: hiiman health effects. Amsterdam, The Netherlands: Elsevier; pp. 157-185, Rosner, 0.; Markowitz, G, A. (1985) "Gift of God?1 The public health contro versy over leaded gasoline during the 1920s. Am. J. Public Health 75: 344-352. Rothenberg, 5. J, ; Schnaas, L.; Neri-Mendez, C, Z, (1987) The pilot study of the Mexico City prospective lead study: neurobehavioral newborn status and prenatal and perinatal blood lead levels. In: Smith, M.; Grant, L. D.; Sors, A., eds. Lead exposure and child development: an international assessment. Lancaster, United Kingdom: MTP Press; in press. Rummo, J. H. (1974) Intellectual and behavioral effects of lead poisoning in children CPh.D. thesis]. Chapel Hill, NC: University of North Carolina. Available from: University Microfilms, Ann Arbor, MI; publication no. 74-26930. Rummo, J. H.; Routh, 0. K.; Runmo, N. J.; Brown, J, F. (1979) Behavioral and neurological effects of symptomatic and asymptomatic lead exposure in children. Arch, Environ. Health 34: 120-124. Ryu, j. E.; Ziegler, E. E.Nelson, S, E.; Fomen, 5. J. (1983) Dietary intake of lead and blood lead concentration in early infancy. Am. J. Dis. Child. 137: 886-891. R-15 DUP040009745 U.S. Department of Health and Human Services, Public Health Service, National Center for Heath Statistics. (1984) Vital statistics of the United States, 1980, V. I, natality; Hyattsvilie, MD; Table 1-59. U., Department of Health and Human Services, Public Health Service, National Center for Health Statistics. (1985a) Vital Statistics of the United States, 1981: V. I, natality; Hyattsville, MD; 1985, table 1-59. U.S. Department of Health and Human Services, Public Health Service National Center for Health Statistics (1985b). Vital Statistics of the Untied'' States, 1980, V. II, mortality part B; Hyattsville, MD; table 8-1. U.S, Department of Health and Human Services, Public Health Service, National Center for Health Statistics. (1986) Vital statistics of the United States, 1981, V. II, mortality part B; Hyattsville, MD; table 8-1. * U.S, Environmental Protection Agency. (1977) Air quality criteria for lead. Research Triangle Park, NC: Health Effects Research Laboratory; EPA report no. EPA-6Q0/8-77-Q1Z. Available from: NTIS, Springfield, VA; PB-280411. U.S. Environmental Protection. Agency. (1984) Costs and benefits of reducing lead in gasoline (interim draft: J. Schwartz, J, Leggett, B. Ostro, H. Pitcher, R. Levin, authors),. Washington, DC: Office of Policy Analysis. U.S, Environmental Protection Agency, (1985) Costs and benefits of reducing lead in gasoline: final regulatory impact analysis, Washington, DC: Office of Policy, Planning add Evaluation (Schwartz, J.; Pitcher, H,; Levin, R.; Ostro, B.; Nichols, A. L.); EPA report no. EPA-230/05-85-006. U.S. Enviromental Protection Agency. (1986a) Air quality criteria for lead. Research Triangle Park, NC: 0 Tice of Health and Environmental Assessment. Environmental Criteria and Assessment Office: EPA report no. EPA-600/8-83/028aF-dF. 4v, Avail able from: NTIS, Springfield, VA; PB87-142378. U.S. Environmental Protection Agency, (1986b) Reducing lead in drinking water: a benefit analysis. Washington, DC: Office of Policy Planning and Evalua tion; EPA report no. EPA-230-09-86-019. U.S. Environmental Protection Agency. (1986c) Review of the national ambient air quality standards for lead. Assessment of scientific and technical information: draft staff paper. Research Triangle Park, NC: Office of Air Quality Planning and Standards, tl.S, Environmental Protection Agency. (1987a) Letters from Jeanne Briskin, Office of Drinking Water to Frank L, Mitchell, 0. 0., ATSDR. U.S. Environmental Protection Agency. (1987b) [Letter from Jeanne Briskinl, Research Triangle Park, NC: Environmental Criteria and Assessment Office; October 9, U.S. Environmental Protection Agency, (1987c) Preliminary results: the aging solder study. Washington, DC: Office of Drinking Water, R-18 DUP040009746 SiIbergeld, E. K. (1983b) Experimental studies of lead neurotoxicity: Implica tion for mechanisms, dose-response and reversibility. In: Rutter, M.; Russell Jones, R., eds. Lead versus health. Londqn, United Kingdom: John Wiley and Sons, Ltd.; pp. 191-21$. Silbergeld, E. K.; Wolinsky, J. S.; Goldstein, G. W. (1980) Electron probe microanalysis of isolated brain capillaries poisoned with lead. Brain Res. 189: 369-376. / Smith, M. (1985) Recent work on low level lead exposure and its impact on behavior, intelligence, and learning: a review..J. Am. Acad. Child Psychiatry 24: 24-32. Smith, M.; Delves, H, T,; Lansdown, R.; Clayton, 8.; Graham, P> (1983) The effects of lead exposure on urban children: the Institute of Child Health/ Southhampton study. Dev. Med. Child Neurol; 25 (suppl. 47). Sorrell, M.; Rosen, J. F,; Roginsky, M. (1977) interactions of lead, calcium, vitamin 0 and nutrition in lead-burdened children. Arch. Environ. Health 32: 160-164. Steenhout, A.; Pourtois, M. (1981) Lead accumulation in teeth as a function of age with different exposures, Br. J. Ind, Med, 38: 297-303. Succop, P. A.; O'Flaherty, E. J.; Bornschein, R. L.; Clark, C, S.; Krafft, K.; Hammond, P, B.; Shukia, R, (1987) A kinetic model for estimating changes in the concentration of lead in the blood of young children. In: Lindberg, 5. E.; Hutchinson, T. C,, eds. international conference: heavy metals in the environment, v. 2; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 289-291, Tola, S.; Hernberg, S,; Asp, S.; Nikkanen, J. (1973) Parameters indicative of absorption and biological effect in new lead exposure: a prospective study, Br. J, Ind. Med, 30: 134-141. TRC Environmental Consultants, Inc. (1986) Exposure to airborne lead from stationary sources: an evaluation of proposed national ambient air quality standards for lead, Wethersfield, CT: TRC Environmental Consultants, Inc.; project no, 3220-551. Ulvtind, S, E. (1984) Predictive validity of assessments of early cognitive competence in light of some current issues in developmental psychology. Hum, Development 27: 76-83. U.S. Bureau of the Census. (1983) Census of population, 1980, Characteristics of the population, general social and economic statistics: United States summary, Washington, DC: U.S. Department of Commerce. U.S. Bureau of the Census. (1984) Current population reports, series P-25, no. 952, projections of the population of the United States by age, sex and race; 1983 to 2080. Washington, DC: U.S. Department of Commerce. U.S. Bureau of the Census, (1986) American housing survey, 1983. Part B: indicators of housing and neighborhood quality by financial characteris tics, December. Washington, DC; U.S, Department of Commerce, 8-17 DUP040009747 Winneke, G.; Munoz, C.; Lilienthal, H> (1987b) Neurobehavioral effects of lead: the reversibility issue. In: Llndberg, S, E.; Hutchinson, T. C., eds. International conference: heavy metals in the environment, v. 1; September; New Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; p. 66. WoIni k, K. A.; Fricke, F. L.; Capar, $. G.; Braude, G. L.; Meyer, M, W.; Satzger, R. 0.; Bonner, E. (1983) Elements in major raw agricultural crops in the United States. I. Cadmium and lead in. lettuce, peanuts, potatoes, soybeans, sweet corn and wheat. J, Agr. Food Chem. 31: 1240-1244, Wolf, A. W.; Ernhart, C. B.; White, C. S. (1985) Intrauterine lead exposure and early development. In: Lekkas, T. D., ed. International conference: heavy metals in the environment; September; Athens, Greece, v> 2. Edinburgh^ United Kingdom: CEP Consultants, Ltd.; pp, 153-155. World Almanac and Book of Facts. (1987) United States population. New York, NY: Pharos/Scripps Howard; pp. 217-247. World Health Organization. (1986) Regional Office for Europe: air quality guidelines. [Review draft, vol, II, Lead, eh. 19, pp.1-34]. Worth, 0.; Matrange, A.; Lieberman, M.; DeVos, E.; Karelekas, P.; Ryan, C.; Craun, G. (1981) Lead in drinking water; the contribution of household tap water to blood lead levels. In: Lynam, D. R,; Piantanida, L. 6.; Cole, J. F., eds. Proceedings of the 2nd international symposium on environmental lead research. New York, NY: Academic Press; pp. 199-225. Yankel, A. J.; von Lindern, I. H.; Walter, S, D. (1977) The Silver Valley lead study: the relationship between childhood bipod lead levels and environ mental exposure. J, Air Pollot. Control Assoc, 27: 763-767. Yip, R.; Norris, T. N,; Anderson, A. S. (1981) Iron status of children with elevated blood lead concentrations. J. Pediatr. 98: 922-925. Yule, W.; Lansdown, R, (1983) Lead and children's development: recent findings. In: International Conference: heavy metals in the environment: v, 2; September; Heidelbprg, West Germany. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 912-916. Yule, W.; Lansdown, R.; Millar, I, B.; Urbanowicz, M.-A. (1981) The relationship between blood lead concentrations, intelligence and .attainment in a school population: a pilot study. Dev. Med, Child Neurol. 23; 567-576. Yule, W.; Urbanowicz, M.-A.; Lansdown, R.; Millar, I. B. (1984) Teachers' ratings of children's behavior in relation to blood lead levels. Br. J. Dev. Psychol. 2: 295-305. Zaric, M.; Prpic-Majie, D, ; Kostial, K.; Piasek, M. (1987) Exposure to lead and reproduction. In: Summary proceedings of a workshop: selected aspects of exposure to heavy metals in the environment. Monitors, indicators, and high risk groups; April 1985. Washington, AC: National Academy of Sciences; Yugoslavia: Council of Academies of Sciences and Arts; pp. 119-126. R-20 DUP040009748 U,S,, Navy* (1987) Data on results of analyses of potable tap water samples. Obtained from Mr. Chuck Roydhouse, Safety Officer, David Taylor Naval Ship research and Development Center, Annapolis, MD 21402:. Vimpani, G. V.; Wigg, N. R.; Robertson, E. F.; McMichael, A. J.; Baghurst, iP. A.; Roberts, R. R. (1985) The Port Pirie cohort study: blood lead concentration and childhood development assessment. Presented at: Lead environmental health: the current issues; May; Durham, NC: Duke University. Vimpani, G. V.; Baghurst, P. A.; Wigg, N. R.; Robertson, E, F.; McMichael, A. J.; Roberts, R. R. (1987) The Port Pirie cohort study - cumulative lead exposure and neurodevelopmental status at age 2 years: do HOME scores and maternal IQ reduce apparent effects of lead on Bayley Mental scores? In: Smith, M.; Grant, L. D.; Sors, A., eds, Lead exposure and child develop ment: an international assessment. Lancaster, United Kingdom: MTP Press; in press. Wallace, J. E. (1986) The cost of lead based paint abatement in public housing: final report. Contract HC-5685, Abt, Associates, Ihc, For the Office of Policy Development and Research, U.S. Department of Housing and Urban Development, July, 1986. Wa lter, S. D.; Yanke, A. J.; von Lindern, I. H- (1980) Age-specific risk factors fdr lead absorption in children. Arch. Environ. Health 35: 53-58. Watson, W, S.; Hume, R.; Moore, M. R. (1980) Oral absorption of lead and iron. Lancet (8188): 236-237. Wecleen, R. P, (1984) Poison in the pot: the legacy of lead. Carbondale, IL: Southern Illinois University Press. Winneke, G.; Hrdina, K.-G.; Brockhaus, A. (1982) Neuropsychological studies in children with elevated tooth lead concentrations. Part I: Pilot study, lot. Arch. Occup. Environ, Health 51: 169-183. Winneke, G.; Kramer, U,; Brockhaus, A. ; Ewers, U.; Kujanek, G.; Lechner, H.; Janke, W. (1983) Neuropsychological studies in children with elevated tooth-lead concentration. Part II. Extended study. Int. Arch. Occup. Environ, Health Si: 231-252. Winneke, G.; Beginn, U.; Ewert, T. ; Havestadt, C.; Kramer, U.; Krause, C.; Tbron, H. L.; Wagner, H, M. (1984) [Study of the measurement of subclinicaii lead effects on the nervous system of Nordenham children with known pre-natal exposure]. Schriftenr. Verwasser. Boden, Lufthyg. (59): 215-229. Winneke, G,; Collet, W.; Kramer, U,; Brockhaus, A. ; Ewert, T.; Krause, C. (1987a) Three- and six-year follow-up studies in lead exposed children. In: Lindberg, S. E.; Hutchinson, T. C., eds. International conference: heavy metals in the environment, v, 1; September; Mew Orleans, LA. Edinburgh, United Kingdom: CEP Consultants, Ltd.; pp. 60-62. R-19 TABLE A - 38 WASHt NfiTON. O.O, O Q\ .0a? m w 51 I< g '2C m< z it? I .o X JS- $ (0 X ><Ui IfV o Xo - >< Ui o 1 :Z< aC:l 6 u. p x o X X 3 -O o ]vs r/> XUI o *CM-CM0lA oo 8 C.OW C'\M--6i0 ooo. lnf-H o *~o o fossisr HP o OvifVp O ' X --Y *-h tf\H M.rt W CO O P0 HzUI ouzi SO Ov 1 0 $ r- UI,i .X somov P \COM MjO d p JT-r-lirt o COMmftiZm o oPtfBlOiOofHU^CCOoOMs ooo <Ms P dd*inN d o i0 CM SO OoOOott.oS0O QsJTOi *0*T >0o oHs HrtSQ Cho'd CUH d PH <MH O o ^N p OOP OOO >fc*H COiAO oo p zUJ X o o> so O oH u. p X Ui m X I OOP cOr Ocvj Pr** ~W O o OooOoP oo H"in* tf\ oOoOoP oO CM ooo ooo (VOv^ VO 0 O .CmM OHOsTOiOVPr-3vhOP0O* soOCOoMs OoOoOvoOf* OiOs. CM OOO ooo ZHsoCJ -- o*sr r-NO o o in n* OO0vO.OO8*vMOPrt} ooCooO >OtO-0.COO--MVOO0COMt oO v >H i- OsX V.UJ cox P Ovp OOvX < 90 H<Oz .H w -J < as H vOs>o<w6r>*[-oo\ H O H Z-J Z UI zoOoO x<o.x<-- O z uQi*iA- ZVO*- 9U -></></> OvX <x v OX < H A. H X OJf z O Ui '*0 H .X .. --* Ho uS>O<l> o ozUioOQ-.oOm ZO*r D0 OsZ .. CNO COvX < Poc-a: 5 X VQ0 O' 0 1 O OO -2 ZOO < oH .Oupfkttk Zvo*- H 300 < H o H A-39 DUP040009750 TABLE B - 1 AKRON, OHIO CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND ACE OF HOUSING, 1980 NOfl in**.<r WCJlA O O o (60r-.P19* Op partTV CHIP 6O 0o? o1 HP X <3 UaOLcil p- flu if p .o IT niOi Oiimx 9o iftffp 9PX O CM NX. O tAf-9 O X99 O5 h-f-9 C.^*-Npu pp **f*N 9 N okp 9 * r-VO 9 O h.* M. p Ifu*n-rO*t p6 - 0*19 o WON o *-WV0 p ,*4f.jsr **-C-MxMx3 o o p CM 9,9 o p 0.00 o -J coo o :< fc- NNh inm>- >0 CJ O CM *- P00O,P0 9.9 9* CM9ft N O X OooOoP tQfVrPiOO `m* rt o Qs 9in o 9 .9 1 O N- .X .Id P 9 O P 9 'oX P * I w o O Ift P X Ul m .X5 o ,|ft Xp * '1 Ul ae Si <X CO > <1!S3N3 oooooo O O in >0 9 9 OOO OOP * > CM *-.<M9 o o . 2T* ooo ooo 9 SO *-CMp O o CJ ro jr* ooo OOP 900 fftirt oo .9 so OOP OOO fil** o o o X ooo 0in.--0] 0 *- N.XX oO 9 O CM OOP OOO 940 0* Nh* o o 9 n 9* OooOoO OCM9 o o 9 ooo ooo X9N.99* oO 9 CM CSJ (pfUiCl o pS ox*c-e -J I </> O op oc.oo uO otf%* 9<S5 > P OlUKJ < .90 -J 2 U* X 0oOX*-ZX < hO- w >*o H o X H- M9aCui9OOolAOOOin* o X-9-r* z 3i0M OvUtJf 90 09X -1 < < w * 0X9o O x \OM 9 v> * P --[ 9.00 -< *- oUi O.tn^ X9*- h- 3MM B-2 DUP040009751 APPENDIX B TABLES OF INDIVIDUAL SMSAs WITH A POPULATION OF LESS THAN ONE MILLION SHOWING NUMBERS OF YOUNG CHILDREN BY THE AGE OF THEIR HOUSING AND FAMILY INCOME The tables In this Appendix include 85 SMSAs with total populations of less than 1 million where the U.S. Census data permitted the population to be separated into two types of urban status, "In Central City" and "Not In Central City,.* They appear in alphabetical order by the city that gives its name to the SMSA, The data come from tapes of 1980 U.S. Census enumerations, and cover children aged 6 months to 5 years of all races. Their distribution by residential status: "In Central City", "Not In Central City", and family income by age of residential unit is shown. Brl DUP0400097S2 TABLE 8 - 3 ALBUQUERQUE, N. HEX. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MQNTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS ANb ACE OF HOUSINC, 1980 .J 0flOf* A *. 0 < HO iriMO -.0 *610 0 H ovcjd . to 00*? O 0* (SI S3 0r I c f* 0* 9" MlftM 0 O' f o**ft O 0 0** 1 o 0 o soo>r> 0 m .6 0 0 I UJ Z 0.00 .0sr0r^.vi0no A* 0 !* .f1t^ P > . A 0VO0 0 0 O* nOf* o 0 ooaom 0 0* fOM ui o 0 o ooo 0eo.h0.f0lo . o .ft inm 0 6 r- Zwlft Oft.t* O o 0 dicing "" 0 ' 0 00* m eg m ft..sr*> o O 000 ooo ft..iMir.0ir **vft O 0o o 0 o .to 1 0r* 20 Ul z a .* 0 VO 0 p 1 u. o O IT 0 Z UJ m X0 0z tr o< Uti Z 0oo0.o0 0Pm-00 o 0 ->0 ooo .0.00 Oo OCMJOMftf*V 0 O OOO OOO 4000 do rf^t>) OOOO KfilA ooo ftw VO 0o0o.o0 o 0*".<O flO CM *- 0 ooo c0g0.i0n oo IT| .o0o0o9 9-UMTS ftsO*- .o oft ooo o 0.0 0 *-- rift fo** (A ooo ft0.0 0 0 09"0*--0" z >u 'V.UJ oiz >* 5 eOvOi J< .<f3r-.02o -<J oO^rAos ** > o .0 >' z 6 * z UJ *z>ooooo <*- u WO * taoa:u5x. O 2 z\o^ 3tf> > H o Ji UJ 0Z <X Wz 0.0 Oo.z0AcX -J < O Ul A*-0 .K p *04> 0)0 2 +- zo wzo oOooO> xvo*3V>0 UJ 0X 00 O0X < OA ^ <- O0Z .o CO *-.. Xw <o 0 <1 Ho- zwooOoOA a iA ZO^ h 300 8-4 DUP040009753 TABLE 6 - 2 ALBANY-SCHENECTAOY-TROV; N .Y. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS SMB AGE OF HOUSING, 1980 rOCkjiA o -*Ho<- PwcPyw.tfJs Orw tfy.iA O iASOO (SI SO o P OCO T* o< >UXi .pwoa. AC * * 1 *oTi o .* hi X POO .0 0sr.s0Q oo J**lAn.Oift .o r> o <y Mirv .O 0IOTs0OlA.OP0oJ\ OO NCsl iflQlA O **.oN(N\j f^jr.Ch o . * O *o mcy?yT> oo oocoo UY rr-PO oo .m ^r SO px. o OvCsOis'oif * o9* ft OSO O Nt- Oo 9-.d> O P^TNC o o *W CO\|AOQ OO00 O*O0*->.PPn30- .oS(os_SOoi Oo' u ac a xo ,VoP5 ioTI i XLU O* xoX2> -O Iofs! I, eUci 0.00 o xO>P0 .o* * OOO o 0.0 0 o jr oi~ xr CM oo*oo*"!o(o(*SI oo irft * POCMOOJnTpO.Pm> oO m obo oOVoiAoW (SIP oo ..r*? .*OoX-O*oOAWtoPOO AoooO (Si OOOOOP pP ro o X* .OOP oWoiAofv *-fO os o O in 8 oolAd-ooOOrlooOA -moosr -I--S.UJ > JPOtOcUBf Si O o OOVX *<it--o-_2o -i .Xh< o^ros <*c/></.1> o O ^X< ->--J x Ui o do ooo 6 * - 3^0gf X o in 2V5- > OiWC QsO OOO^CCv*CX. >00 </> I o oo uPiOoOA ;o *u\ Xr- </X/> ,5 XOT <AoOAO0<:*J0o/i*>*\tl.itOXUOfcJf <Jfoc-i- PUC*3fO.00o-*i.O0r0-s* B-3 DUP040009754 TABLE B - 5 ANN ARBOR, MICH. Q00 p\ O -.a s (O 3 -J mom .0 1o **9\b o o*" oixvo t-f* Q 6 or O >- X u> o Ul o poo o ,o . . OO P CM 0 < 0 to mm o 9 --_ f> o*!* 9.,9i-N0 Oa ,z 1 P f* 0 9 3' H* .< 9 tom o .O 0) z * 9 z >c Ual 9f- mi^so. O ' O NP*0 6 . P f<fl zt Ul O z Z IT .3 r9~ 4k W XS oz O pvez 9 If o.tosa 6 9 *-to o 1\ + .4 fm> CJO O o o r by >-1 Z Z A0.*WA . O* OZJK o o^ f^>mto 0vr-fff-m^ o o .o -ZOsO' o CsC-Mf*O. o ov* OOP 9-0 SO o CMf* o .1 w :> .a -J <h O OOP o P!*>O<O .o 9 > oooooo cy<sr O .sm0fl P* OOO 9Os0m.i0s* ip* o o 9s CM CM w x <w > m oaa 00.0 0.00 o OOP ooo oO OOO o OOO o oN 9 sf**m . 1 CM CM.pcwa CM mt SO OM>* '9 SCQM o <0 z>-- wZ V .* zz oa -x so 0 hi -J OS -- >o x as p " w oi ooo ooo m.QsOs try o m* m OOP o0m.0m0 m oP SO >0 OOP Or-9OMO ** r ps o o ts fm U o in < i z z^ W mJ < U. a Xo 9 ITS Z9 p+ POO 0.0 Pips o CM CM OOO 0 0.0 CMP-Qs pm. O a CM 00.0 OOO CM OP ." o o mo 9 w Zz wz ;z o w .X > IU 9 #w w > Ui Ul bi P z >*Ui 0X .9.0 H* QMS S' 90 OoO%vX -J < -J OsZ < oo mi Z 9X < lr o * h* ,9s Z OsO OOsX O < . * s o o to 3 ffi t-0 -J 9X o <:Z < %*-. K * CO Z V> l o >Z-J ZUl 0.0. zoo <r- u W o A Z w OJE % O o z 0tO 0.0 zoo UiO 09.Z o CO *rO 0X 00 01O oo mi zoo < wo * JWET Oz<X ,z o *m Z)Or o *m o AO*T 1- o m o Z sO,m o 9W 30<A z 300 >- 9 00 B-6 DUP040009755 TABLE B= 4 ALLEHTOWN-BETMLEHEM-EASTON* PA, O <O0v 0 X J <E9\OVO . CM- CO =3 o < CM H *-<M O rtO VO o - dvcu . * X k) or^rt 0< Q Ci*M<*D* *-o r*o '^r-.f* . OO X< 69 S CO 3zo '2^ ocy CS.l .Ot*v XT.*4 ft . f-WOv *h" Ovro Ov Qv O - 6T* < XI Ui O a. yrt Ui r oUi' f-h-irs o o XOift *n>o 4JCNf>0 .*.-C.UoSsO o I > 0.0 u. mOiTv so> o CM CM o <*3 OOO .00.0 >-jA.cy o ** Os OOO .. o o CM ffi CM -CM -iT w X < w > 0.0 0.0 *-\(M m ** r- OOO pOm O(B.OfM *-Ov OOO oo Qi.tn.3t *- o o os I 81 31 I.1<19 OOO ITS I OOO if*0os<lOO so OOoO Ov --` *- f* Ov Ui U. o< . ir 0 r- Ui I j CMO +< flO X o* OOO o Of*vO*O*3 SoO *-<viu\ o\ OOOOOO oo M OOO OOO CM ta-f* o tso CM UJ 1 nX x u o 09 0299 ar hi o >H- ONUX tox s-M -- OvO 0 Ov.X < -a ><cx1j - -J, X< po^r*ir S0^<*/*> O CO *- </> I o x5 x Ui o xoo a wo Sx as< X *IT\ Zsor* - 3V>02W u Ui <X OvfE OCOKvOX -<i Xi-- O*x ho- W **-Q H* O V> . X-- v.x>ooO H Ui*iA* zO .X&v<O/><.*/>r 0V6UCi ovvx -<J ^ K 0<) ^<?*.<O hO XW J <z/<>oli>oo_ H<ho- zO3UvI>0.%.*>iA*% B-5 DUP040009756 TABLE B= 7 \ AUSTIN, TEX. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, T980 o m o --b o 90-St m o OWN o N9m o 9 IOo* hr 9 X >c UoJ 9*- as t UJ a. 8a .9 tar> 9 *<NJ 99\0 Q o 000 m mcvi o cnrim o ----c 9**9 m.9 CM N w9m4of\ foev FOfO CVJ CM m,sr o OO rhfi) M?Sf --d --e p ONW : a\ o \--0tot9ft oO .co9oo0o9 o CMN CM q 0 9 1 O N UXJ a .9 -R XO *9I- t o O IT OWS 9** CO Xo 9 it X9 OO POO .coco CM CM 9 ** rf-tmmmw oo oo ooo mN9 o . 9 .0 0.0 Toor ino* -- o CM N 0.00 OO CM CM m. o 9 .* 0.00 OR-O'OPO ~CM o fo> m OOO o lTVN.9 0 0.0 oo CM .mo o\ CM O in ,iA 9 OO Q O 1TV9 ** O m CM OOP o sOp^O-P--f oN lA.IS W OOO ooo .09 r- CM CM o CM >H CSUXJ tl-NUI --a PO9sXQ -<i p 0.9 tC o <N x 'N~* </> :_CZA>I <A 1 O OO SOO <-- Ul * aO<'s *m XvOi</></> UJ -<J ovs .90 -J KH- 09-X < X w 9 **o o u <A V> | --X OO so u< * *in o x*- X 3V> 9U 099Z0 <H-i- < 09 O X < 1-- o B~B DUPG40009757 TABLE B - 6 APPLETOH-OSHKQSH, VMS. CENSUS COUNT OF CHILDREN OF ALL RAGES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AOE OF HOUSING, 1980 -J OVIA'O O < <nvo 6 Ho O 1- co Y or;OTs- hr .W2 O oksi a. *0 O' UoH1N oIoA> kd OS fi. .ftj .< K Hi O'fla1 OlA2 on of-- *v .' .* fO so fo>o o -cyfr * -ft .COt*-OfiTp\ . , O 2H-.0J CO O <n T* O CO .* 1 f- z u -4 NO - o k. I 0 ijr ec w X 9 an 2 -H o CM2 tn o n OO .*-. mi . o in oo 0.0 0 m H- 1^1 *-N P O To" lAlA O WO TP srtot*? o Ot -N cyf> OMAlTVft ais-f\`2H oft oo * " .. o eyjH-m V-CVI.t > O CJ tp 0 0.0 .op ;N:8 ^2 1- so '2 P OP oo o2 m o h* .2 oo o Nwm m o .2 c.o oAw. o mvC *?*l* o r-anp *-2 in o oT-* CfVt f^-f-tTift ihW2A* T* en. .* tTvTi.pfp* o .*- O oo VD2 tft r4>f-t o 4A fc* mi OO 0,0 0 "V p f-- POO 8-00 2 ..2 i-y\ p o IH H- OOP POO co m TP >o o o T* to > UJ H 08 >^UJ o ftj (9 O ox < o * H- -o J ot OS . ,<2 < *-- H* -- 08 VOCO W H </> >2 oo 2-1 ki osoo <-- CSX -08u<. -.2 UJ.O * -an -2NOTto<o > o Ui .J OS '< o .J as ox < T *- ;2 2 OS P kJ AT* O 1- p V> 81 2 O 2:00 UQ ^ H* ' -ran o Z}p 2 111 OS .O ~J ox < O .* H* < 022 O to -t -o H- X w V> 4 OO ;j 200 it UJ h- O -an o 2*0 *r H <ov> B-7 D U P040009758 CMO CM*! QiCUift O jAh-P * * -: > *-lA.CW O p .* (APIA O . O - * * * |AUCM .**>% ^ -.*.***- *p-.* p. 0PvlA.*tA. O * t-fH. p p ui -1 -J ?< < u o A UI 3g UI a 2 * 3: o <ffi b. H ae a o 1c p UI a -J p a < UI O 2O S* ,X g I UI h***.** * . ' <U*-in 3'J^ o Nrta* . OOP. 00.0 *!*A -33*0 * p 90 . * . 8 ^ 8 ^ O POO P*OrPjr OOO 0.00 MYPCM Jrtijp.M CM P 1A 0 .*1 CM . .# cy oo <g8**8 ^ . ,pn Pr*imAiAif 0.0 OOO 90P.CM 8>n w X Of Xw t*- X <=J sc X o *- it O 8oh x * UI .X P a in x * i Ui CxL *f*S0 S(A ooo ooo h-OO <m*~p iA O oo 0.0.0 POM 0 o to N ooo o wo?fMotiiohA o0**s OOP oo o 0 Jbf p OOO ooo 3VCU lA At SO P CM *A V0 NA -3- 6 * CM o oo *PlAP rfrtr CM " OO OO ->-cy P <A UI vui .L ..X p -J X a O 0 X o u<* ox o <z < -f* o *- * <O0 p 00 > X o .X-J UI 0,0 .<--1 UI 0 > ffiZ O x< 3U. X X\Or* SV>P > H* u P UI -J X < o -1 X h ox < V- X 4TK UI " o 0O *Xw OO xoo UI o O <A O X.P-^ X 000 UI X o J ox < - < P 3-X *~o O *-- X 0.0 0 0Io oo .xoo Ui * Q *rf\ o XP*- >- 300 B-10 DUP040009759 TABLE B 8 BAKERSFIELD, CALIF. CENSUS COUNT OF CHILDREN OF ALL RAGES 6 MONTHS TO $ YEARS 6Y FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 <y<o o tt** . Oi8AvO *-r* ; O 909 *0X0 o *-CM*Pk CM*"! . 9 f N>?>.if fo X >0 Ui 0 o X1 UI 9 X IT . so co oo rOfo <- <v m p o T 09 0-m0<r\ p 4 00 *-fnvT\ 9 NOtfN tStfWO f-in 9 ** r0~*^4sNrO oaoor,on tty re* xXu> a1 . -i O' x--o wOa I Ur 9 0ifi *2 XUJ X om X O' wXXi ,0P0OO..O,t05fST 9IA 0oo..mof0coCopM iConM oo0o.oo3 ,CM 90 0 00.0 VDf 6On JrO ? > O o --j ic\ M o*9O"* i0O<rVa0tf\ o .0S0"JNi99-ONO00ON fOIT8 0O.O--0k Oi0n ffO OO .oo Of <SJ IfNlfVf ri CM to O' oCCoMMoomroomr m otCO-sMoO0^fOo3CM* ofCCMM O0*.w'OO0JmO0T POS >W f* O0N9X -J Si iSfnex o <-6 Xhr oo^or*xx >< #- U. <*c/></t> x<\ *>--J 9.X Xui O c.poo UIMn* - 3Xb<. Xf X<9/></-> O tJ -<I oOoX IX* oo.x XUI O.JfCoC U x-- A>VoI>ooo UIO A h- O Mft Xvfif X 3<A) Ui ox <' ,o094oO-*oX :O9X VV>AOFJ0-OO OO -<J XUJ9 0. -- O iA 9^ X9VO>r0- 8-9 DUP040009760 TABLE B- 11 BIRMINGHAM, ALA. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING;, 19BO h<O CI'O-Wif* Qf- 0 0o** .o0 Ir" 0Cf> 0 Woas *PCS O1 Or' >-srz O ?**--* ' oo V pip *- too wcun o o 9 Otpi.Ot P ulA-artrOix o9 0 r-ftivp 9O5-- iA<V ot-<\i -- r* 0 Oo .* PJO *-NlA * p O o rOf-0 p .r v*p.tfia>r 09 ***0..p* o 0o#-- r-90s 0 O .I* r^tojp *! Jh.lA O O O-- r9!A o lm--n *> :0 -j J<*o--- 90 0 ooo o-soco ^rso*- oa io 04 .0 -cPn z Ui QOS O' SC X 0 9 .o*4r as O' hai G ,OlT X a. 900 00.0 p*- t-- o o m 900 090 0-.P^4X OJrtsO O 9CO 04 !*" 090 OOO .zee so r- m en O 9 9 CO owp0..ior0p--Wpo0o*s oCoO 4* 009 OOO WflVr* 04 i-- O o .m 04 04 900 009 fO*Or04 ^Os o o pur\ -- OOO OOO P-sOiA r-trtJT 9 9 ,0 0 OooOoP Oo O-SfiA 0O4S 009 0 09 OsQOs wars pi- 1-- o co n w OOO 009 com in com # o 9 .*> 0 04 OOO ooo mp>0 0 o 0 P > ss*VUJ 3 -J p- * .<as srl_ lPiN tz UPi X hi OV OOv2 pJfg o*vr>O 0.0 ,Wo oO oA I -J oac .<XHZ OOOO0tVf.t0Xf ,h<o-J phi >a.v*>* O: Ip-- __ 0IO z-- h PzWo.oOoo* Z 1^0 oa oopaoUcti wh<* $ .2 2 g .sr* h<~1- wsQooo.%ootf\ O 3TO*- B-12 DUP040009761 TABLE B - 10 BEAUMONT-FORT ARTHUR-ORANGE, TEX o CO Ov UMTS Q prr- . 490 POW:*v0- ,srj^.K r h OO WON o X u *-m>0 . ooo p % za < **V- 00 - I ifNmCM : ~flQ 4/> .9 5h 40 z <m *Z *O0' UOJ ~ XI Ui <9 csi\sp 2o P-PtfN Q OV.tA P fr-pci PP 9 p- m UXuzoi .0 Jf't* m*etvfi\m O * ovcor* m h- lAvC O CM CM.7 p >ffl orC*O*oOrSy'oPCM , oCM OP--OCDM.OCroM ..tf\ -0oJT.oO0.Oo0N OoCO CM SmO mx >o<6 I(\ 0 1 ior.rooooCCM\ Ooro rO- O0O.Om0 .AoosO iOTkOOrfO-OW oo <Xo ,o za as xUi 'w w(o<0 s o u T" .11 IT X *- oooooo C-.6W M3 oQv owOomOoto .pm* ooao i-. :r*wo -* u. Ui :95Z MN 0<--opvo0*-.ofm0* Oo r* MoTo.otAoCoVy- ** CM poCM.moCoMomS .CM UXi Uxoi a. X 9 CO 9vs > hi -vuj 09)0S *I(<"f~)- z--o > .Z9x<--.X-<uJ1. hmm Q -J < uozUac*i z* * OoCr*SPO-*vXSO V:xUO95>ViCoo>\10V>-oo*m>-- -1 <Hor -J <X z Ui z-- z>o OCCOvntUXeI -*s~Vxo vZXU9><iN/oo>O*Vootof^>V\ -J H< b~ <CO XCO <9Or>6CtPOO*0T%n.S.v;XUOoXXJ < fOi- --1H<O--1 zUZ' NioOo-.owirv\ 300 B-Tl DUPQ40009762 TABLE B- 13 CHARLESTON-NORTH CHARLESTON, S.C o s0o ,0z -Z01A o 90 CM o 9iMO o < 0Z9 O 0 9fZ- o 0O oX f- 90 z O' MA o tTM o !Wtf\ 0 uo. OUi ON.rt. 0 rtCMZ o Pft-Z o O 0 CO 9 .u\z- Zift oo *7 0>06 nvQ o IS..CM9 o mtn O O h- . H0* .*9- < -H* .9 POO 0 Ztf\ -- o O P CM* o <0 Z0 JftOlA 9rir*> o PPM o Ui 9 < o-- as i a ui z e. tf> 99 o ** zz o StJX Ui o or- o -- 9.0 o X IT Z'W** . iOOlC o Z90 6 sz :9 -- .* NO o -- *- 1AM *o * -- mA o-- Ui x X] I t<-1s .H1 OOP O(>0O3 P" ZfV o 9o OOP OOvONOr CM 0* 0 ooh9 CM 000.iIr00A\..m--00 0ooO -- CM .z X(<UAI > 0cc1 Or-' 0 0*0o .9o*0 * oo% 1 0.0.0 0f.t0f\0 -- MVp--" o<\i so 0P0-->:0f--0!>.C009M poo> CM a O x soufii <X Z Uaa-stI .9-- a X 09 Q U --cli P z I9--T ,O0.O0O0 oo CM -- zo OOO OnO>O0 0lf> 0 OOO--O0O--iTOOzk o(oA CM Ui P X . cir Z .9) *-- 0.0 0 OOO iA<C - .CM oo .z OOO OOO ZlAf- " r- oo o PO OOO OOO 9WCM CMn o O z 0 o z Ui X .a. a: p XQ > .1-- 0 > UJ Ui UI t-- 9X u 9Z 9Z >N.U 90 i < 90 -J .9 0 -1 WI o C9X < z OPX < Q9X < 3.C O < zC -i < O* O ZZ *--O uo* fr- uz* Ui OA zz A-- w O >-- < O ozz h- o v> u* OOWwuaiz t-- x zx3<fiUS<->--. . X z Ui o z-- 0</> i/> I O aU:I OOo.OoA oZ3V0>*t--r>\ u 99 V> .1 o z oo -- J" UPZiOQmOAA oz Zo<0/><-/> X </) <0f>0>I .o0 N<~ o Uzi oO oA Z3OVVO>--i0ft 8-14 i*i DUP040009763 TABLE B - 12 BRIDGEPORT, CONN. $0 X 1AA0 0> o O ur\j^ o < O.iOjO 50SOIS Q o 05 h* inM-ir.. o O.0 O fr- ** O r-r>0 0 bO. Ul ooo CNlJn O *"0vO O 8O CO o P-.MO o t** p O <r ' o.1*- o *" *-.cp o *- CO 0 * " :<X f O f- a f-- c- Off?* o stSOC* A nffift . * p X >0 Ul O' MMOuN*On o p o o? o QMUfc- -o p o CQ-< X 1 Ul o a. IT! O Wz f-n-in o o *-, <r* o O^ST^ O o in rnvoON CO IANS o 7NOO o o OS tO.M p MP u MM*n P > bJ e -J x I . o 00.0 o OOP o >CD . .ul .0.0 < w >0 O'f^i OMifN .u o -U ooo \0m r*MW u* o N.r0 ooo 50-tno a-iAf* ;r .O ON fM >0fU<i5J 1- g OOO o IA O o O*"s . up 0.00 ooo to o o .^r OOO ooo rOtAJff to O O M X o *:OxT r* Xo Ul W z XuA W - -\ ooo o 0.0 0 . OOO o ooo o OOP O OOO o X os (N-N0CO r- Wiftr flO .Ov" ON ON 03 p um in m ''"NO *0 PW u. o o IT < Osl a: X u LJ a Xo ooo o 0,0 P o OOO o X if\ ooo o ooo o ooo o X .ON OVMff 50 iftsO*- M ffroNirv co M WW flO >0 intnh .St 1 Ul W tc a. o Px > K U. o P > Ul Ul >sUi >M- On OS OvO -J 1 < 0sX ON -i Ul c*x 0S.O r P O0\C < X OCiX < OCv < DO - u U * J- O *' u s -J <X < X O JTOC o N0<l> o H- X Off o Ul **-0 u O <60 < ozc o 05 frX S0<- so . u y> i o _ </> 1 o w V> l O v> .> X oo X . PO CO oto ZJ Ul KOO <:~ p w o -* xoo U.o -J xoo < w.o X SIX O >tf\ w 0< X ZA0P- uq O XsOr* uo o *n xo* p XU 3VHO X D00 H 300 B-l 3 DUP040009764 o P * ( flNO PP0 CM CMP 0 0fm oo pI9fIA* o9 ' 9 pr-crsTiJA O 9r* ui 0T-0 0 q 0 " m P 0 i*CVI*> pj *-:M0 P*.CMP #PKV 0 !B^OQ0 O o 3E o 0$ a 2 <0 O' g -g O0P $ CMCym g 0* CM*-P P c**s*I*r-!0 9O#* uyp** 9 -.*3PCM**iPA 6O 1 ui ap CMPP iPr Mff*N 00 jfrtrt I4RR O PP 9 PP0 O **P O s-J POg*9 O o o nmooincp 5 CM CM 009 OO OPn Nff ** O CM CM cooooo eo OCMf* f^pp* CM 009 0 9.0 P.99 tf\V-P 9 O P 0 900900 O f>r- 9* *-pp (TN 090 O 900 .0 pp>f- CM h 9 00 0PO9C0M CMP 90.0000 O r-op 0 CMP I** p gmgRgN g 090 ooo O90O0P Oo P ."CtnMw0 tCM > tO QgPsIXdf j< 'P > *KXw- pooi ooa g.-? 5 SSS 3 Id POO OOvg < o. h" OP.OS ** 0*P V> oI oO POO wa om>* PPid OPP.XO W< 35 oOP. P *o* **- >- 5 0<O > I W .< POooP w9 o * X0'*3VM 6-16 DUP040009765 TABLE B- H i CHARLOTTE-GASIONiA> N.G. toV ovAom o .0 .****.* * osts> - ma < pw eg vo o . IAHH MvO oo tyvp oo*4 %wa o 0O 0*0.* 0% o ~ f. oo" VOX '.* K cypo- d X bov-sr o 0.6.JA ,<yh- 9oo** %C 0i -ta*!- 5 5 X aX ;XkXwHUftJ.r V*tpOoJf Cv*' o O-OVO b CKM.lAljAA -o9o-- XOsH' o 04 00400 o or* Ov" f*<fOyS.op d o o 0 0^0 o lAP-0 o JT00 p QX IoT COOO *-.CVIvO *oo* Ovqi'A8Z^ oor* ffMS o J-- id XCL 5 >a 0 -mj h< ooo o XMo.OSoMOo,<OSP 0ar Mo _2ooXTvoo\or\oo.i0- o o s<\ti ooo o0 oOsoJ> oo St f* 0 ST X 2> lA O m x 0ov 1 XkJ irOo-*v OOoH0fOo0k oVoOOv 0o.o0-o0 (VCQ X*1A- oo04oo9*oo * >oof cy :x . w0 -XoJ OS X >o0 0 U. oI l*0oA-4.ot0AfOo0p) oo VO .o0o9.o0 Cv nMSi'NA oo 0 fToo^-OooSooJrOT- ,:foofj scyr X P (OAs uX S*- X u. o Xu X0 oifS X OwN u. XX ooOVoo*O-COooN\l ,*o0sr oioa"ooi*A*cooroy oNo ooo notfoNoN *-Mt A ooo\ -QX >*- bO aco ain .XL0j S^LU COX 30 HO H<XCO XJ> <xa<xtX* >Hmm* o -J <XH zUl P X bJ Q0poVvv.ZoX oo^*c. VV>O*V"i> oo. xwOooo-oUoT* -J -H>o<- w J< JOOsvOx XK QOO*vZ ZUJ ,0*Z*-Xo U 0l>0. X oo n HOZ 5Xxwovooo*o0ir-\ -J < H ovwx 9 9O.*2O -J <H- .< -0x O0.x 00 0i o ioH --j ><H xwO2S0ooo0roo0-* fi-15 DUP040009766 TABLE B- 17 COLUMBIA, S.C. to _o oas <33 OPO p fty*Opmh .. OMfft* p PPPIMP po rtf*o o mpf*- o fo u P op o f-HlA . mn-p p .* Q povooa* oo BfcOypJ oo pf>**> . Osip O I . 3HJP<:a< xh- p IXuoU *OoI-S cimm o N.pey op pop P P-P:P> . mm o Pin i** rflsB o p 3X ,U `CIO O f-op o X ,WM cOviOin oo mop . N .H o mcyi**-in o 2 H- OO4ffNOOSOWO:O.JT osO4o* ooo gs. *- o1o*0!4* O9OmO0OoOO9o .ommmo 3-f~ gmcsi m ooe e cooo*o* <y Sit i .m*>om* fc** I a cN XU Ofs S oS;-OXx 0) X -- >0 XO O*I-S ooo o oflOosOoOs m m ooo ooo o 0>mVO so p 0.0 o OOP o 4X.P-P o t-tlft U. oUi o in3 OS -2 OOO< as o Ui o Xo 3 IP ooo sor-m o o \C CM POO oo m O rt r* ooo o oosof-mo o CM m UXQi 'X o Xoo 3tPfi Q ss V--a- oocO*uOzi .-H<J Hh<0xO | 93<xp<1- <J x .UXo1-I x r- Q**^.C >o</> V.Xw>oooI ooo -qjtso**in* 3V>V> HO wJ QlX o^i XHO0-*7X UJ *". P 2 KUi gOg* *oX- a*99*0m * Ho H U X < OOP-jr*2.x * tXWfi <0/*>*O1o. oo ^ 900 < UJO * 'O oXp**m- H 300 8-18 DUP040009767 TABLE B- 16 COLORADO SPRINGS, COLO. o <<c0h COM --r 0\m O iftNOOs o _i . * * < st^ s--m . CVI.lAr- , o to eom o .*-* * m\ rP r* h Ui o wO t*> lA.r* < 00 f^OiO o V fO.VO o .0X0* . o . &Q\ . r-.CVlA O Qa: < o< f* ** m: fc* 1- 5 W O' *-X3A o . i . '5 X NO Ui O' o Kt 56^ 8 6^ ST.vp oo r--jCM j\ o 0 f^CM -3,ar CirQ UI Q a. .If! O' .v* u O'p ro 6 oqo o * PfW- p 5 .at in mcam o O' *" its*** o T"* o o CSI *"IS* *-! . w X fi- fw> < H* POO 090 NO.Ovr"* *~'OOv o r> 0 0.0 900 tfYCV *-*SO o 9 * 99 0 0 90 * r" po 9 in r* I* * * CJ tcoe u<i > .1 900 o 9 00 O :oo.o CO 00.0 0.00 9 0 0.0 . o> t*- * n- tn r mjPk o n 1 .0**001 9 tA 0x9 On X* w9 P> X X Ui O* X jOS Q X oui -J o * * 0 -X O' o -- 1 u. o 9 n oo 9 PocOoOo 9 >o CM PO 0 ooo 900 XCO*- cy --u O fO m 9 00 OOO CM SO *-. rUMA .0 ON ip* *" X.< O' X u 9 X 9m X O' * * ,Po-OooOo 9 ft- r* 900 090 CVJi-f- 9 oO T" OOO OOO . Oo .r- CM Xo -J > Xp >- Ui Ui UI H- POP -1 o n a: ONX >sUi MX 30 5 ovo .! C**X < H- < o X w OONw X < >- ON On X O < *"0 .x.at o X O XX o < oat o <z < *- O >- Ui **-o I-. M -r-O 1- om ce. se<i> M t- o> >X oo 0 NOi/> v> o X OO -x NO</> M OIO op XW w ooo too 00 O 9 S/3 '<*- p wo * wo < UJO * ox C *if\ H o -m H* O %tf\ UJ 0 < X X NO *ou. -- O Z\Of X OU><i> o x>0.*ov>v> 6-17 DUP040009768 TABLE B- 19 DAYTON, OHIO CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSlNC, 1980 -J C\J O* H< O .cXuSmO*0* O or or-ift (OOO Nf* o o 0*- 0 N mx n 0 o o :001o i o X0Kaut 0*I- wo POm IT O IT V0r- 0 0 4-SCO OOn X cywrt o . 4NO 0 *-8 wX8 0Q tAN4* ; VOW^ o ptf>x' I^n OO *-r> 0 0 O'4'O O l*A"*CtA"J.>0fN 0O rrtOOS * W<Vi X --.6 --v6 Vo o .0 p 1f\*9 OP **,WVJ 0 '0 o*> f*>0 P !F{A}I#OJO -0P .00.0 e OOO o < infs-x *a H- 4'Of^ 09 H o . 2W2a O-' ,w w .OS AO X Q7 tc ui 5 OOO OOO -- irvcu o09 OOP OJtO* P40 o0 m OOP OOO *-.x caxa\ o IA OOP OOO KMACO ?Oift * o p IA OOO OOxoP *rtO O w IA OOO OOO oom r-X CO o w ,x W 0O.O0 O0 0 o T-*rt-iOx w 0O.O0P0 x^ 8 --y6 CMS.** *.x o o .x 0 PPOOOP <**. *1* POO OOPM MAO CVJ p lA a> w POOOOO COCSJOp M f* -- * o N --z SU P <x 0 1cc Ovtt oS oo<s*rs fX- olO < uO sWoo* 3U5. *-- Ox9*0o4%~(0-A oxw v < 5<2 xfi u55 8?o 0.0 mi flf.OO <OHh- 90WX00O4**l>f*\ B-20 J DUP040009769 TABLE B - 18 DAVEN PORT-ROCK ! SLAND-MOL !HE, TO CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND ACE OF HOUSING) T ,0O3' \in -J < o. .'-ft o f- aor-pt^T-O 0 o Q o p * * ,OCor*C' fo*"- h Z .UUXoXJi oo of ffs OifUXX*f1>J -J -< O H* pkptfV O *--efct70 o 'PO-*Op" .*-.0 O o ft ft ffOtO. .o P SO ft o JfO' MPA. *oo ft ft ,*ar-<fvt Tp" - Z" p ^co >bo .0C0M 0l0fAt..O00T of.9C-M' O..9*0- O*c0v-.P^90r .aOo' F* * VO Y*;. P ooT* ftpvp o PO* *P!*. o Y"6ft'6 .do* O0ofOv0ofc-.0To0f0itf ooo CO oCOO' zUJ ios s ,Jox Xp uo. -.o O' 1 m P UxJ aXo 1oA z OT"s U1J xX moooowmooCM -oft 9 mO0.O0O0 ~9 ,OvoS rOoie-\fOo2txOot* Oo o 0O.P00 oo in SO 0CoO oS0O.oCi0nM o <o o0P.o0.So0O ofmt 00C.00sO.00S .oo<o OoOOoffttOoOp ooo#o o0*f*t.*oC0fOto-0iOi--n , omso >s,UJ w.x oo H-Q <z w * .> ZUl < T* X e< Pw .> h- p < X Hz ui o z W ova: oo Q\X o `V 09CC -o v> <J> o .zoo UJ *in x~- -J < *o > i-- O UJ -i ox < Os O -J X O.OX < ** z e-srx Ho UI o o so<J> </> o ;Z _o xoo .UJ o ^ I*- o -m O z Z2U><f> UJ CNX OsO OOVX < < O * OJTX H- o V) x >*- o H p JO oo -J xoo -< UI u o -m o Zr h- P<^V> B-19 DUP040009770 TABLE B- 21 DULUTH-SUPERIOR, MINN.-WIS, 00 ON O z NNM . r"-fZOZin OO <0*0 T- M.cpp t-.Z'P :CSl>0 0 O O ,X Uf <<5 '<* oop o P*-OZmO 4o9 *M\0 OO tfVUTNO P 0-4 co dF>\ oO 0*0<- OP.CM ,.P.cy o OSN ku >O0s0 ec ,UUo.li< z 0 I.o*TI 0,0 ON POP , ifuAO 0o ?Jd o CVi P Os 0s CMf** **ONoo 0m ifttfO o ^ pO its . 4T -- PO O i" PO tf> U1l z l u. ooo O 020 o 0.0.0 o OOP o 0.0 0 o OOP o w> CD < Z*-iA o u* CSJ o H .Z *-.irv cvo 00 cvo o I-.\QN in .i N z U<l > in . o O ooo o 0 ooo . OS *-z*n 0.0.0 0 0.0 r- On r- m o o! f> ooo ooo nunZ o p 0 o 0 X *- Z ON W zz o :Z NO .0 j On -- so Xo o f" 1 ooo .0.0 00 0 CM OOO ooo *- r* U"\ o o fr^u ooo ooo ON.PO PO o O PO z w u. O o om < Os z Z ,r Ul -J <a -J Xo O IT ooo ooo ooo o ooo -O ooo o ooo o u. o Z Os 1 WQiN Z S-C44T 0 NOStof CM z mom NO * POP** CM Ui zz u< z z o -J B** > -S' H o u. > Ul 0 JUt Ui o 'v .{6 H* 0NZ 0.0 PZ < oo q J OsZ OsO 0Z 0 OONX < z O.ONX < OONX < z o 20 Htf J o> zz ** o K * K z ZZ o O f* H- .< ozz o o < z < i"* fc- Ul *-* 0 S-O u* o -- -- z vOV> o N0<1> X soo CO >- i o V> 1 0 o> o 0 o CO 3 Ul 0 >z oo Z-J Ul zoo <-- o Wo ffll o *m z< z Z>0-* JDZ] D<M> z oo zoo Ul - .o o DV></> oo .-1 zoo h<- Ul o . o m o Z0-^* 200 B-22 DUP040009771 TABLE B - 20 DES MOINES, IOWA CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME URBAN STATUS AND ACE OF HOUSING, 1980 NO-Jf p <nQco MOCM.cyi o uvuv-*d N* jjs.Oscy Os*S"O TpO^ CO Os N0o!S| s s Ua.i c IT .05 I Ui z -J < O H OsVO47 o i" h* , *-OS 0 .tfVf-f* Y- VO oo m*o~ p a1--WoNiAp OP 0.0 QhO 04 CM O 47 0Or:O0inOt0n o CM tfi zQ NoOON 0 Z 1S*34 X3 z DOO 0.00 CO.OvtO OOO ooo OArt.f" "# o M "SO ftiA 0 *~>oca . Os p CCOYSlfOs ITSAO CM *-.sfS . o P h-OvCs " ps in CM r- PP*.~O0'j*.OSC0OM fo!- yp e MoroOo .so moooojor- oCoM JfOssO o ~ewp* r- CM vO *~,cy>o .09 . V0O3T r- CM >0 OOO 0.0.0 t-VOO-s 0447 Os o o CM Pr CM .a00r..|00}.080^ .o tOos OOO OOO '**-0044VSOO OOss OcowOoinsOoQ mo >w '<HV.-WzoOr .HZ<fZ`fr.-W>-l--<d*l >WV o -<zwJ zUl P z-- O*40*O--7V-ssuacoZc: <3sUZZQAOV\IOQO<M*OOO--Olf\ -J <H+O o -z< zLJ O.OsvUOZi O4*-7*voZZ .W <Vho-- . O z HOz <szWOZr0>-<JoOO0ofOoifA^* 3V>0 < Z0 --t <wJo- vvwozcZDO*Vo..<o*sOo/>o->*\s*o.Uo1zoZOmz>-4*" W w<HO- B-21 DUP040009772 TABLE B - 23 EUGENE-SPRING FIELD , GREG, t0o ,0N Si CONOCO x to**,o? oth *-cyin o <5 . 5VN VO to VO WvO O o Os CVIOn *-3>J -- cyjp O P p az id "0<> o <or>ifv 0 pr*3 o So co to i*jrt 6 . 3fticM O .- # . p**o o p -v CW.n o o -- co P *-p- o 9S o *-- *" f- to o -tT < -Op o p'-o . 0 On NO-NO 0 -- 'on z SC coco 3 6 t-eyo P UN PUN o Id Ov a<s 0cc r* 1 Oj NO o .*- 3WN 0 -- <WUN O 06,Q Id o CL UN O r* W r*S tfVrO p Xo rOtACVI P OUNUX O XQ tn o 3tf\ UNf-f- ON CM 3 W o *- fO.UN 0 *-<>3 o r* .* i u cc Cl I 0 0.0 o 0OO O 0.0 0 OOP o 0.0:0 O OOP - -- --~6 On 0N3f- into tofi ---u n u n cum 3 v*" UJ s u* > d *o0o1* 0o0.3or0^--o.0OMN oO SO 00(O.000-.CU00VNJ otNooO oo-*ooCVJoo*-. *- cyrpv .ooC3M or- Izd 0> cc wuo<3 u.d -- X o :\COT0"NN* u. O UoN CC O 0OKCO0V.OI*0O :OUCVNJ" ooo toOTwoOOo-N .oot0o ' OOOOOPOPU*rN> VooO UJ < I*. Xe3Zo o un Os u01 OOO ooo oor~ o0m0oo.^o0o oOCMN oooooo *0 U* > O* n o30o oQid fr. > u. > w u UJ O *vLJ h- On ON O -J (AS 6 OC\X .- 30 o *<-OzI -j < O' .3**-O- oS 1-- o f- _J ONZ '< .0 W z Ui 0.0 0o.OV- X 0.38 Q -J < h- . o Os 3 On O aJ oonx < < o '* : 03 0 -- o to *- O u oto 3to H* 0 NOV> w >1 ZJ <-3 h- z UJ o </> * a: oooo :UO mx O *UN z V*o>vo1>oo. 3 00 UJ O . >- O *>UN 55 -J .-< w 00 0.0 3.0 0 Id O * Q*.UN s < z ZNO -- su. 0</>V> zo ZV0- o ZovnO>t-o- 8-24 DUP040D09773 TABLE B - 22 ERIE, PA, CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 -J OSS < HftN O *- CMin o o H oimn 0 OO1* O fONO p O' ~. .1-- . woaeo p 'p . Npz*- ina* P tnoip P .sT.tn-?- . O ON Z 'O WoK .O' I W&. iOn r-*- **! Alf^O PO V3 *-*rm op mom O <vme\l fti P P -- 50 F-- <VJ-VD :P * >6. m 0 * * ^Np P O O P o mm r-euvo 6p ooo 0.0 0 o cw ^cy in O' ooo ooo mow r-WON P p in nr* ooo o* jo-mo o rfU- CJ 40 I r> Z O' zw r-i Q -j a ---ux NaO uo. :*n O' XW T- :a z a o8 Z O' WXi ooo op m o CpO POP ooo On CVF^r oto OOO pO-nOo O. in ooo o o**ror-oo o a*. m ooo o OOP o e>0 OooOoP O o JT&O CJ CM M OOO OOP r-Or-PfO*. O p ooo o0oVomN Oo' if ooo oino<mwoo oo oo >sUJ z 30 1-0 <x *-- W > ZW <ox Z< aw >w -- ON ,o -j o OONX < o H ZZ O < +* z NOV> > 0IO z W oo zoo p W P *IA z z - ** a v>v> vt- P Ui mJ ON < OsO -j X OVX < > o %' ; z OZZ O u o H* u NOV> </> o Z 0:0 ZOO W * H .q -m O ZNO*r Z av>> Ui KZ OvO OOZ < o> i-- < 0.3* X o ' **-o J- Z N0</> iO o oo zoo < wo h- o *m O z.o*1- p>0 B-23 y. DUP040009774 TABLE B* 25 FLINT* MICH. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME* URBAN STATUS ANO ABE OF HOUSING, 1980 *J < s pmP o *o-<dgdm . ddd o d o > omm ddd r<Slvp d ,o opp odd IfNCI CJ Q d P po.P *~P o d p iftOX p or m i* d . *-- O' X Ui . o fl w CL o iT ' p*-- o m . w Acs. .-1 < b~ e (IliRN p mom o -.cam o cacam P o o OOO ooo m.fl'O o o -.I"!* CP o-co ..UXX_LJqi vX IoN 0.9 1 UOq o IPT UxI X oIPT i u1i oorCooS!CooM o0<0 C00:.i00m00jr s-W..Sf foo* oO.eg oOcaoOm ;aopcr *? *VO*" o o* mono O ` cam P o ooo OOP f- mm M)CtA N o o m -3* 0oca0o<wv.o**0,<o^ mcoa OooOoP <9+*S* i-OJCO .ooe*J*gt LPO-OCOiOmP oo p*-0J>O h-m 9 NriA **<egp p . o o IBB -f"p >oo ^CJW o 0.* ooo opo nrt.O p*--m r* o o 'cOv tn Oo OoCJOoAO m5) oooooo SaDjjri3m**i Ooto Cal opo 0T-.m0^0 00op > Ui Si 5>wUJ 1<-z0 - OsSC PO J .** -J OOK O < **- +* 9) > CC U X 0)Qoi/>o iiX-J oua x UKzioOo**Om-* 3L 3VW > I-- o UI s*.a iw < oOQx u X Ui O*O"K0 -Ot-- P *?a X OO +* xuoio.oom> o X =>&</> UI cPO OCX o* < 040 S 004*!*" o O < H* cwoooo"poin* o H- Z3V0O0f B-26 DUP040009775 TABLE B - 24 EVANSVILLE* IN D .-K Y . CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BV FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 pm p otf\9 o 9.9.9 . O p . '*.' 1*9 9 .9 o O r- t* -r* Zlu 90 O Z1 uO CM m *r iOn :*U*iJ* Z CL u <H*o- wr-p O zm o T- mtf\ 0 o.o o. o ooo tn o j^-map ftJ VmOm o 6 o OoOoOo Y-mm pOo r o0 *" ,o f- Z U2 * Z o -I -- 9 X o .* I u. : IT z * ui s zO If z , 1 UJ z .0- ooo o ooo o :Nmh- -z ooo ooo vo m o o ooo ooo *>CM o o m 9 m o f*h*i-.O d o 4*9: \# o d *-ao o mcyrm P ft! <W9 o O OOO o 0m.f0t!*09- 9h* ooo ooo r-iffrn *-9 9 o 9 h* ooo ooo h m 9o m 4 ooo ooo %fti f-,m 9 o 4* M o *99* . * O Mh? 5 MO o*<<M-9 9 IftlAO O * '* fl-fotn MOP !ftl gfgt.Og 8ft! 8098*-#8A* f8m* O**O.8NZ . 8 > Ul z 0su o -J Z p ox < 3>.-0o -J O OffK o <z < Y" Q h- -- z AO0 V5 H- o > Z-l <-- z UoJ zoooo UI * oz o *m z< 3L z Z9** o UJ < oz Z oz < 1- o ji" 9Z O Ui Y-O * p X 0ooO zoo UI O * *o- o *m Z9*- z 300 5 IS 2 o B-25 DUP040009776 TABLE 6 - 27 FRESNO, CALIF. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO $ YEARS 6Y FAMILY INCOME. UR&AN STATUS AND AGE OF HOUSING, I9 6 0 fOCNO >o^r r- O . . -zmOs O fp* co I O' oxxwUi OOwo''! I o Q- IOT' U> O' JO o -op ir m*> O 6vom * QDifSP- ovr^w w O O p *** CM*Q 6: ?sTrw P. t -.-o .-Ot o* OuA -r-m ir- o o meo so^cii p wo O **.. O - Wi"" mJO-aS*t . <vo ---- oo? o ooo O.0S armcM * o os -f* CM .0.o00o o as CMm*' f*-> XQ-J VO Xu 1 XXu ,OIoT' X m P o OO mm -- cvi-sr O o 0O0.O0 lAdO-CmM *Oo m OO 0.0 0 0MACM fOOVFO o so CM oompomo *" CM m ooo OOO m m so a -S' -oa-Oop-oOm o *-wr> 1* 0-0.0 OO CV-3\{\i r-tf\lA *~.<M O m st O0co:m00 Otr 1-0".O' 90 OOO OO CM. ^vo Os Os 0o0o^.*o6m oin *-> CM >vW <AOX .Ns<1--o -x--0i> X_>i .XwXC f>- p -1 -.XXhpU<JX voOO>s<0P.r/lv>*x*.XXUooQcJ -J < Ho- xW3qzo0o.*0om-* -- > -J X< XUJ p X io- X OOJ00Ts*svUX.KXoJ 0XW3oX*OvO0OOO0OO>0omA- -J **o< - w< X fo*<-1- 0O03xUX-Vlo*00OOXOoPO>-Ss-OXS0U1.oO*XAJr *O<- B-28 DUP040009777 t ^ q M[ q 26 ` o r t w ^ v n [ , 8 n q .- CENSUS COUNT OF CHILDREN OF ALL RAGES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 epf^in iAP4* -CMin . r^.0K^ p fb-jr f* |S O bp\0.tf\ ' - CMTC . o .00 I opp- K :UZJ o P\Qi P* Zt OWN Q oo>o CM i- VO O 3\lA fo\o -p .ebinp<M*-m p D T-rovO O r^4r oo o o srso o AO*** o o :OVD CSlsOYr - MJ p o p r CO ckarvo 0 O P COpvPO CM K O of-* C0P.CM ^<Min .o' o .r- ,0 0.0 ooo vOOv CM-SVP p o vfs VO ** ooo ooo - ir iA o o CM OJ 0.0.0 0.0 0 *-.pPN* CM o o rPr- :*9 CO .0? *-* r o N. zP UJ oz -j O' >0 X O' p t u. o tfV z r- UffJl 'X o o z (ft P 1 UJ! CO a. ooo 0 0.0 oo mcvj O lA 0o.o0 o0 CM 00 CO T"fO o CO ir\ ooo o of-OovCoVJ oCM CM CM, P ooo \oOCoMo0 oo zr CO ooooo P\0 it .o in m oooooo PPlA oo f- >h->sUJ w PZ OVO -J OX oo <-.oz a _j < z OPS oOJC V3* V>- O u<> oN- V3 - V> .1 . ZJ> :c<o--x wz o zUJ.0Oo.o0 o *tn z0U<. z Z<v/o>,<^/>- > o -J UJ PZ < 0*0 -J +z z u Oo P*S 04C <H* o 0 \0<A v> o '--Z zoooo H* 6 o o *m zo .Z VD DW .o0p.so0rvo0o r* o 0O p ooo o -.ooo o -- pC*M COr oooooo orr eo^co o IA vO UJ PE o:o -J Oo PS H<- ws< ojrs; oo O .h- V3 0 1 o oo < zUJ ooo H oH- zq\otn300 B-27 DUP040009778 o OCOfc oz CO Ui s .za CO .5 I<- w x . CO 3. Ui :X O u Z > r1 X u<. > CD < UI > lA O h CO -x f-- X o X NO Ui < u -i < 2E u. *o to p z UI & . < .a as x zu u. o H 0\ X wX o o <0 bJ -i <H* o XCO Ui OOO NmNwVm0 p 0.*f?>-0v* r-fc- OO O NON.NfN* P o :o p o Ov z >0 ui 0? sUaci * * 1 a. iA lA ui X < o .H 8 ^-o ** *-* NX Q * . lA.f-*Vp 9 - vOOX Nft-O o p .0.0 0 OO v~ VO ry 8 ^.o n tf\ ft Ov Qn N .* ft- t- 0 . o .* r-mvO. NX*0 *- p P-P*0 A* CM .cyft- o o o t-- OO OOO roOv*^ -!- en o o M OV n CK.** P m.Chl* P r*f!* O <vnncy ***. UYiAp POv o o Q 0.0 .OOO XiftOv OiCWp *^x P SO so (A q os t . ftZ Os ui a / o> -- VO X CN o ** u. O lA Ov X fui X m X *O >v* 1 UI X a. OOO .. OOO xtA A* OO .OOO NNO W o o mOv OOP OOO iAX t-x'vo O ON ** * * 0.00 0 0.0 ,o\ CM n V- cst vo OOO OOP l>XCO mitnU O O ON r* OOP OOO Of- N*- o o o X* " OOP 9.00 irvf^r-* carx P o Ov N* OOO OOO rvox cyvo o p ON ' OOO OOO CViXX CM'VOmNm P O N > Ui H*sW -- ON OVO -J cox o OVX < .9.0 5* K <1-z0 -i < x .*0 O ft- u CO co h* CO t X.>J .<UX.--<_ X Uai z o OO ua-Mft z<0^40- > U* o Ui i ov < Ov i oosx < - o * h* X ox o UI *-o Isp NOCO <o i Q .--X OO 0.0 1Xo ZUoivoo*mtr*t <o<o UI ON OVO OOvX < o I- :< ox O to X VO%COf0 u* (0 <0.1 p 0.0 -i OO ><* >o- uOZ>N4o0O%4tf0>- B-30 ii / DUP040009779 1 TABLE B - 28 GARY-HAMMOND-EAST CHICAGO, IND. o00 pv iAsK o *"-- -- 04 t-*- ro o ^ . ifi .O3. O' CM <m*~\o . flOf^ar o CO 0 o' S' W Z'OO . 0 JArZr>it\ P 3E ,o 0Sfl > Oafs P W t<o z- H* S Z >0 UuJ o*>- ZI UJ cH a. tH o W>" \Q o p o 4, zUI o o .A-t* S"Z O O Z;tMj*.Zo 0a S.*- CM ;0 *-.p o < *AZ 0 0 O* 4K9 och* o 0. o f* 0 6 P CUWZ p^.ar r- r* SO O c o > CD 0.0 0 o -.<.J ooo o so w 5 SO (AO fO CM . ooo ooo fOCM (y(g.N CM o o n <NJ n ooo ooo SO OvO CM*- z o o IA (A SO SO z>Z<ui to 0 oC>O Zw of*>1- OOO ooo Z.Os o o VO CM ooo POO 0sO. 0 O CM OOO ooo <*> tfYSO O o Z .in g ?x CO Ui zo ---4 .\Ofi' oooooo Mr- oo CM Ten- ooZoo*-Mooo oo lA CM o0**.o0o0 -- T" o po- IA CM <o o *n z .2 fUflI P 4T< u. p O zo OOO 0.09 *- CM ** MM r* z IS ooo o OOO . -M<0 O M* A K ooo ooo CMiAtS .3" rose o o Z Z CM z z p >H* OTzpp CpO CO az JUJ p >,W vax 90 c><02--ZP-- Z->J <-' CZD<uS. K> 5 .J <zu> z UI o z OswZ OOOssO 0O.0*.o0 <vzU/o><oioo/>ooo OZsO><A9</> -<J hr O P -J UI OsZ -< Z OP O0X ' ZH- o* 000 O ui *" o p V> 1 o z oo zoo zou- UI o A :o ^ ^ Z.sO </><!> . UI 0Z OvO O0X < < o 000 hr> O V3 A^-O h z (OV> 0fo oo J zoo < UI O A 4r- O ^ A o zs- I-- 300 B-29 DUP040009780 TABLE 8= 31 HARTFORD, CONN. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME* URBAN STATUS AND AGE OF HOUSINO, 19Bt eosp*^* o .-J < p6 O . p-v-otn TOSCO *"*eo O o p trt.COO* F *. F-F--.V n so P o o o 00.0 o to boo o os o o OS * pwo o Os >0 o^rm b Os csimcvi o b IT -O' , .c IT O' sbsOfs* fOMCV oo * UJ < G. -J 009 0.00 oo < r^pso *rt H O TO r-- 9-- 0-.0* OOSO os o b r-r^ih * o.fo.ev veo o op ** Of^fO inso oo CYVO p b 0 * booooo CStS-Jt riflf!* 0 0 0 Orts ON 00 ifVOvifJ . b o P '*"* O0O. o sCOvifv o > i***'. o N*- b OVF--01 r-To ir. o OOO .PovOa-O. *!- RT oo rt Nm o ooo o flO Os 0.00 oo ** " 1 o f- Os OOO Ooi-Ooo r o0 U` ooo ooo SO r-.irt r-O ** b o CM .Os so ooo ooo oo Os tf\*rtSO 4T N t O Os oo oooo ON.CM ..csim 0 0 O >o ooo .00.0 *- ifSO t-inw 8 `* oo co r* o 0.00 o in ooo o O sosof^ Os 8 n<M os i UJ ec o> OOO OOO SONN r*V o o o N ** 0 0.0 ooo .CM CO Os JTSO O O Or"s N > > UJ * Os OS \w .092 3 OsO OOsX < OO f-O o o srts. o <x < P" o * H* -- X *0<J H- V> 0 >X oo X.-l u eoo < -- o UJ o ft .OX O iA 0< X X-SO.^ .ON o </></> ut -J Os OS ovx.< OsO -J OS < W 0 ft *- X a-ee 0 u ftt-O o \0O> </> o .X 0.0 . 9.00 wo H- o ftin O X so X 3400> UJ Os OS OsO 'mi O.OsX < O -* . < ocr.tf o (A ft*0 X SOO> fn Vi O O0 w 90.0 < 6 -o ft V-- o ftin o Xvo>" >- Z3V>i/> 8-32 DUP040009781 TABLE B - 30 GREENVILLE-SPARTANBURG, S .C . flO P-SO>- 0 *-N>? ,* o WfOer> p* p<*vvAp oo CSi>lSO* o :X w S3 eoro&i T- 0 x< a rtp? o ww.n O 6 (MN \j IS* <y*o p < m < >*-- .<CisC - sp>0 ^SOSV.Jr . * >?*. sOCcOutfS o pso o O<o<Pio .6 9 |0OTHi *- os o esiircg p 1 PVpCVJ fg jra* o fo ps * Al.QAt O w cc CL < >0 ooo - o .OKift *- cgoj fo- OOoeg'o.P**--soo .o00 ..fOj*ym.O0*0-O:OfCNOVJ o p- CsO < .>UJ o CXO wSO <cc < w cc .3 uo a . o to CO , o T~ 1 P-l W .*- cc o o -O o in cc Xw0 AT * Ui CM OOO o o o " eg . o o eg OOO . ooo mp-m pp- ooo o.. JT O a- W OOO ooo Os*?* ro . o o m a *?" oo ooo CM *-0J tf\in tfS eg tg ooo Ooo .US ST V-US m p- ... ooo trs o N o o ooo OOP ...Win **rt O o to p- . *N.Ui w* . DO H-O <x . > Z.-J -cocx< ou. > p < cc hX UJ X -- u CC O' ox .'V a-cc *- sc</> #> i o oo COO .wo* irs z-- </}<S> -j < p.o V *- u UJ 1 C .< cc O X -4 .< z aoc p UJ *- o t- o <S0OV1> jz OO OOO uc P- o m o z DVXft UJ cc o -1 ox < O'* >!-- OJC o CO X SO-</-> >- </> 1 oo oo < WO A o m o >- acxo B-31 DUP040009782 TABLE B- 33 HUNTSVILLE, A U oO0k 'i M^ *-. 90 x --Win 2 9 M M.jfBM OOw 4TIA O O op-m warw Min 9 . O 9 .M l p * I-- O * U JtfOi 8 w 7 0 " s * fid in O 1U < 0 .. H* >*4 ow WP 0 O 9 tfVOk^O Mlft WCUkA 9 0 9 0.09 900 mm O O O M 0 00 9 90 ^OV w.wm O Os P OVOm . 3 - M VO 9. d .POO . * h-Ovftl NO 9 d 0 A1 mmo* O0.4 X.X K:M O 0 - * in is* p-Min 0 .00A 09 0 OWB wmw .9 d 0 boo 090 MM MAOOO 00<0 m prti * so^w >- in m . d 49F* 0.00.00 srcvips Ml OS M r" 9 O in SO W O 9 00 *A 0<0 OOO 0 b O f-- win.m W .* 01 090 900 8 ^ ^t WZ b w r** 0 0.0 009 Fr*OOs win 9 O -.O' Os O _ t+ XO LJ - xA 0,-J O 09:0 e 009 bob 9 1 0 0 000VO 2x cK *- 900 Ov"" M t-Ntf M 9 900 NINft N.W Os m woo warn- O O jf h- c 0O in flfi w 00 0 0001 a d ml X O. wM oob MM O 9 0 009 900 tfYM f>- *- 9 m boo uvoo O O * en lil I > W > hi o 01*- osce O hi -J . a W s 'S.W 90 -J < V .j OsO -J ) O O.OX < X 9 ox < 0sX < 9.0 h C .-J <x < O* O.^fiC rO O c w * M I 9 >- X _O0 0 0x-i Ui fiSOO < WO * ax *m cc< SB X>OM O wj </>*> >" O A H X OffK O W0 0**v0-0 *- 00V> 1 x -- eao Ui * 1 0- *m 0 arvo*- Z 3V> O h- < O0X O 03 4^0 Z vo</>. 01 00Jn v> _2 SCO 0 .0< wo h- pin zsd*> M = </></> B-34 . ('* DUP040009783 TABLE B - 32 HONOLULU, HAMAI OCD p st&'Q . O lA(A PN0tft &> *N-vmOirA* o p COosro- : may : 32 2Id Oif p : CQ PiCm . cbf-.x* lA.VDf* O * cocvo o . o i P 93 o --6 >p P' ico o < v> 0 5 SoO3s ftzid ociOdsr \po p 1 P.(A pip . OnA oo .* ' O *-miA !OF o i-cniA f-- Id op O . cssrst CMCMiA oo <2T CM evf ifiA 3-cym .o T-fOiA p 5 > . CO CmVOpJ.mnOmV lA <y f9-- 0ro0Ovo mc--rvCoM .pOomSt p0o>C0oCoMU.o0prPo SoT APO .0025 < Id > 0 0.0 O OOO OOO o o 0.00 OO o o r-.ir CO AO NO CM f*m o *- A* v~Sf fv *-COiA lA CM id .X oc Oq z .ftm u s -J P *-- NO .X P p l* u. 9 IA P OO OOO 4? 47 CM : O m OOO 090 lAP esiPCM -- O cv CM CM OOO OOP pro .*>-- -- CM O o CM lA m 02 X d < t3IZodD O if? ZP '* oo OO r* CM ft-- -- -- CM O (A OOoOo O O CM CO CM CM *M .X OOOOOO mp CooM f5 P x Id QX -J u. > Id y id UI O ft- POC -I Pfl2 pee >sUJ umt PO ..J < PO J PO H*. Z WI P PC < 9 * d X PC < ft- * ft- OPX o* , KU -J ostcc o X o.trx O -.< ostcc ; -<x < >-- o ft-- Id o CQ d- P ft-:-- X \o</> >- v> O No'> 0 z NOV> <0 0 1 o V) 3D CO > .z oo :Z_I NC id O zUiooo* ' r_ - OO coo (do oo J .sso < idO ^ zUJ o SA'S *tfN X < Z ZvO -- u. <ov> >-- O (A o ZVO:^ X </></> :h- Q *(A o ZNO^* ft- 3W0 B-33 \ DUP040009784 T^ q M[ q ~ 35 ^ --K s o n v 8 MM[ , ` M ^ .J r0too--\ 035A .O93 -JKOHm<i * '* O * w**z OO x.a.wa f*a Wu ih68-^ 0*00.* Na .* o 0:# ,0i^ 20 .X u0. UQI < Xb O<0 1 NO*.*^*N*.6*C .l O4 OOr- t*fU 0 00*- hO 0 fi*omw*st 20*! < 0 ..f.0*' iS0wc ZC5D 0X HUX0XUX*II >90tC- IT S*OW N' O lAlA .OO >Oa0Oma.s0Oo.a 0w5'a iIaS&a j*a .afsra1!* OOOa . *> Ui -x 0 -X OMtf O i0n w O O OUMO 0 .4r*- b *-.*>* 0 bt*fYa *-a SMOiSntW01 O O O(P 1 UI > -XX 1x > so -J .< poo .0:00 s*r.0*i.sr Ofm 0 r- f- W its boo OOO W'OO b 0CVJ f|Tu" o v0O0Ob >:w 20 Os e p* 0 X < UI > in 0 H* OOO b oo OO nw m 0n .Ofs OOOOOO ZC4- O iOn -.*> JT 0 boo 0"0lAW0 mob b 040 4<V0 (O Of- X*' yz r* . rtX 1 .0 X Q -J * <0 X 0 *1- OOO OOOOOO ZbN O Ovfi lA W OOO 0 IOAONO 0tn >*rt tft 000 m00ru0 b,a"m 20 UI O < *s x X - UI < u. XS ac 0 .if 0 OOO OOO 0 .^SWOlNfS 4400 OOO 0 O*jOcsiO.ru 0N CSI obo 000 OtfnMmftl O b 0 O 1 u z u XX X a mJ > Z C O u. > UI 0 UI UI 0 >z X 0u w 13 0 z UI 0 j" ^u 0a0o -J M30X H<-5C 0 0 -j < Xh- ox 0OZ9-X \C </M>-0 V> 1 0 H< OH z-> <- XUI 0 OO xUI oOo CBS O m xx-u3 z 3KI -J ox *X<- 00 ox .0 * -J <fcu -UxI ozx *o *O 0 ><i . </ o X 06 X 0.0 wo O 0Xv*m*- z 9VX/> ox <0 OtO oox 0OZ*K *-0 <-J W OH 0X MIC -J < x^ui2oo2-* U- 0 **n O 900 B-36 DUP040009785 TABLE B - 34 JACKSON. HISS. 0 o ,z z(5 U. t<a <z, 'V) H<-' w c<a CC UJ "X o X > .J X .< U. >* CO p .X < .Ui > m o OT-s H X x :V0 0} UJ o < J .< . u. o z UI ec -j -- X Q u. O HZ o p U5 .3 <0 z Ui P h.O i<-6 rCMof^jOh P g eO CViA Op\ ** .*ft O .' o ***>.ln p o OS n- > X VO ui euci *i- O- 4T o m i Ui -X a. mi < iO 1-- pm p cgvp o r-*n ^40*- *-mm , .com Wf*. >-jSr o o o r .OOP 0.00 PlNi" cy\oo\ O o rr CO IT- cox lOClsMifpt 6 P p,a"cy o ,.iCM ' fMp , .pVpi:N) P C<MMC.CVMt.iXA o . m*ncy O .4""WNifi : p-p-X OlAJ o o ooo JCOO '- STer o p ooo .00,0 fn corn i-h* o o o CM ooo 0.0 0 votnp m.Oyj .o o n* o eo .a f o hZ O' Ui fX mi OS *0 X Oh o *1 u. O ml X * Ui '1 5m Z Ui sc ft. ooo OOP mmvo f.CVI o o VO JT oPo ooo cy m o . f* OOO OOO NOJTW f" * o cv w OPO ooo rnoco Cvi o o o n h- boo ooo oeoo O o ift *** ooo oo 0 60 o o co " OOP OOO O lAj m(s o o p " .OOP ooo %o est CVpSr^r o o 60 <*> Poo ooo VO O CM CU p o o Jft > UJ H OS NfcUJ -- 0\ -J x o X < OO o .* H H-O J o^rcc o <Z U "* .e<c *-0 \o</> J- vi > Z_il H- Z UJ p V>lO oo ZkJOoO. - X Z< z o -m Z%0^ 3W -- </></> > s UJ -J PS oo -J X ,ox < *z- *. o jrs h~ o w o I" p HO</> 0O .Xmi oo soo UJ O - a -m O Zvo*- Z 900 UJ -PS OvO J OOn X < o- f- < 0.2TS o CO *f~0 1- X 00 CO 0 1 O .09 J soo < Ui o . *- o -m o ZO^ B-35 a/* DUP040009786 TABLE B - 37 KALAMAZOO-PORTAGE, MICH. CO Q> *"tfSsyX AO O OVOijN p 55 *-CM 0O cv .00 O*~.tfmY 0. Q X tel 000 O .jf < o co lAOlA * CO O s- o 1ft o CM p* p STNI^ , 0 Czl < ma .0 QVMA ZH* OCMf*-p <m a: .0tel Xt tel O o. 8 -- cytfi 0O SI' my .o.ift cva-*n . p <0.0 0 0 CO4fftMnsr *<*>M\ O MA <ojro p x 0 IT8 CM*?; O VAcfvOr.Or*- PCp-M^0 o0 uI X u. OOP o 0.0.0 o 0 0.0 o 0.0 0 o .00.0 o 0.0 0 o aa> :*A0CO <0 *- CMMA .0 CM7.C9 X *- tf\ jy f!<Mlft jy p* CM aw: U<i > US # o ooo o . 0 Y OfO 0hp-- o CM ooo 0--.lA0C0B .. ".ar OOO O ioa'tofMoA o sf *" ..to o CO X .Hs* p Xtel *0x C5 o X , ---J X * oo o OCOO.O*** Oil o Xo ooo .0.00 r". o e ooo o o^CoM><on o n CUOJ I O IT ON Xtel r" J c CQ aXX O8o' 0o.o0 o0 jr*** .** * oPoO *9 Om0C.fO0-MBP0l o * MS 00.0 o ooo o f*C*nMjlrA x tXel tel X&. Xo > > UJ 0 tel U >stel H* mm X O -J mi < X 0VO X o -j a tep aCO teCxO tel' axo *<-.xu > ZJ .< -- oXx< . Oh. -1 < Xte> :tXel 0 oo.o% x ox! xO v> 0o xUJoo0oo* o -in x3.\0o 0-- <h* O X . X < 'te* . * 1~ X tel 05te-EO o 0 0</> o X oo .B txeloo a mirs O XrX 300 OOvX O P. . -H<- W< oa,x *.*- 1o- .X 00 0O -J >-< kxJoOQoO O MTN o x^- te* 300 B-38 D U P040009787 CENSUS COUNT OF CHILDREN OF ALL RAGES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1| to Ov CN IQ*cO o < roH* CJCV4 0 O 'r* *rf*os 0f*CSJ o. P -r- -f f*.60 (SUM <7 P oO -r* .o -CO o r> 0 fr .0 X * up O X1 ui jft. 0 vi . ON o IA 0T w Z .a. .pp-0 inf* so ir N 0 O O *" fO N Twm** o 6 .o *--1*)>0 00.9 <y cyj . o ooo 09 0 co<*w POO o -- ca CM rtiAf?* car*' o p o* ino.in r*ir\r* nicgp o O' o 9 0 600 P cycum. 0 . * .0.0 0 .0 0.0 %s0*0 a-soca ** o BO CM CO 9.1* so o ca Wl* . o spApca . . O 060 in.*6 9 .6 o ** pmr* o o ** OOO OOO 90CO r* r- CV O o r* 'st oCO O**s? o r* z o> Mi Z-aj 9 X 90! Q u. t -. 9 IP 9Xu 9 Xo .0 z .I9P w.1 Xa. oocaoo-- poo o 0*> oooooo o o f**t-\*s-oa m a ooo ooo *~vo inar r* p fitn*-- oooooo OO COCCVMt tn oooooo O *"0.9 4T ooo ooo arcom O of* nc no 0.00 o 00.0 o tnOkQ60i 9 OoOoOo o o ScOacNaO*rro> ICTOS OOOOOP i0fs0iT*t0n . o CM a > Mil H oc *n W MX 5 oo 0X -6 -< 90 o h- t- O occ O <z -< .o w -- :Z tO0 M W </> o 'Z oo ZJ w zoo 0<3X3 o Wo % O in C < z xa** awi a tot > f- .Ui -i 0Z < 2 90 OAX 6 < C* f- Z zz o Ui ***,o U vO< t o z 0.0 Z.O.O WO * w o ZaT*9> z a tot ui 0Z AO ,-j OAS < o% i- .< arz o to X \0V> (0 to :l o 0.0 J zoo < wo .* w o Ain o z*o* w pt< B-37 r DUP040009788 TABLE B- 39 LANSING-EAST LANSING, MlCM. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 mwN o i- l ift o tft-.*J CM ft* oo 0 f* W* O <M0COfP.CQ 0o CoO i*" Ot 0 zp wp o zt wo .a. if Ioft PCMPCvPUT oP ptftp ft a nr\tft o .ip p Ov.PCM o 0WO . ft* p 3*lftO ift* O or- nftC-oMop Oo CViftCM .* ft* O lift*? 0f*-rt CMP O O o sAiflN 0 CMP O 1 4 OOO o 0 0-0 o <r r*0ift ft- H O |rt jr * OOO OOP o p CM 0.0 0 OOO p 9A *\p * " CM o O CO 0 CM OOO 0 0-0 .-M3N r-*-0 O o CM 0.0,0 OOO pn, oo * * fO o o m z ,z OOO OOO <0*30 wo o o o Ift 00.0 o OO-OPfP*- o f'"N Ift 0.00 OOO " ON ON o o 0 p 0.0 0 OOO ^>o eify ,o o . CM OOP OOO PO*" PP o o ft* OOO OOO jfPW Ift* o 0 Ift o 0 0.0 OOO Oft* O o 1ft ft> > UJ 80 ~ OH-O_ f<<t0*X --a <eJc ft- oO0%l*O f<tJ* p0m%-9>*-0o0 >O- lO X oo W .00 oo U WQ p*lf..t. !i Z Z P ** 0W ov>v > ft- U! w< p0.z -J Z 0X < fzt* ez%z Ho* w .**- ft- O z <PZ0VOoI>Ooo wo m- o *m O ZP *- Z w ON -4 0X O* .< O WX pv> *- (A <A I O W< zwoOooO* ft- O *tfN Oh ZoyP>*<*/>* B-40 DUP040009789 TA B LE D - 38 KNOXVILLE, TERN, CENSUS COUNT OF CHILDREN O f ALL RACES 6 MONTHS TO 5 VEARS BY FAMILY INCOME, URBAN STATUS AND ACE OF HOUSING, 1980 *-9lA < mvO . O o H ocaoi 0<0r !** W.JS o o 9.0 p*^rpY-CMIA o' o o O CO Os o p** Os t- o Z' UJ no Os 0 .* cc i UJ o Cl . Vf\ o 0 .if :os rW -O A> J < o 1-* OsOsfO *9o---.** , o . CMtfYto \cOv-bo-mfo o o o lACsi 80 -- 9 -- o o ooo O0s.fO0S0O m.jff-fo o o r* Ort'h j&tCM.P o o .o osmco so.9ea yp o o o OUPSP009 CM o o. *o" lfthift- CM i- rt .lA P o vp 9 src\im ^-- o o o - T" 9ps:h CMCM9 CSirojr d o ooo ooo mcy\o INflSO p o N OOP 0.00 CM (A CM M3 40 O CM o o 9s 9 b 0 .CO Os ** .1 o 'Z O UJ r- :o a -j O .* x VO OS p * " u. 01 o ITS Os o r ui m X o Oifs n: Os 7 UJ cc a. 0,0 ooo f- o . CM m 0o.o0o0 f-- f!*.9 .** ** o o CM 9 ooo ooo mOvCU oO 9 .9 'VUI ox oo *- o <z ' H-- . >6 OX ec< 3,W > H- o -J < K H Z UJ P z UJ Os OS 9s O OONX OA .090 **-o sp</> </> l . ,oo X oo UJ * o *sn ZvOr 3W J < U* O H* OOO ooo *~.iA\o *- Os b CM CM ooo 0.0 0 N0S09 r-9 o o CO NO ooo ooo so OS NO CM 0o 9 >I- u -J OsP < Os fi OONX < H* 0 % H ,3E UJ 0.9 0 Q o H O sO</> 9> O z oo -- POO UJ O ^ fr-- a *8 ^ o ZNO*- z ov>v> OOP ooo VO CM VO CM CM o o 9 in ooo OOP rr--uiYroe.tfos o o " * ooo OOO bob t -.CM o . 03 .UJ OsP OO -J OOvX < O ` fr .< (ft 09P O i-O ,K X sO</> tA 0lO -1 oo 0.0 0 < LdC - *- o o Z.NO^ J^- 8-39 DUP040009790 those for 1980, 1981, and 1982, employing the 1983 rates for 1984 seemed conservative. COC data concerning legal abortions provides ratios of abortions to live births (per 1,000 live births) and a rate of abortions (per 1,000 women aged 15 to 44) for each of the states and the District of Columbia, A national ratio and rate are also presented. Information on the distribution of abortions by age and race are also provided, but these data are not available on a state^ basis. We used two methods of estimating 19$4 abortions for the SMSAs and used the result that provided the smaller numbers. The discarded method consisted of applying the ratio for each state to the number of live births that had occurred in SMSAs id that state in 1984, The sum of these calculations was then proportioned into race and age categories according to data available for 1983. The alternate method consisted of applying the rate (per 1,000 women 15 to 44) to the ld84 population estimates obtained from the Census Bureau projections for 1984. The resulting total was allocated to the race/age categories according to 1983 abortion data. A difference of about 3% was observed between the two methods! end the smaller total was selected for inclusion. The NHANES IT prevalence data base, 1976-1980, for distributions of Pb-B levels in the population, was. used to estimate prevalences for Pb-B criterion values for 1984, using logistic regression techniques to adjust the original Pb-B prevalences tp 1984, Adjustment was necessary for the reasons discussed in Chapter V and Appendix 0, The estimated prevalences were calculated only for women of childbearing age residing in SMSAs. The prevalence rates shown in Table VII-1 should be considered while bearing in mind that the criterion value of ID pg/dl lies ih a very narrow portion of the Pb-B range. Certain preva il ence values in the table, particularly that for the older group of black women, appear to be unusually high when compared to the other prevalences. However* because of the narrowness of the Pb-B range at 10 pg/dl, rather small changes in the meajn Pb-B values will account for rather large differences in prevalences. The geometric mean shown for older black women is 7.3 pg/dl, compared to geometric means of 3.4, 5.2, and 5.1 pg/dl for the other three groups. The pattern of increasing group values with increasing age, discussed in Chapter 10 of the EPA lead criteria document (1986a), can be seen in the means for each of the two racial groups. U.S. EPA (1986a) reports an increase of VI.I-4 DUP040009791 The attempt to estimate all pregnancies regardless of outcome Is based on the recognition that the various outcomes are not Intrinsically relevant to the risk of fetal exposure to maternal blood lead levels. Legal abortions were Included since data are available for the extent of this outcome; fetal wastage, that is, spontaneous abortions before 20 weeks of gestation, were not considered since no data exist. , The estimate of women of childbearing age includes some proportion of women who will never experience pregnancy. We know of no method to estimate this proportion. However, we believe that consideration of the number of pregnancies in a given year provides some measure of assessing the size of the^ surrogate population at risk. The Census Bureau pro|ects future population utilizing three methods of calculation. The sorcalled middle series projections for 1984 were used (Table 5, U.S. Bureau of the Census, 1984), which provide estimates by age, sex, and race, and have a 12% error for the 1984 projections (Table N, U.S. Bureau of the Census, 1984). These are projections for the entire country, and to establish the proportion of women living in SMSAs, the 1980 residential distribution was applied to the projected 1984 figures for the four categories of women (U.S. Bureau of the Census, 1983). The data available for 19841 live births consisted of computer output (Division of Vital Statistics, Rational Center for Health Statistics) from which we had established the number of live births for each SMSA as defined in 1980. The births were identified by race, but not by age of the mother. We used the latest available data, 1981, for distribution of live births for each race by the mother's age (USDHHSji, 1985a) to allocate the 1984 live births for all SMSAs. The fetal deaths for 1984 were provided by the Division of Vital Statistics and were allocated to ithe maternal age categories within race groups by applying published information for 1981 (USDHHS, 1986). Information for 1984 legal abortions is not yet available, and we utilized 1983 data. Examining the data available for the years 1971 through 1983, a peak in rates appears in 1980 and since then rates have declined very gradually. Since the number of women of childbearing age has increased steadily, the actual number of legal abortions continued to increase through 1982. In 1983, not only the rates but the actual number of abortions showed a decrease. Since the decrease of the rates is quite gradual and the actual number for 1983 below VII-3 DUP040009792 Ziegler,, E. E.; Edwards, B. B.; Jensen, R. L.; Mahaffey, K. R.; Fomon, 5. J. (1978) Absorption and retention of lead by infants. Pediatr. Res. 12: 29-34. R-21 DUP040009793 TABLE A - 1 ANAHEIH-SANTA ANA-GARDEN GROVE, N*"i^ -J < * oH OWN o * > 01 (A CM 0 ttf- O ONS O *or*M"} po OOP 0 w*r o o (OW. f*' o. 00w*W po iAW P Q J!" (T ' I U0l I * WlA 0 OOO \o o tftAQI . I w o -*. * * ` o N.f* 0 oynn o 0wNo O 0 W0 ,o JTlA*- O*-.rW*.0. o oPOoOo o0 .x.ffar * *-.r > POO ooo ^WW 0O>- r- 00 o o flO tA o ooo o<0 oCOoO O.CVIS0 s* m T" 0 o NO On *A oo poo p 0.0 o r* 1 rtovw n WO *fpp ooo pop ooo W.tfVO a* o Ao* 0 * ooo o oCm4o0t*>:o0m o M o NO XO UXi *- o .NooO 1 ooo o6oro OON o jof ,4T 0 ooo oOfolONo- OrMh o o (* A iA ooo OOO W W*A NOCp-ylOtf\ o o .0 IA to IT XO Ui 0 .X iT wo O' UI ooo 0.00 o m8 ^ 8 ^ >o ooo o ooo trfMOCOSvl InA Xu fc o 21 *g -I OS 9) X*Hs.UJ 1 g* <0 > 5 g 2 &*-u gSx S?r ac*o2 < g o UOi-Q * t2- o2 J g UoJ OJT 5 o H 0 o O6.o8%S<A% ONO .u OOvX OA g < es*raQs o !* s pv> 0 o1 oO -<J 0W0O.0A H> a IA s ito 2 xayMj*- Oh X9VO>r0- A-2 1 ] i1 i f DUP040009794 APPENDIX A TABLES OF INDIVIDUAL SMSAs WITH A POPULATION OF OVER ONE MILLION SHOWING NUMBERS OF YOUNG CHILDREN BY THE AGE OF THEIR HOUSING AND FAMILY INCOME This Appendix contains 38 tables for the SMSAs with populations of 1,000,000 or more. They appear in alphabetical order by the city that gives its name to the SMSA. One exception is Table A-81, for Nassau-Suffolk, NY showing only data for the total population in this SMSA, which had no city large enough to be defined as a Central city. The data come from tapes of 1980 U.S, Census enumerations, and cover chi!" dren aged 6 months to 5 years of all races. Their distribution by residential status: "In Central City", "Not In Central City", and family income by age of residential unit is shown. A-l DUP040009795 TABLE A - 3 BALTI WORE, MD. CENSUS COUNT OF CHILDREN OF ALL RAGES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 <Vff K<n 0 S-pK? o -- *8 ^ o ^-WVO O OOft ' .K; JT 9 40 t*o-rf** oo K SB VO g2 UJ o .0- IT -a .tr .U0J -j v<~ >o OSJf , sQr o S3 *-iA<n MmT oooo **3\O--sswO VO >0. r* . ND0 NT K '-- *P auryjy rue\ ooK 8 ^ K r-<n.*T 0.0.0 0.00 A<"90 KNvPa* soo. jr 0O.0Oo Or~v.Ws*Ot W.,3* 'r* KiA V* O o - 1 0 p- X LiJ rr OS a -j SO .X p 1 w o IT CC UJ CO X O IT X UJ aX,I O oo o SO in 0.00 00.0 o 8 ^s t o w OO oo o W.rt h>mv} -.KK o o ip pM ooo oo N.PlO\ ntA in o 5T rs 0.00 ooo fOr-sO xr -fO o o T-- IA 0.0 OOO .*- WOP- CM o Os p> n ooo ooo flipr hnrs* r* in o o flO Its oo 0.0 0 0*O n*soro* 9 n ..o ooo PS** oso AIM o Pm. SO IA > UJ K N*UI -- as O -J (OZ 30 o oX O' % K< KO .-1 xas O <X < i.-0 K K -- SO0 (A K .0 . X OO x.-jl w KOO <K p UJO % OX O Min OS < .X ZvOf- Ob. 300 P UJ -1 as < o -J a; ox < K o K z OT O UJ .* K u 00 0.1 O z J- 0-0 ccoo wo K a ^ o Z9K z 300 UJ AC .: -J o < * K < OT.tt O to .*** K X 00 w 01o OO -J 0O < W- K O m.8A o X9K K 300 A-4 DUP040009796 TABLE A - 2 ATLANTA, GA, CENSUS COUNT OF CHILDREN OF ALL RAGES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS ANO ABE OF BuUSiNO, i9 6 0 b.M Pf-P foca*** -0 P O -*Y* .o 0CO *I o f.> 0 0 < Ul . tfv 0 o 0IPI:, mou\ P . evi.cvi .0 SfYin .p ?d*> dM O wtfvcv o to tf>vb P CVJ Ca.iT P btO** ib.i"C4 -9 .T* -r-h- 0 O c 'T" t --8 6 * 0WO3<V so 9 O 0 0*-0 tf%04T r- CO iA 0 P PiTvO eocy^a* .y- CM O 0 O fOPCU f-dd y- r-- o d p 0 p-r^aS M o y- CJ o .tfVOM** Y-P-O WCSHTk Q O <1-- O 99 0000 .nfC"\Olif"a*r-T O 9r to P- 9 00 N0 M0 9S 0.C0M*P* OS 090 POMOAO.O oWa f0*>Jr-- O0 0PPr*- O CO c* 1 0 Z O' Ui Y* p -J o SO Xa o u. o o if OS p Y" u 0 o O JE moi .1 UJ ;oc 0. ooo OOP Os&'tO Cvir-r- oo Y" OOO POP CO*- f** o o a o fa 0OO OOP O N 9^ to ea .oo 0 O * OOOOPP rM <M Y- *- OO tf> P h- 9 00 009P00 Y- P P 0 ITV 0 90 909 fyU* JmT tpa O PO * * OOO p0O.,fPa0.-c.0a *-.P Oo p N CO OOO 900 Wh*0 ca-ovo *" -* JT o 0 !> 900 OOO fjMy p y- o 0 M > Ul 0P >sUJ mmm OvO -J :S ;9<K 0z H* " 0 -i < P OQ\X OO0*P *- o p</> H<* O 1- tfi J- </> * o Z. ->J ZUl oo POO < -- fil 9p.W< O z * Ul w O MTV Zp*S0<9 > K 0 Ui .w < pp 0.0 -J p r OOvZ o* V<- Z Ui OZP O o p pi/> 4J> o z oo PUJ OOOA H- o .m zo ZPY3<A0 Ui 0P 0.0 -J <w w OO0 oarp p<"`^/>-O </> o K< O H* -3 <h- oo Pw.oOO a .u n O h- Z9P</>^</-> A-3 / DUP040009797 TABLE A - 5 BUFFALO, N .Y . CENSUS COUNT OF CHILOREN OF A LL RACES 6 NORTHS TO 5 YEARS SY FAMILY INCOME, URBAN STATUS AND ABE OF HOUSING, 1980 ON P NOO*> NIOA o o NNh> IS p o9" msoo r-Wsp p o ** ac HO X SO Ul o u r* X Ul A. O ,IA O IT O' u oco o ooo 1 .*>*. Vo*. OON * . *-%0N o o o co--tivso- o OooOoP O o vhD*.fSro* 0 CM 1 0 1 o Uo<ec4l O -- SO X0 YO- O 0OO 1X4 *- m X aX oo8 * 1 LU AC O' O onP Ooto oionoonoo CM 0 O 0P ooo oCMoiACoU wno o Oos N OOP o inoif?.. O r- Opto ATOtf\ P o 9" lf\ lAP p P 0 SON ** Nh* O 0r* *O NO.to P mp O p OOO OOO t1ff*.0e0o o ITS 1A P OOO OOO a*f***N *-OsO -**AO Oo O oOsctP-5SWM0o*3 oor ooV:ooOOoo0S t** O p* * -OotoOooOoto riro.*s * oopJCTM . .OooO*1oP*- *-PO CM ooCM 0 N ooo OOO oNSnOoP o o SOst CM OOO oopooCM *-0 ~CM oo o SJTO *S.U <| OOoOssoXX <-J O0*4*-AK ^O* IfJ<0- * xtou 09O OO XO UiO <* O -lA s.i4 S00 h<XJ oO ooOsOxxUl .<h4 X OAK O 0Ul sOAV*>*, >* X 0x1oOOoO H O AUJO > ^8 O Z'Or X S00 A-6 DUP040009798 TABLE A* 4 BOSTON, MASS. CENSUS COUNT O f CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE Or HOmSING, 1980 VO i**^* o <o fOfOfO o o ** j- o CO .O' o *o h* P X \c wa o X1 ,U1 o X it] O' * a IT of* ui CO CM .4 < frO 'OfOS- n h-O -n o o o .* floaom O VO so *MrM o o >oN MM** oo o o * :ODO 0.0.0 *-mn o co o CO O * l apj X oi 14 :Q UJ >o6 Xo o 1- u. .O o in o Q V" 14 ffi XO 5 in Xo 1 w tc a. ooo oo:o *#>! o o 04 M OOO 0 0.0 tfYtfYCO Ctiftr* o o CO VO ooo OOO oo coo * .co vO ca vo.mov V0OV*> r~r> O o * 0S.<r-*r sr^sr * o o o * * 040 OV votno '. 6 o .* * pmov P o OOP 0.00 fOrt K Cvr-m MO o n o jr ar" OOP ooo trv.o r-WOv r* a o v> M M OOO ooo 1-f.Cv MifsvO w O o rt OOP ooo r- p40 voiovn O so 40 n*fveo r- cum *~MvO o o o TT yjesz flYtOJ* T" P* P . o o W>ON * . **40 o o o CUM.*AO> 8Ap *nM>0 p o o V-- o,bo 0 0.0 VO VO Os oWofOuYnT o o VO nr- OOO 0.00 -T CM M `!T* O o o .4r OJ ooo 0.0 0 so von zrn CM O O OS p X ooo ooo XOflO.O CfN:as r-CMAfi o o o fir \w wx so 1<-20 h CO .> <-- OX ce< X lu- > 14 H CKO OvO -J o OvX < _1 o O^rctf o < --O >- cc H V> 1 o X oo Ui ooo u UiO - O >tf\ X ZVO.S- -- </></> ti ;W 4 < ova: 0x0 -1 OC OvX < >-- O X OZK o 44 -Q H* O vo<l> MIO X -OO A- KOO UiO *> - o -in o ac*o^ X 14 vOS OS.O J OOSX < OV n < OX.tt o CO %r-0 H* X voo> </) <0 1 o oo ^ ooo < UQ -- ..C O .XvM n 900 A-5 DUP0400G9799 TABLE A - 1 CSSCiSSiATU 0K5-K`tV - S ' B I Me e Hi i .oj6 M .* o * * J .*> g i *- *i* *.* e- JTN- Q O >m<* e ^. "'*S g s* . **jr M <y* o mf*MI t # ei n p *4T O A IN#1IS9 p f-oirt o . e*M o po n o .* . g<V<K AKlb o * i . sss g JTOif. O g ooo -Nlfk I SgSJ 8g< bgmbjgfviigoD :gb fbK3 > * Ok igg 900: CM 8 i ill 1 fillW fii* n ** || g f*vOO n KN HI * !i in i burnt m fit gg| MAb hOOi CVl f 111 1 #< Ok til MM A CM ggg g o*rcov*n 6 r-W # Z Ife > _*j 5w lil O I5 IfP*si t Ji * 5.2g o III P JO *> S fi_ b. fi s ISS "* So * I- .fl *IA S S5 it. s g* o A-8 DUP040009800 TABLE A - 6 CHICAGO, IL L . CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND ACE OF HOUSING, 19*0 *-*- 2 **OOv o CM ft:* p 0*s0s!* g iftom * *C M 0>*.C4O0* O. COi 1 fe O' .SWB SC .UCLi |T{ * IT o . * *>rriSP O f-.*L c*cy 6 CM CM* . ft* ^r-Nr CM CM U*) W* lflM.* g.-CO prtN If? ,NOH *-> o HlAiB v* *WS g <NN (C UY- VMi-i-fN* * w f**to, n .*.* <o . opo -- 8 8'C *CMCO AOf* o en f- CM OO POO OlA** * CM *0 o 40 CM ft- OOP oo f-OO* **t*tcs O Z t- 00 QOO tAOMJ ft- i*VV0 5 9" 9" Ot O o o tf\VO* H*OCM ?"9& CM O (A 0.00 o tftOO CM *0 CM poo oo ftftlft NO **CM * o 0% w * ooo oo r**fiAW*^ f.*0 * 0 o H>i*0 .* .'* fii-M *"* O CM MO .o0o0.0 oo *>wn e Xbrnso m conM) _ -- 8^ *~ *- CM Sgg **0**o0in0 m*h-- CM W vw 35 H2O*1 t/i z-j <-- gf w ovo: OO*i.3 ft. *;Z <*OWOz00*A.*OOoO1l0A-f.PO(tA*ft i. p aHP u z H- KwQoftOotf%\ S i 1 iS *o- 2g I9zwOO%ooo>oiTVft A-7 DUP040009801 TABLE A - 9 COLUMBUS, OHIO CENSUS COUNT O f CHILDREN OF A LL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND ACE OF HOUSING* 1i 0O9k moo o * ' * .* '* < KrrPttNfi , e **09.01 0 -fl'wKIWr* 0 poo p p 090( W.Otf%* ..* w-trp<>n* o .*-** <D *0*0.1* -OP .9 uooe ftAftlA P o ff--sWo*m 0O fK.owr wow oo wAo*-oK** o ,o K***no.*iao' F-WO p p p-pCM fiOOvW O NW O ONr *- W lft P OOP aP*OK.O -<vi p oos*r in xUi :9 --J M3 52 O IT K w i OKPOPOOOP ..ohIoA* 0Ofift9Oh-0P fOlfVW ooo OOP _ 0\9OK* W OOO OOP Oh-in * O o 004k St o4O'To4OIAfo PcPf-n* lOrA* POOOOP 0 -TOWP P tOOt.NOOOPPt *-sr, OOO >os-t4oO*uoN* ^ M o HnO O OOOOOP Nfttevti Joowrrt OOO OOO Wh-O x p.Wm O O Ok nCO* OOP o O`m.OnoOno t0n >*UI ss *-o 0 33 UI 5 t- gXU_i O0PkS pOiSf-tec. >*0 2 >r o x OP ~ cuiooo K %iA X 900 0O0O0ft90of*fIMt-tp0xoo zWoOooft O ftlA ZPK 300 ^-<hoI* .A-1.0 DUP040009802 TABLE A - 6 CLEVELAND, OHIO CENSUS COUNT OF CHILDREN O f ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME* URBAN STATUS AND ACE OF HOUSING, I9 6 0 c*Nm o I hON A - <*sr o ONOP.P' o t~'t* $_'* k 588 f. op. p g*o*P# Alj^ P> g f-isifM. * * .f Q Ww0ce p*9IT ft P8 ^ 8 nm8"^ o ' . Nntf O - o **f.- e p g OO.iA . 999 .'4 0** *0 oo ,**.*** o' mxrt** o NlA O OOO 1POfA a2 rf IM M lA P k W g . = U. ,53| ** hf l P tL sss g oMopoino m WMtfl N gKO* *g#N*AgP* |MC* OOO OOO NO** P-ffOV .*** O rO* ' IgSsm*o i? Mg IW S|S MPPNn *4> igo| SA* ,<AOf" H .# lA ggg *>IAMP Vr1tI in f*0*! fc 5< *5 is i * t5 2g <P9i* ohauiceO5p. Oo >L8 ^ g hi I S^j * W ? o grp Sf>r2 -- Ul % f- O VIA I *<Z> hf oil * *.5S S jffo oI A-9 DUP040009803 1A o 8 ^^x o -J -* < vOV3f- o6 ^ ^ w r-fttfV o o 1- * Or-O ft|S o o o o X 0 1 o p* *- O' X UJ o* gU> rI UJ o. ion .0 x 0 0 f UJ X xl tAOuA "***0 p o or- ' JTO\0 UfttA O o -- ^ OX *-ftlA o o p! rtf-ifl lA.mr- SO o 6 Opv XXft .* * * XIAO ft|S O o o r- W... p. sO OlAX r-rtiA O o o tA*. *9 so #>CS r-A o *p y>x flOVSlA ft SO p o o p XPlA lAX r-*5iA 9 o o -J .O o .ooo ft< y ft*- kOOA ' OOO POO sexrIA0O o o f*p * OOO ooo .MftX MOP o o 0 CD o *?-ft X u* *9 rrtnpo x Ui S<C UJ > 0 ooo o so ooo o 0P" ft.A** 1 00.0 ooo ft0O h-0\ X o s* o VO ooo ooo J3'0JT .m o o 0 r^> VO V) f- 'X z 0 Ui 4m o X o x% 4 0 *- vo X ON p *- ooo VoQ oP-op fttAOpp o o ooo ooo jsrtfjr sft ft o O 0* * 0.00 ooo OftfA xw.ft o o IS 0 X u *u p o< O lA 0 X fC 1~ DENVER-BOULDER, COLO UJ ca Xo ooo o ooo O ooo 0u. X tA X0 oo o OvftiA CSJX0 >o m ooo Oirt 9 h t-1 rTfA 0 ooo 0VOO p o (A ft UJ Ui X Op asc j > 0X *- u > u UJ UI f-- 0X -4 0X 0X ; V.UJ 5x0 5 0O O0X o* .j < >- *-9 -J xx o < 0 l X O0X < l- o * 1" X xx O 0O O0X < o* u- < XX o 8 <x < -*-o 1X \o<*> H <f> 1 Ui p O ku vo<^ W> 1 o Ui -- o >- XS3 < V> 1 o TABLE A - I f 0CO >X oo X J Uf xoo Xp> oo xoo oo j xoo XCO < -- p UO * 14.0 * .< ut o > DZ a *tf\ u Q *(A 0 lA 0UJ X < X X>Owr p.w 5V>M o z\oX 3VXO o X5.*^ H 3VHA A-12 D UP040009804 TABLE A - 10 DALLAB-FiJRT WORTH, TEX. O oC>O e .Xmm ifi S O' X Lu O /wU < o X < W IXU 2 <0 X ..a< x O ui X O o X >-J Sf5cEb' o V3 X w< > iA tO-- to . X (hX o X. V0CO ui Q x< --i < ib O z Ui X a -- X o u. HZ 23 O o Hfl X. C0 :UXi s.d * 9r-mr*m9 .0 o *o H- 00 CM tftOv. o d P fnsOrr 'o Ovdvfi CM VO o O CO 91 f* O' * t-- ov X \o UJ 0N Xf xUJ ion O' om *o s* t Ui X& -J o H .x.teao CJV3 o o 9-- CMf!CSi VOOv. *-W 1ft '0- d or <3*-Vp lAOO*- X-.X o ooo 0 0.0 OmA lAiOrj~ wys o o CM CM T.r? ifjfw <*.0 O' Q O 0v*KiAf* CMvp e d or SO ro O o ro* ooo ooo CM .09 CM OsO JA n r"r* O o CM iA r" tTNVOO - C*" o o o f- ^rifs CMfub * CM M3 o b o -- - CM N9 * o o yo* OOO oONoho* tfMAVO cyoh- op |U .VO CM O ec o> o fZ .O' UJ .iX o -J O' -r 'SO Xo o *u. .1 O iTi O' UXJ *- 9A 3 in Z O' 1 Ui X a. OOO ooo COOJ? r-VO'O o o -- ,JT CM O.oo ooo VCUCM OstOn ^n O ofO VO OOO ooo r-A-Os St Of*'*^- o AO CM OOO OOO o*-r** O o CM Q ooo ooo i*fASPA^>ifot Wep o o Ov M3 o oo o ooo V0AO*STrS-etOry* O' oto CO tA ooo ooo (A COM wX nCM oCM o o VO p*v 0.0 0 oQvofOoO XOS O o CM .i9-- OOO ooo O O Os tfViAO CM oo Ov o 9 > UI >s.ui >1--- Ox vO J cox sH*oC t<-- z-- o < X OOSZ o O-3-X +1-0 ^ </> < O *- A H- <0- o X-VJ z Ui oo zoo < -- UJ * xz O mA x< X xsa*- SXl . -u </></> > * .0 Ui -J ox < CT'O -J X OAZ < H Z oO xVx H O UJ *-o - t? voei> v> o X oo xoo UJO - h~ O Mft o XvD^ :Z ov>v> ui o\X OiO _J Oo pvZ .< t- <CC s S9 a: vo+<1/>-0 o 01 o -j < 0.0 xUJ oOo* *- o %tn o X vO-- 300 A-n "f j j / . if* > J > f S r 'i > j ' i y \ J }. DUP040009805 4o0 x 3 o X W J<O X& . <. tn i 0 -C<O CC W IX ><3 Q <Ul > U. O X QO T 5" Utol Q < J XO .X mmll LiU < u. <0 XLU O XwCC 90 C -j X >* p X u u. O X 0 0p CD w CD X < h- Ul 0 <*) p ! P < Wlft O Vp.lh.OV flO*"-. CM ** t*sO-iv h*iAN> W O t .o <Q OH I I* . I X - AO Uol On cc w a a- in .O' Ul X <*>0. a,ao tn\Q O O O irojja* VOeSOOtfA^ OVD 4* or>J3*c*m\j oo oooooo oo 0.0 So rr> T* -VO OKrt ..:> MAMA .*0.601**00 tjfrfOC.wVI ooo o .00N-.0N05 C4 (>*" *n if fil.OAl tncviw CM i> 0 Xin PA-l*m0 O o or-fo'0-oo0* to a.*m jor v o .C0C . n w X 0_> 0 x 0 u. *t O ir XUl - X X9 t0f* X 1 UJ fld 0COM.O0COO *-cu 0 ooo 0 ,v0o0^.u0r ' mjA ooo 0 00 0 f"f,i* <V| ooo 0 .0lA0.l0A i-atof-- .0* A49l* 00a OoCoAo CWX-W** . aO ooo 0 oTo*CoVI . OOO 00 r* M9 * * N O (A o\ CM OOO oo<o*9 CM P *flO O tOo to CM ooo aotoomo O >*W >H* Ul 09 o*p ml 90 *~ <!C-D x*>--J XJ < -- P -J <CC -HXUl p o0 x x*x *v-- 0 <0 00 U9Q00. <u* h0 SOxU<X. X O *IA X*ov>v> >H* P Ul Ul .< x u* X UJ X ..0 ox .o0ai*ScQc ml *<- 0 p i\Jo>*io x 00 900 wo: fr~ a -8 ^ O X*X Ul X 0 w <0) .tXo ox 00.9.9 v>v> -t<- 10* ml H<O 00 w9,o00 *lA Xf^ U A-14 DUP040009806 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND ACE OF HOUSING, I9 6 0 f-< Oh* O o CMCWIA --C8 Mm lAlAO *.C9 O O O KO0 0MPlft O P ox Os r- O O Tf 2<M * . * ' *-, o r- X*UOow-:I O'8T8 **" a UecJ &. P4lA OO CMCMfcA p O O .00.0 OOO o.o Mi--p W.WVO o :0 3o--> .2 r UJ e Q -J a -- VD :X O1 u. o iTi w s X 2 U ec o .0.0.r0- CO CM OO oo f**CVJ U\ V tCoM OOO OOO UYCM !* -CM 2 o o so to PCM 0jfO s- .r- 0Ov*** f** P O .OOO t* --cr toCcoMs CM tTv W .o0o0.0 CM CMfto ONJT o h O oo VO^Tt uve f,c o *"r OOO OOO .ITWT2 ifvtMin -r*JT o to m cpo.x O r*f* T" 1AN0 lANJp r-- CM >0 0 Q f-- OooOO Mm CM pr*t**O-- *iOo\ CM O 1A M OOO oo *- ST iA *" P Or OOO OOO m.M r^tTThr-CMiO-- O X X OO OOP O0rt CMfO Ana . sr t-- OkCtiCl o.o0.z0 iS S0 .2g g 0IO x-- zoooo t QUJ . ?O X90*0- &vcUe o -6 < OOAJtT-*QQJ HHO M <8 O <4C su.ioA IO-- XQA*lf*k ,t- 900 A-13 DUP040009807 1 ****.'*:**', OP<` * '*"*> O 4 P . * * I *8fc 8 0 w % a f>4T M#t#fth . --o--.8r6*.* . ** 8 i ! Jrf* 8MNYA P P* JtfOtl*-\ oo o M .* .- on.to oo ** - f-Mftj4ft 8 cvoy<* e *ss s *v<si o ssis i 15 1 $ .i0.l011lf**0 1O n o 04* 8N<808 0t 8p X 1 8*<f9<80080 8" ' CM 88 *<AS I 088--* n8 wr8 888 8 n-.w nf- p I1 8!*?*1 2* I 2O aeVH- A-16 j DUP040009808 CENSUS COUNT OF CHILDREN OF ALL RACES S MONTHS TO 5 YEARS BY FAMILY INCOME, UNBAN STATUS AND ACE OF HOUSIKC, 1980 -J fi-T-*C!j* P -OH< mjfW d ftl SO o** H CMCUm 0 .0*C0M.0f* do <y roso o O' Oi (A^ro r- CM s 0d 4ofit\ O' o * IOT 0.0 T- O r- m iTv P fmc.**mts-0cpol>*.- o .Oo1"' OsCOfO > . *-C0 o *o ? ^rcvi-9 sO\0f> <Mvo O 0 cj-avoo . ;^*CM T-W.SO o o OvQ** o ov.od o or * sbcr-rie>s P o f-- iro\co CVJTOJ *-*CM>0 <u so or * so com i-cvtn PoOoOo *O-sOSmO WMO\ #m0 oof* oofOOooN oo .os st.:m om OOO ooo irvpvgs r* com ** O o CO m h- POO ooo CB CM > STKQro o . SO SO CM OOP OOQOrPo :*- fiiTp- o o *" o ST oooooo SO CMP JOO.Os * >* oo ST ST OS ooo ooo 3\CM -- ,os.j M o o Os m m OOO OOP T-CVIlfS '" '.CM' O o CO Os O0O 0.00 *-* oseom .MlAO CM O o St m Os CM OmOosmOoOlmoTPv CM"* o o mITS -*a-! * ooo o(Do.COor ft*0 r'-CMP- O .JI OOP ooo moo *-CM o .ST SO to ^UJ X o < H3O0 H<Z CO Z< </> UJ z U UJ Oz<X z oz >H- O u ml <z u- z OmsoZ OOoPSTs*CXC -J < H* .o UJ *-o H* p z - VzsO>o<o/1>oo UJ A .1oz- .m Z.so.13V)0 UJ 0s Z OsQ ml < CO o9s* X oA.f9f* eO .< h- o *- X SV> CO CO 1 -J -.< zUJo0o.o0*. o- m ZMD-tr A-15 j DUP040009809 . -i wo o I , v* .* oo* !* ** O SS3 8 ,#>*> o ?88 8 wimya o S88 8 . ' *8ff 8 CM Op > > . O * 9 CM O CMP O ON O MU s&s s ^n*d* o Sirs* p5 <1 1 8S Ch< f9* 1| xo p oit. BItCl j!l ill i g 888 8 *f--Coo r 8M88N 8^ tfw# CM CM *<*-M-* .*N0V. O 8 *eio o ~9iOk - * r"fwA 3 >88 8 MTOt* CM Hi A8dOT8Ohv-r8ffN* 8S AI0*0- CCMM 8NO8V14L 8*--OimM** O'.W f.* 0 ' <r-MCfM^i9A p -* *, 3t PCM* F f*On 0f* S3O8g8p6 t-o CMP 9 888 8 J0T007i0*1- MlmA ioOTCoOM)pOr* .iprn- 0N# CM CM 3 oil * * %8 I C 1A0 H 01O :5 5o O _X_ Ou S^ *(A .. - 300 J o\qC $ slJ 3 5 .g x &?pa| H yOo*0 8 3 *M 0 < 8?< <5ot*- wo oift 9ar<vMo r>- A-18 s \ DUP04000S810 TABLE A - 17 LQa AfjGtLtS-LOHG BLACK, CAUF CENSUS COM? OF CHtLOftEN OF ALL RACES MONTHS fO YEARS BY FAMI LY INCOME, URBAN STATUS AND ACE OF MCUSiNO* TS80* NO o S .ce .Oi A.M O> O.* ' *.***\^a6 *^ ? p S e Hi i KttA * r* -p o fWa aAa P. l*N jo tO.f*.#* ep .fe 9 S$ S X s* 0 O &**jNf*Ao o*o > o 5r* 0 00 l*<MT .|*.WnIiAn ofO- *>N0 jr3f* QAr N8m8aat8'>s *6<- oI 8 -s 2 t& _ 1c 9IP ** 888 8 # 88 8 III I MAN 4T 888 . 8 ` 8 6 j/t o 9 888 8 S W88*8iA 8 mr*<mVf jrtt 8` n8jrN8 %08p 888 *.m** r-AJf- 8 0 W Jr* 888 8 AfiM Al mA 8.m...9.w in YlAiO I ilS< S-&?S u8 Kui 5o e* 9S0M0l\ ^ JI < 5 U m O Sto t* o ->rs I 585 A-17 DUP040009811 zw6ooofr0dna 02-V V>V>C ~*PX *W O* fO*l 009 oo oi v> HO O3*^**0 H ' - +. O: >r~- aoxvoo x* m H O H>I r gi o H on; 009 -- oo x 0. 010^ a, g-** n XO X o S> r 3jv0 vo0vo 5 r m vtA.>Xo6 *. On 003 8? 09 Sxp xso o O'O *>P m a * H< Ut (4*4 ** UVO-J H XT -*P o oooooo ra S0<-Jt* o o mU U4'P ooo ooo ra ro \Op0 xUoo4rooJiTaOoo^J u*O4 U-Ol'-p0H.s0. o ooo .* ssOoo' u-acra** oooooo rtoroao tlooaarioraaoai o ooo simjs racoo Oov 0O*OVtOQ o ooo r*fae act * 6X4O\jtr-sJ3 O oooooo Vooo>lt 0ooo4 oo-ro*oos X Jl e XO m -- J0* o-n 1 J-O* Xa p r*-- o -- xm -w" X0 1 so S' IQ ra o ra -* ra so ra a-k OOUl a ooo o ooo oO OPSO-*X-* o Nro-c*BO *4NO O' s-l o w-*x V) Kfl . so -pra Ot oj -- ra o ooo o ooo O 09 O OS SO X o W-*p oa 0^ WMX o -*ra oa o oo P ro o arutrv* Ok ra 4X0 SJI o o ooo OOP o o u*ra -- aw%o SO-* pCarCaa-W* VJWS O ftM-. v*ou o wins X m Jl a 01 m x m p -4 O S' o O W-slO Oo 0C0K-4Qw o pro-* O Qwov om uc0 o X' oX m >r r x S rn i 5 X Vi H O a* -m< >so: vs w < a o xm. x. w X Vs HI 5 e --^ >x o s m o -n. X' so s o TABLE A - 19 MILWAUKEE, WIS. m6ooorodna 6t-V 99 --4 o \ji Q % O PI > OOP f oo 0*9 05 <OOi X O tfi o P.tf > * O' > Z'OO r* QIO 30 VO n mi (M UUm 0 CaOivO o ooo o poo U! W --T vp w off a 9 OvOvO O' OOO o ooo x*: f\>.p* . M OiO\P VJt fS3 oe u> o OOO o ooo 006 z o O k on OOP oo 4 _ zmm O 9 99 a H O-- n pz;. z: 4 * o H > Z'OO P f- o 30 VO > f- m O -4 < 4 M VJtOV0 O ooo O ooo XT M-i* O 904 m CAl o OOO ooo w a CPU* OB OSNO Q OOP O ooo 990 -i*0*Z UK o r on POP OO' . 0 19 99 4 O; O pz-o -4 , *. >' Z'OO r O'VO P m -* z , O PT. Z. H P > r" o --\ -4 < n< >.s> ZS> --*>: P"Z *< 9 4 Z> H 06 ZCA m'v 9 9 990 O ooo o OOO * * 6> 4 0-9 OOO O poo w * -4 o OOO O ooo u p n t ^ pz 9= C O' nXr m -p -o v* O *n i -* o z Ov -* r* o P -* n; pz 4 O 4 *^ P' O ^ * OSW-* 9 r P OOO P OOO wii 6 Mo* P QBQSyi o zrui A* p - 9 *-* Z p U50VO mi P o O4*VvMifS-*} p Ov-Crp vo mro-* XT 9xrxr 9 jr-*- O OOO ooo Ml o xr rp rp o CBVff OV o CKOX mi o: mw-* o 9 4X o pPO* *- oo CKftf-* tuwro p 2T-4P M M* 4VOVJI 9 *f\9t*8 O OOO OOO * Oo. wrojr 4^yi O'- t*l U VJt o'o ro -\j b 4g*P a o p xrr mt,W9U 6 MfSjVJt o 4 > n pe m t P* o p ot mp p mi P 9v zom p H mi P *4 om1AP OB O' O P V49A9NC-K* P 4 49 O P v* ouix- O' 4U19 oO Wrv>ff0N4r o oHr> TABLE A - 18 M IAM I, FLA. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 H86000H)dna 2Z-V itx/yes v-*i;*o\sae *00o3r7n oOoi <l> 9-*rO* *; o xo \0 m !< ** oofs> o-* roo o-oa> o ooo 0so5>oo04ooOi ooo jr u> w oim* Si -4 o OOO o ooo 2 yc 02 CO m S30 O ci'fl I J-*PoX Ov--* OP?' o 9 .TM z: 3 i * `O' o o vo ytrs-* voPnO VoNonioooOoiouOi OO CO\Jt\Jt o 9 m i c Ji OO OGU-ACK J*SJ Om '9 r>*fion OiX 'OH O 0-4 O (MWW 0 -*H3 O' H O O 0-4 O O CrfVJl CKvoUi CO c o o H o X p O' 9 rii H i fTT <0 X co < I o 9< ao X m co 1 c 50 O & m o X" 2 X a o o TABLE A * 21 NASSAU-SUFFOLK, NY si86ooowdna tf-S -*OvZ Vl*' o *ooons oo O 1 </> H O H V O' > X T*' O m > r 3j. {A > 6 * 8o. na 0 07 oo O 1 v OOv -H O -** O 7* ,o >. r Xo'gO 7 VO' m x o n > z n x >r* o -4 < -*\X *V'onO QooO 9 O <I/<0/v> * OO7-*'* . xsoo nO7 COoooK XTo-* oooooooq two OoB --* -OoO4voO.-*oO--** -0tAo3* tQovOtb* oooooo u* os vivo CD -si - o ooo ooo VO OOvfO VI Ul Ov o OOO ooo VOO* Vito-* MOvUI o o OoOooO Ov VI -4 Vivo W CD OtoOv o ooo O' OOO' Q* Vi Cm Ctod -C4D VtoO o oOoOoO to 44 Os -4 JT-4 O OOO o OOO >7 55 OS H X Woxn>*wcM^ 30. n 1 X J* G X n 7' o n 1 o X; O'i r~ 7 rn X -1 a 1 QB o 4 CD -4to -* av Vivo fa Ov -*oyi O OOO o ooo m3- o --*1 --* o O' b ooo m3 o >1 -A. o -4 VW o *4^6 _* o CD-* . o -^ UVT b **OVtJ U A mJL VI OCBOV CM WOi o ooo OOP --A o --4 -- o sjpr o to CD w o 4-- f-pxjl o 'U o 0> ** uto * a 00v VI Cg * 4 OV* w -4-4 O OOO OOO al -4 -4 ro o o oo o V* to-* o v 8 o qOv o o-* m3. Vito-* OvvfJ a bttoOv -1 o ->4. r 7 7 m i4 Jl o 7 o m. 1 a4 7 o n ev X H A4 -4 0 1 O' o *4 --4 -- O' -4VIOV o OB Vi *4 *4o o-- o OiVt o Ovto-4 o sio-* o Pu -t a H > r* TABLE A - 20 MINNEAPOLIS-ST. PAUL* M IN N .-W IS . CENSUS COUNT OF CHILDREN OF ALL RACES MONTHS TO 5 YEARS BY FAMILY INCOME* URBAN STATUS AND AGE OF HOUSING, 1980 TABLE A= 23 HEW YORK, H .Y .- N .J . CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAHILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 f-Pf- < mi -----9 p ;e*9K jf o o cur* O CM CM 9 o 0 cPrO1 Ot w *c0r o Ua.l ion 0 PTUIT1*Sl aoc.. s o m.09 P 9m CPMO#Oa9 O P :0o.o0o0 -CM OP CMufttO iA-hr*w9 p .p 8^ 040 04 ofa1oos p 8O :8a u a: iigO OKfl o ;0too CM Ifk <30 OC30 p)p^ f*iACh rt\0 o * CM .in OOP OOO AOCM*9MP Of 9 oo OS CM () -.0W- o o p 9 ***-p* 0 tfSt^p pr-<r> o p O0.O0P0 m0o PNI r0o-e:o0oom0 *"CMO oo p<C*M ooo OOO --OmMo9 9 o O P P 9 ooo .00.0 f*ON m9 *-9 oo o\ C* m OOP lKiftf9tivp O i-VWIAt9ft oo ooo UVMft CM CM 9 o O . OOP O*O-*O * Nr0f5fJfV9l - P- fO Ooin wO IS oooooovooov ooao CMfWCMjys S> ooo ooo 090% OirOv .(ftO o o Os o CM oooooo Noc.vso O.ftJO* oo p CM CM 9 *N.OJ .IHsP.XUo -C*j o 11 o hi ml OvCC cc- OCS3 oAoZ ml < Xw o 090 V1>0*1*I93o Ko _oo Kuaa<oOo!o>*O**in>- CtOhSi <to OoOA.O9fc-C*vlOOCx J< Ho* Xto -<J WconOOooP`.N FhO- 3OzIOA*IlAAf A-24 DUP040009816 TABLE A - 22 NEW ORLEANS, LA. CENSUS COUNT F CHILDREN OF A LL RACES 6 MONTHS T 5O TEARS B TAMSLY INCOME, URBAN STATUS AND AGE OF HOUSlNO, 1580 J . * . . qit^.sr P s>- MTh-hffT<V *n o CM 01* O o 00fiC1 ro>PrC0M* o p NO 6F-fW O oO P0O rothm cvwin 0 o .o <AN -- o o XUoH*i tjUCLCi 0ion wis1 CL nph so TOO MW4T o O o jsr coco * * foeoCM o o 0 0.0 ooo P{M-COA.CfM* ` -*-CM o o its 1 :P T g UASi a p u. ooo o ooo o esoOs ooo oOoNor Os asJO o oto 9 CM Oi rtOS m -0e1oiwp O0 oo5 --m -- t.oo * o 0.0.0 ooo OhWsrnr .oTfO* O 0o0 os0o.or0* W JTfO CM o CM TO OOO ooo TO.lft.tft o mo jCaMr ,0o 0o.o0 ^ ---- r-r-CJ Aoop m ITlWr* WftUA o; O O 6 ^ ? t o *oeo OO OOOOOO o0 Sr>OfC>PM4A Oso CMCMP *- OOO O Q O.N4 lAOfiO CM Oo o tr 0.00 POO tta-tts CM o oTO 0 4T oooooo CUtO'O O 0 co oo 90 CO CM >w >%Ui Si W - O Oxtc OvO OvX O* .<-I Sg ^ *Sg OS >- 01 O ar oo li u coo O WO ^ O lPi PM Z X3'0O0-- o0OeUf -J < X(/> CO 00OOo00TaiV-*%o.cOXc hH<o> oo -J OS oo ><- ol*J%cnA o h a3s ^00** A-23 DUP040009817 TABLE A - 25 PHILADELPHIA, P A .-N .J . O CPO 8 ^ --8*? p r- X X3O o OlfOX fUOkCO p. W PA i 01 ui a 5 o . AMA#f> *t p *-CJ t No AO4? *3$ g 4T aos OO .3 OS Sc X '3<K WO X AC hi OS o *I- ha.i o it o 8 ^ p OiOJlA hUS> f*01*F**' g *** 0**-I*0*p?i0* . Ul I ,tfs 001lX*o0Xxn O OOii" pto01r-* O T- 6 *8 ^ p-OMA O o o UI i 5K sss% .-I ?C oooep o so O P tfl Ocss pitfse f sOOOOOi-sPPO f-F-tfN *- fO X01 NFS j->lft 4.01001 1 m g s *-*-X 55 to tn noolA n st*P*:mP ' ^S0 JO XUl P* Xo -i Os -- 'S3 oooo p hi X Os - w I tht*(tVoOt> m 8 o ir 2 U0l uO. IS * s? UXIi S h<**C)pV-*P* ffP"* pnnoMo *X fift Xa p 4#0 O* OX w NOOl g slu ick 3O u CC3OO S .*1 , S*uj to 5 e\f < I-- to *- <* a*< o-tv>e*- o x5 11 2u auO:oSo> O Js oOsSi -i hiX"i O%X**"X s g u .to X-- tcooo1 oo K hoi * PX 3S oopx %*g I at X X>Op* 3 WO S^ g ?r A-26 DUPO40OO9818 TABLE A - 24 NEWARK, N .J . CENSUS COUNT OF CHILDREN OF ALL RAGES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 OtfMA O xmcw p q 8 S h-40irv ->* mo.x r-cyso p AOr-eu (OW4 p 4x n coco *- o p socoon *-f* NOt Uoi JTrt.F- oit r-OO --o n9W f-xo *-1- p lFif*-40 p OJP* -J 0.00 O oCJCo4SoA o 40 X.* Qr--Ov X CO ooo ooo 04f*0 eoi.o ^o o >0 <r* * CO O 1 o f.o soc o 40 o .1" IT o .m 94 tx1i ooo ooo f*-X o o 94 r* ooo ooo TO-CVr- cyTx" o 94 40 V" ooo 0oXoo0 tfvoew o X * ooo ooo 94 rt---- o p* 4*" OPOOOO ow~ eg M - ooo MoXo3Co4I *-X o o00 -. OOP 00.0 i-sotn WON W.cOOs O O CM w4* 0*4 ooo ooo T4004 *" cu.x o a to ooo ooo ooovx to O . r* CJ lA OOO fO^fMO-O94 N .4"" X o .to 00 Ui Ova: >gw.UrI Sbi ><-X| 'e<c ovo OOO*t X \oO*x0-a: -J H<* oH Vi V> l > X-J ui flCoOO Si o loZa>p0**i>n <*><9 . Ui mJ Oiac < 04 -J as OvX < H? % ? x x o Ut At" O w O AOV> 40.1 o X o - |S*JSO* fOcr .SZvO>"-* X 3W0 OKUI 040 -J O OvX < v H <Vi *X*-X h X 40</> V,i v_>oI -J osoo < Uio ' > o %m JO- Z34'Of>Vr> A-25 DUP040009819 TABLE A - 27 PITTSBURGH* PA. flO q -f* as OtOro q N 0 3 P 0 *.*" O p * in 3 <HO Qtst> o CJCam *o Oft.ft O O *m PO- O*OjPH O P O *- ,z u. o UI o < (0 9\n o o ec r- cam b caqp O niftO O p^K' .0.Pft O zQ .0*5 r-jcun P 1 *-p O v*"" O .jm <o IH q 3 'OJO o >9* }~ q O 0lftH O (0 z Z 1C wo q q**q. m p pqp--qq O P O0tO O O < K1 a x Ua.I o tp 3 q* ui o vON N o eoooi O' *< O OP 'zq m N'Olft O' - cam of-- \i' wcajr O p-W'O O qrca O r-CJ'O Q u > -J Xa. 1 u. >03 -i bob o ooo o < q VO * m*o<?> X* H ftl 00.0 b ooo OV03T ONW 0 q m Hcao. ca ooo MoPo-olA voeom iHcao. O Om Om V) Sc UI > il> O J- qq . O' 0.00 o ooo caoao !*o** i oooooo H*"JjfTtH9 ca o 0 q 0 w ooo o01-V0oOoO0 ca 0 0 VO m 0 eft :.X zUI :qp** ZX Q X VO UefIt .J 2 >0 X O' W U. ;1- footoof\(oo> o or ca ca m ,o0,00.P0 qqm camMo 0 0m p 0 ooo mooovcoa 3tft00 0 0 A0O -jr oO < O' z OS ap* UI -J 1C u. o z UzoI X -.X3z Ico*T" UJ XX ooo or*NoOo n^Ov oo 0 jPpH OOP ooo jzflom p+-*~jr ".ft 0 0 f0! m 0.00 OOP mmr> 003 wmrmar 0 0 0 IH - ta. X fc p uo. H* X Q p *N.UI MX 3 H<H-Oz-- > Ui J"p qz o .-1 . qqx O A 0.3* X X< H r-O eft i o -) <o- K mm P -J ovUxI 5 oot2 l < H UZJ p oO ir.*x e0f.*t0.*i o0: 10 q 1- UI OqVOX -1 < gqX OJTX <K O 1-- $ eft :ePft zUI O ,XJ Ox?l 3U. ZUI u * xo ua om> Zr* 300 * fzoc 00 xuZ0ViooOofmH> 900 -1 -< ;h xoS UIO A 0 *m HO- 3S< A-28 DUP040009820 TABLE A - 26 PHOENIX, A R I2. WON )AO v-CMSO 0 o o <M*-fN PPM CMVO O O P tDOtO : *-*0** pOMO O -. o O ^ariD vCQOtA - r> p o O p*iryp p N Wcy.\Ooi o o ?*tM O WN 0 .H- OS 2T M5 UJ O* o AUCJ doo iv O r* .O O **5 N* IVON O 0 0 ,0 CM *-cr.sr r-fOiD Q \OlDCO r-jfp oto.jr 3*WW r-lD o ,o O P O.OO 1o-foOoS CM'- O 0 0rNVO O <00 Os f: UJ oc Q .J U u. o oc UJ m oID OOO ooo CQ-a CM -lDCM CM 0 o JT as CM OOO OOP Oscara- ova- i- 0 0 . -- oop POP JTNOD CM CJfO 0 0 tO :OOP 00 AOj-r* mr-co >*o O O CO O w OOO ooo NO ID'S* CVIOlD CM O o ID SO m P 0.0 POO iD .CM iD csir-*- OOO O O OP o iDOTCM i" OOO OOO IV^rcO .STJTCD *->o.tv O 0\ hCM OOP OOP ar.osvo -a o pID A ooo OOP aacsi N.0 **=N o o o O ID OOO OOO os~ ra<SMD o o o CM >W N- pec v . ova nz U OOsX < SO o . H NO -J O^K o <z .< o > H* 0 \0</> (0 h </ i O X oo ZJ UJ OCOO O WO ax O N(D cc< 3U. --as zsor 3<i> p . Ul t OiQ& OvO 0 0sX < 1 pOJ3*-K IN o o w<0 . .> I o _je oo KwOoO* - O ID o zw3V>V> w mi 1-< m< X PJTK '5 K 65 -J KOO < wo * N- O *ID O h 9X/> A-27 % i DUP040009821 TABLE A- 29 RIVERSfDESAH BERNARDINQ-ONTAR Q! 0 x -J * Chr- 0 vQcy o 0 CM CM O 5o < CMCMMS 4* *-cu>o O t* K- W46V1O^'f0 ro- .CM in CM o *~CM0 or r- fMO o minp tO O 5? O CO 0? 0 .* o o CM 4* 4-CM VO o - .0 O O 4** o *r X< rr *- I-- < 4- 0 X *0 .x* in*** o .X <M4> 4vOt<N O f oo 0 --oo .' O * fivfl"* o ui e *-cmp o jr- -.CM vp rO- -CM0 *o* < ec t eo Ui BC ,a. [tr 0 vooitrv 0*00 d*h,OV a O u X if.^ o 0im r-fir.ar o cooo -OX o,p 4*0 in T-.eOJf oo 4* 41 eQ. > 63 .ml 0.00 ,: o ><4* J-OVNPOJ o.* ,'JT 0.0 0 oC.ffv.oOphoO* 0 0 m* o.od o o0>os,o^r ovr-: >oo o in CO < iU > o o -CO O' Oo4-vO<c4 m o* -if 0,00 o ooo 4O<0VoC~M oOv 4- ooo^ooa-oo.o o oo CM * V3* \o CO X xu *- o X foiC J X , ooooo 4-CM.0 o 0n* ooo \oCo*r>ot- o .0 0.0 o ooo o Min 4r to ui u *I 4o, in .C4XF*"* 00 :K\4rTtOO m floor*-\X MflQO 1o X *- hi :X OOO o ooo 0 ooo O .< x mo* *-- I CoSoJAO^- CM p*nn <0 0,00 ovm (otncfi o 4* 4* 4* OOP mm X0r--> o Ov m CM .41 X a. aac > .4* uo > UI ^.41 4? o .1 cox U --K < 0.0 * >4 O Ui J OV.OS < O' O -J X 4* ocvx O A. < 4- 41 Oifi O' O OOn X O -< o o o u to CO <4-X0 < 0.76 * .4- CO X 4 A00410 O > 2T.J <-- AX X41 P oo CUiO O. a *m X41 o H O 0O X oo KOO 41.0 > 4* O -lA < oag o >4 X0 0iO.0i O J EQOOO < wo J* H O >iA K< X X*C- O 4- 900 oX X'M900 O 20r4- 900 A-30 DUP040009822 C286000fr0dna 6Z"V *4 -*C>Z O VI'- O -4 * om > 009 r oo a0 </>o* X -1 -** CO o 30 xr > --1 - > xo r~ so 39^0 m z -*0vZ o VI* o -4 * m 009 oo -- z 0 n "4 O r4 o-*\ Z4SO % zrn -4 r> I'OO O0 9 > Z0 r* tn a -+ < coo>c 71 C -osz v* o z >XZ * om ooz o m --r >z oo Z- < ' o ! to <ft?i z --4 o ->*z-cro >r Z> -4 >r >o Z'DO O' o 1o(c0 w f* < hi ro ft> 0oo o4Oo0Oo0 o--*k oo4 ooIMV oofoO*ooK-l 0- V w -*0*CK 0 XThi o OOO o ooo xOomrk-i M* voooir-oovvoo-x*r 1othoo0) VI v*4i -* *4 oooooo XT hi hi O o hi 009 VI 0 -4 IV ooo: ooo .A OOoJft oOoomkvxoou*woo-X? -IooVV- oousiirooVvl-oo'OA to v ooo o ooo 0vmp1A A 0oo1 i-: 000\ zXCmzcD om so mrOz:' 0o Sru Nu> w-. Oft MVlOv o ooo o ooo CD VI -* mi -40VCO Oft o OVIC4 OOO O' ooo to Oft o *' vi-vVi 40w o ooo O oo o: M*' o vfSJ-A X?<-*0 <**&aOv OK N` o Vipse O' XrV A O 0V~A * ODOhi O os-* -- o -J -A o -*090 O' 0 VI 0i Og* 0www***.*J. o * oo 0GKQ-9^ M hiMlO - * VI M -4 o Mlhip b 0V0i ** Vi CM --^ o b^sivo 0V- -V >? s 3 fn S 35 --A" oQ Vi -- Qsoaos P?' b b b o C\M-* pi-M o mz x ? a: O 0i M -* O 0OO b ' *4 IP-* -- o VIM--* F QvyiQt o -*O0 3 > r TABLE A - 28 PORTLAND, OREG.-WASH. CENSUS COUNT OF CHILDREN O f ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE O f HOUSING, I9 6 0 t'Z860oot'Odrm ze~v II-*Ov'X vt * Off 0 039 a m OO x o </> -4 tf) *3--l 0>Oi o -** X> O X0 -4 . :. 1S ss wv 39>0 PI Os <o J0-* pa pv0-4 ooo o OOP it* 8 0 JT0UI 0 o OOO o OOO si u* Ul: UU**OS 0 o p UooooUooI0 os . aoo Ul^4' . M^oojsOoooVoroa* VI* or' a Uoot 0Woo-voo0o4ooj?r ro o c* WlrN 4WW Os UWO O' OOO ooo *4 o uifu* 0 or o q pi o ufto Ul Or oras tiora CooBooUVoo0 * OK KJG*-* J? OU 0- 4 rau ooo p ooo 4 o PM-4 o *?# 6 ST 0*4 * p m - . * ' - * ifml ovuw Pip os o o aitlw*' 8 --K -4 o OS0U* o 4*A . - Q 0M* Op* KrUaI pa atA 0 OB WX O-*0O4i o oooooo -4 rora- ml CBOHf O' O O'O' p poo ruoa . ojraoruoi O' OOP 30 rn i rf- U0i X c o x; m. mo 00o1 o n t ml 0 O x. Os 0 ro* X m 0X *4 0 1 0 OB O ca ml mi so o\wa ra 0S-4V* O ooo o ooo mi P arc*ro Utb*-* o: da-* 4 o cattffU p aoiw Xdip * o o -04*-4*4?U*r aI -4 O-4 > r X w i 0 01 o 0 at .o 0 Pi 0 ml 0 *4- P 0QB O' O' otra-* O <4 -* -* o 4 * p wOft o bbra 0 Jrwru O NU4T CA0TO TABLE A * 31 $T . LOUIS, M O ;-IL L . CENSUS COUNT OF CHILDREN OF A LL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 S286000fr0dna IS-V ST XT UoTo\--*NoVJt O ooo (4 II XT' -4WSP 9 (MOW GO o ooo N u*-4Jr jr U(mC9 ooo OOO XNioArjrrogi 0 pGoOo -irt-i* 0*4 o -N-^ O O^U) P-4U 4'OKI p ** o O -n IOJT 0 dtrtOi He -w* \i * om g'O'Z i * zzo Z\oS i PI x o -4 --z; mz 3 0<ftC s I w II-*-o\x o * pi 0:0 9' x PoT O ; X' t V> -I 09 3 > 9 1*2 '2r r cw -4 . is xvo o r o*o PPV 9PI H< -J4r >t*0*r4o 0 o ooo o ooo ra * 0V -W oo oooo w *-' N *0VCrt VOOM O o OOO OX?f O' VVwO0>-O*0*--44 oooooo OV NN-w 4?-4 0 ooo o ooo titbit Oi roeoov ooo o oo Crt fru " OOO ooo 4 0 o41 c 3 m z 0, o 9 m e A 0 OS b nw* o -4 JT ooo o \JKrt> o no vo O -6 \6 > vnwk -4-*-* o o* >o ' o xwu VJIVJI O nn V*NM o *x?*o*w CK.fr 9' m a8 0 1 m* P ovro-* V>fl)VO XTCrtfV* nxt n -4-4 o zp v (ft o x f o 9 PI >r 9> O m as 3 O < P>I 9 (A < i za 2 PI C 9 I 4 > Z o & 8: x o 0 z \oo TABLE A - 30 SACRAMENTO, CALIF 9Z86QGGfr0dna 1?~V *x/>e -*,Z. v* 0 O - * om >, 0 0 X '.r* 00 0 1 X --* $ --I >' >r* * m PKfrG X VX>Cz7 0 H * om 003 at OO X O 1*</> 0 . 391ToO. mat *H * O -H >r 5ZxsSoOO r ^a PKPC * X WI 0 * om 00 9 OO O*0 o.-***\ *5g 8 JDSp m mm X a m. XHX >: *> rtf ---- . Wso O0tfO0jrI0M OOO PS N> SI -0*.0r-.T0N> 00 o Os * -* . Os -* rtf *<ivno o 000 o 000 y COD U -* SOJOIWPOS OOO O 000 O JJBPS4WP-- UW O USGJ-* p grus o -* -* aAP ro P fi**4S0 P ovo-- at O tfW<4 Q ' "tfftfp ftfbb so mw>* y -0*0*0m 900 fill V s soOISsJ cXaT ooe p 000 I9O' NS VDOtfO o OOOOOO on SXltf . wO' rtfOUl 0 000 000 o rtf in rtf 0- cn--.c- o P Utfi* 8 s o P itfvx O Itf yiyiso O rtf^i -- 0 giw p spOsp b CItf OOPS o OOO o 000 Itf O-*S OD fill so (> o OOO o OOO XItT*f t a-*\'J-yrt*f o OOO OOO r*i 1 |3 at 5 CD ToJ5i m50 om -* fPoOS rax~- o X I. WN Ut S)VD 00 OOO OOO utjr -* o Xwfin o. p Ofii* m ojt o 6 8 *t> I s o * mo> pv Xsi O Oifin ppp b cL*e 0 a* O UlCtf-* O faV9l* b ypw 1 > r* 5 m: x osi > 3? ?> m tfi X g Cft jr o TABLE A - 33 SAM 01ECO, C A LIF zz860oow)dna "V >>e -*X w* *4' O-4 - on > 0039 r* oo O 10 03 X H O ** V) o 4 XX o > > zoo r o9o0 m wsSs V*4 $ OB M O ooo poo r W41. vfln6wBvGo O' OOO ooo r M-* n X*CK von *4M OOO o PPO 0<AC X v~n*oX _*o4 * Ort 009 OO X Of0 H 0fli O --**' o m o 33.Br X H * O <4 > xo X P" 5 > f m: o 5 < w amk' mai a -* O' 0 0:0 OOO MM- X' M<* o OOO O' 00.0 *' Ml Vff ~*0* -4 ov -* ** Jr o ooo o ooo 006 -*x X H>.xC vn* o so * o m o *** > oox m r* Ooot 0 X' -4 < 0 X -- 4 4 0.-4* . > Z> Ha x-e? ^o r- ; 0-4 O'C > r* 3Q O 2 its X m< oA -Brco M <4 WItf O ooo ooo M tM ^ 4vn4 * o ooo o POO IM writ UCb -fir vnc ,o ooo ooo X X mi 4 vn ze O X03 m * X vn o O -n i 4 OX 4 r- O. Xm X- ' 4 O: I * '<&' . CO I Ml a* OM 5o? - *-* OOO o ooo m* M.BW WT0 o Nur o 4?JT--i OO O vnp\fl * o vn m* 0*4.0 >*>(* rtf atJh vn vn-4 w or -*rvn o. ooo ooo ant O' M\nM oo -- o -* rwM o vnr o b*n>w o .4 VO 6 M0 OB UU~: caMOB ss o ooo ooo 4 o M JTW ptaM VTM W w jr -* p -* 4W 1 o vnw-* o O Bw4 CB *4. O *4' > r' XX r*i i jt p N om 1X + o nr OV X -4 wfc 4 0 t X/ o A O jjrt>* * * * O' -- 4 vnttf-* o OB *4 6* * 0 vn UWN Co-- b sivnco H o 4 > r o -4 m > Xo 03 rcm 03 o >i o cu Xw 4 03 ~n > oX X > X r -4 oO XX m Xo o *n 4m r>- X r X > om p 3 OX4 X 03 -4 O vn < > X 03 X < | r* <- X o o 3 rn e X CD > X w 4 > 4 eo> >X o > o n; -n X co 0 x O VO Oft smooofrodno 9e-v 00C -*C\2 vi*: o >c m 0oc0r9 0*0* -4 O --4* 8 2 00 . * ca > 200 r .04 rt X 0 > *kOotc2 Vi* o * Om 009 OO 2O * -- 2 </>c\ o -4 -- m O 200 2 -4 ' - O" -4 > 140 2 r* ^ > 2*0 r' n 0 w**OVc2 2-- -n c >'' V* O _ 2-03' -0o0n2 am -- >. OO z OI W 2 . *ri M > 2> O 200 r Ow -4: - O OC > 140 p ~ r* : 94 FI'S -4 m< P 0*W CD 0-4*4 o OOO 0 OOO v; .Pi . v 000 Oi OD'0 0 ooo ooo jr w -4 *-*0 0.00 OO w o CD --* , vPi 0ra9*NoVovI ooo o ooo o vOi0wv 0o w0 ' wo' wP 0' w CK 8 ^oro 0 ooo o ooo 14 w -4 OVIN SO VI0O o OOO o OOO NO-*' . i < vjr ooo o ooo 0u ww W-*04^POo OOO o ooo oO -O4v-v*O.fr O -- Oiw oo wyo*iw 0 Ui0fij ov row 14 HOOD VI O ooo o ooo: w TO -4 OVfV> -4 WO0 O OOO o OOO PJ 0*0 0 WO'O ooo ooo 2 Vi C PX 03 m o V o 0 -n 1 -* o O' X a% --* f* x rn < z w o Vwo\I 0-A \Q-*Ui woo o OOO o OOO- O PVT O CDPO -- 0 -4 o wan p w-*w 3W> r* 2 rin >4 VI' o Jl II* 0OV *9 mz mo 0 O 00_f\15 W 6 ov w o 0 -* . p V0 0 OWW O 0*4 0f\3 f*3 O 0-4*0 OO -<4*--4*C* O W-40 O -4-* OVWOi O Ov--W O -e4t-4ov TABLE A - 35 SAN JOSE, CALIF. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1080 6286000t-0dna S -O->44 r~' v0v-Oo05O3O*Qt>N-Wo0*vQnCBC3trff?ftC\Coo9izK. 4' o *4> r zO6DS. - -j4r. r .*-* -4 04 0 Of ooo OO OHk'' OavMu-rAo 'O -4 o . ooo ooo vt jr T w<4tw 2o JTCOOS ooo o OQO -oH1 > r *<VO-OO*JA0OOo*<V/3mvMOEc osxOr.nN>-oOrO*o*oo So--1t . mX-t SB >r 2 < -4 -4 >r- vuOOoXQ*<NNv4*-O*OVOo O/O**TO>>.nmO<XOooO/v> Ft -- X' amX -r>4*' o <' >s--r.wox>c < 0--2a->-6O' ff IroB><> u ro -4 UW.C04 jrjroB O' ooo o ooo CD OI-* ro 4*4*4 o VOWl o ooo o ooo jr JT VO obvw w raapM Q ooo o poo w l\? *4 KTNOUt rv U*fN?VJS o poo o Pop VO CD Ov.Br VO ON^?VO OOO o poo Ul ON lUO JT- o: OOO ooo *t t vo: x jv c 3 CD m *HO* js O O *T -- o' sO x os o r- o -* m o x. s r o CD o N m* OJ vjijrhj <* 4 JCFv m jrcoo* ooo O' ooo o--vt row-* CD u --jr CP -*rovn ooo o ooo e4vrrr\o)u-^ roc Jf Os -* -* p 4 NOW o ON *4 08 o os r\j--* o -pwro OOfSJ O' 4O-G-0S AifOOS - O' o OO0 - -*4 -* -4 oo o -* . ** 4 09Ut ON to BTOn -m *4 OJ O' o ooo O' ooo -- o PN -^ o J?`X? uteres --A O' p W M ?' o foraov o \jv -ursj 4-4UV b -*VOO H H > *i0'' m t ip kojt o yt -o o r> o o FT ON X' O -4 P !*4 O t SO' 08 O ai* OvM-r* p CD *' b Ci.p * po 4' ** odpo b NOUiO O UTM-* p b CO N 4 US ---a4* r TABLE A - 34 SAM FRANCISCO-OAKLAND, C A L IF , CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND ACE OF HOUSING, 1980 o86ooofr0dna ACKZ O SJI* o H * om > oox r oo O 1 v> 0 </0 z -1 O--* 0 0 X > * o >: ZsOO r XvO m 0ro Os0s0 o OOOOOO c*i f\>- 0 vn O-O 0 SO o OOO o OOO 0Jfc M -* 04 fPvF Oi fO\$ Jr OOO o OOQ 9HAC *-OvZ v* o .OP1 oox oo O 1 CO </>o -r. -* o -r4 X>'Z > r* Z ova xvo n z mm* zom z -X4 >r o H<f ? r\ a* oo OOTOONOOO0 ru rovjtu CK iPovi o OOO OOO Z ri>- O Jr-*jrro 0tois> OOO o OOO -s o-i >r vUO-oOCHOo<O>OAi/>X4FeoZCs0f o--* x>zoO' ZOXm>VO03O _ z z--0mX-i > r om-4m' < >ZrrinzX0>o' <--x0OIP*>-CO44A ' CSOi ip jrro OPOOOO*OO* *4 ovnt** A OvxOJr O OOO o OOO v Xmi Zc o X0m-. 3 50 o X<9 zomXr 04 W * -* (> JT-4M o OOO OOO vFro* 0 .C\OU 0 Osip o OOO o OOO Os M -4 u 0 0 v JrOs* OOO o OOO w rp --v so 0*OsS o O o:o o OOO o w o*K} O0ip O' vnrp-* 0 IP mSO o vnovji o OvJT o: sop -- o pifO- 9 JPO-S b ssout o \jiro-A o 04 >10 b uiwro 0o jrw -i 9 CMSO 9 bob Xm X om .OO' CHIP-* Osl* 0 -* v*46i O ifnpu*v-* >lbb o OvM- o -. S' O' o si\D jr 0o vnfp-i so-sfp b boib o Vjtfp-* 9` jr-jvo 9 bbb m3 o jrwro o jruiO b bi-r 1 > r O zm. CO O' CO zoco *on XO' o sr >r; x smco zzo < 5Xco 0-<' 5 zaozm: x 0>- 5OC- > 8m *on woc* c0o TABLE A - 37 TAMPA-ST. PETERSBURG, ELA l8600W0dna -V w*OvZ --4 > on > o;oo r Hi O -t > O 0>0<v/* sO --ro S*C O0 3 OS > P nO9PP 0e y1**%0* ZO m ooO'5? H O >r~ O VM>OOS 90f--ir* * . 2OP 0 nO z-H 9 > 9*0 PI r* n <AC -*<7v2 vU00* O9m rn -4 oooro (5<fItVOt r9l > 9f*i?0 r f>- XvOp OvO 0 9P -f PI < >9 Xw> "N Z> Oh** OC 20} ?\> m* 00 Povro Ov OyVjiVJi O. OOO O ooo fir- u CD CftCD P* u> OVPCV* OOO O ooo XT P* Ul vorw -4 mw v O 000. O ooo froOo% \o-** . v4n?vwocoo o o OooOofl 0 Na fir W-4P 0 OOO 0 ooo w ro CD VOUtM ccw OOO OOO fir Pa u Ncu -* ox COCrvvO OOO 0 OO vji-*vn uoifot>oo O O' O' mI* CO ro Co coov 0 00 0 ooo a* CSPC - p) NWOI OO 0 OOO ro at fir fir\6-* O ' O OOO 9 9 mi - u ' ui 2 C O3 GO 9PT 0 1* p O Ov P 9r-; PzI; pi Vo0 oo vo coca VooOooO:ooO o dvrss . O CBISSCft 0 y-4i--si-Ni 0 CON 3 Vftvoz 0 OJO&fiT o --~ i- ,,--> O \JiOi : * O Ow n <* 0 0 OUIVJ5 0 mXi0 *fifir 0 we* fir O ONFSS O j?OM* 4T0D a Chpo -t O wirors). OUOV L*. Otk 0' 9m 9Pi z-f Uita O -*4 fir WUIPtf mX sA O W-* O *NVJIOK O C&*Sl VJ! oO WfOVjl O 9CVMJSI>VO firvO-J zom0> wcr o o *n O 3 r" 9o m 2 O -n > r 9' > o co 3; ' 3 m< > 9 0) os < $ o o P3I. 9 9 > O S* >-4 Cos zo>. > m o C05 VCQO TABLE A - 36 SEATTLE-EVERETT, WASH tABLE B- 41 LAWRENCE-HAVERHILL, MASS.-N.H o <O0S 0 O^ift N rrtfy NOOviA 0 (ft iTNJf r <vin OS0 o 0 >0,0 f" *T SO .o :23 O UI ooo 00.0 o S Qas ooo ** j?-CO OOO. Q WC4*Js .0 < w a9os auoOUsSil oNOOS oI fib IT OCVcI rttf\ oo jnincu o uv*o^s.r p VfOV- NO<rVCPU- P 0 ifMTS c tCfSSIMW.tfNf 00 SOI^-f^ 0 OV-lNtlfi o 0 O NcyOveo 5 uanis. 00000lf\ O O ** 0O:O0OO 00 00.0000 !**. $ .CUCU.Ift * * Os r * (V to 1 > tfV o 'I OOOo OS OoeouN Oo*oO*oPp*>* oOos r .U*l -0h* so V) oasi -* SO g2 0 0.0 0CU 00V.O04 o too 04 ooo ooo CU%9CU w 0 1*9 ooo 900 awi-Kirf o so ui u <a: o .OU0Si 6* .az0s PfOo"-SOorOOol(f*S) 000 >0 oooroo-oojfOr oO in Noionoooo^ CooK CU.CMAO ui aos X Q lOu ^ui Si UI 0O>NOS OCX o* -i < *- .0 ur J os as 5 u- oSvS o * .< h- UJ CK OsO oO eAx Q .zW10 <* O-ar-aos o iota aUsI v> i o acoooo mcez< o UQi * aas\M>- aUsI P *Op'OoS MOV> iO o1- X oo oa? au0s o*o*T\ zso*- < ov-o*-e0c o X iov> o> 1 o -- as oo.oo U<* UQIOtfSA ' aassM^ B-42 DUP040009832 TABLE B~ 40 LAS VEGAS, NEV. CENSUS COUNT OF CHILDREN OF ALL RAGES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, T980 ftJO O -J < Pt\I0 H CY'C o O * ihinp m NAO p 6 D **ey off f*- WiO o p o , b h* Pr* u* O zUJ p u ZUaJ. 1 4oA P r* ,o ON u or a. -j .*<o 1- tyff ff PlAin o o o ** ihff n . > : PON N o p.o.o .OOP o p o o*- ooo o POO *aT*O- fP"- fr"f IfXtOPJ COr- Pc--o o o V m.N in 0 \dvpoor>m- p Ofr*ro .b.vom Nff <o o o ]F ooo 0.0 0 fSIAO*- o o m cvj >-m T"P- o o o T* tAf^ ` . p x -nropm *o NDAIW - T i o f"* **" b *-ff ff o O0 O0,O0 me- co *op\fow o o o fof o to P f" 1 o f- -Z p UJ z o-J p Z o fp-- u t o o ec P Ui CO Xo m z .rwpI- z OOO ooo OP *-.ff o o m VD OO o OOO P--r- VQ ,off cyff p* 0.00 o oo Mw ooo o 00.0 fffOO fof *-*ow Vo ooo .0.0 0 ifNCVNO cuff . o o 40 00.0 0.00 W/viA o oin *" OOO ooo OtvrOarvPo o . p CM N boo poo -- o n mp ,j w ooo 0co,p0er0s* oO n- > ia ( PZ >*UJ PO J X o OPX -< oo o* >* H-O <Z < ff Z **-.o oh* .a: SO<J> CO - </> o >z oo Z-J Ui zoo ^ " u UJ *. mr o m z< 3U. z ** X*o-v>v> > UJ -J oz < PO z OPZ < H* o * H* z Off z o u Q %mo<-/>O v> z oo zoo UJ o * t- o tn :0 Ziflir z </></> Ui PZ P.O -J OPX < O * t- < to Off z >< o x \oc/> to > i o oo zoo <u- UJ o o o ZsOr- OV></> B-41 DUP040009833 TABLE (9- M3 LORAIN-ELYRIA, OHIO CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND ACE OF HOUSING* 1980 2 O' {Oftr O *-*- P s p TI P Os XW ,VPO eOc ri- wo .fi- IT .P S' p I a- O *co o. *-P *- f>p r* P.P OO OOP o OOP :fC*WOCNU1"P XP* 0O..O0NP CM 3 .* > * xor*P* o' o oi/vm pro o 9v O O*M P OovPfl <ow T-Y-P Q ee X0C0Q.h*0p* 0o3 p PO0O9 mro X .PX 'Op4> CMtfVN OXf* O OvN SO PO *~ps OVXVO po roop p Oty*P- ooo ,P-O*f*O"<f>0. ~ jpf <M .of0lOo.r0-oO0 O OOv co 0pof0oo,oor0o - OOP** X o' ooF~oor*l oO 0 oooor-ooPO o to 0fCO"M0NmO^:XO00 o tft ox00xo.xo0 o CM * CM OooOoO o p*tT-*V-flXO lO>v* NU OvC 33 5S p -J .K< O#v.e. PV`*>'0 H* 0 1 o X .oo <-- w u wcooo* XCo*z< X ... 3X*000*- MwM oooIsPKrv*vrXSi* < o X 1"* 0Pcw^4OooA Oo. X 3400 as OOP*vXQ ss 2g 0<s <-tO1r 00co0oI oo uZo.p0.^m>.> 300 B-44 DUP040009834 TABLE B- HZ LEXINGTON-FAYETTE, KY. CENSUS COUNT OF CHI LOREN OF A LL RACES 6 MONTHS TO 5 YEARS BY FAMI LY INCOME, URBAN STATUS AND AGE OF HOUSI NG, 1980 <t-HJ- <pf*iA 0 6 --6 w o. to Oh 'O >AO p mw>cr\voi*mot.t o Y-lAlO oufun **wm p .o IV-WJTin o vch PF-*6>J ~ P 6 p >0- M X u O' 1o ir UJ s a. rt Pv : ino.r-r ^CSJVO o ' : mf r- in P *-- YO ifi 43" COP 8 - at o N*OO P CNJONO ncvj m o mr-p o in*aoN.- P-Pm m P . o o PO Csj-sr*~ Y** o P p- ooo ooo . cvrop . o N . ooo ooo *-T JT P o o icgp **"<V o Ptff . OOO mi>p- ON o\ w OOO o S'CVI-P ***OJp O . P* 0oo0.o0 o Cvj pf ooo ooo o ro 04 OOO o lAP *-win o 0in ^ ooo ooo min. ** CJ 4r nr ooo ooo N-f O * frt O o **> ooo oo P"AO.J3' jsun p*> O* UJ Os W3 0I>vUi Osp OOVA, X -j -< P<-.zO W- <0-J3 .03 *o<oIn o C3X< <U3J tf.OO UOJ o * XNO*- Ul J C*03 < OsO -J 03 ChX < >p * Z u o o AinO<8/> tCO.O Uf O o Ain Z<.p/>.<*/>- UJ g O.OiS < H * O< V? o j o ooz X \o<n 0i 9 0300 OUJ ^ B-43 DUP040009835 TABLE B- 185 MACON* GA. CENSUS COUNT Of CHILDREN OF A l t RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND ACE O f HOUSING, 1980 OmAsO -J < 0vs0i*> o h cviesj^r O pspw POffiO ^injr o nh-*1 I^CWP P o o O On o f!0s H- Oi Z >0 UJ oi o-- ZI UJ O o. in O' ^* m 0> r* 1 UJ .Z .CU . -J o H* oo s0.iT Ci r- VO o o o 08 90-9 p o' o # * SO "* m ^T.rO.QJ .&ca.jr o o aaa o Lfs *" MfOlA o o p- .CO \0vO f**"V0 "fOlA o o cvsna- * SC.lfYVO ..0 w o' * o o OOP OOP mm o o o OOO OOO 0SV(M.S0 msp o o rs* *! Osh^iT *- wm o o 5C.OZ meovo <Vrl m o o p 0 * <oso*o c j c s i -a* o :b o OOO OOP po r mco>- *-- o o m (CM o 0 01 1 Z Oi UJ f Z o -J Os -? SO Z OS o I u. o -O in 0s Z tUJ j CO X ITS Z 0s tL Z .A. OO OOO m^r vo w~ o o in w OOO OOO ** OJWCVI o o SO >0 0.0 0 OOO OVSO*- -- so Csl OOO p OOO o 0v0n so ju OOP OOO ir8.0s . *-csim o o -rr o OO OOmOe -o j c \j o m m OOO OOO ** S0.J0 ir..sr o o CSI o oo o oo o SO 0.0 0 OOO 0V0SJP o o . m > Ui t- OS 00 ^UJ ws s 010 OOsX -J < SO OA >- hr .0Z o <Z V) > ZJ <X <z .l--z Uoi .** vvO><fi> zoOoO UoJ c*m.* K z< Z Zso -- u. > *- 5 w -J 0sZ < oo -r ec ocsX < )-- o % u Z Z'Z o uj o - O </> z *- V> I O wzooooo- ozK zo-\ o*m- </></> u 01Z . 0sO mJ O0sX < _ Of < O 4T.Z o jO O X SO0> (D V> I O . -J < )r- UzoJ ooo->oom O ZVO*r- U 3V> B-46 DUP040009836 TABLE B - 44 LOUISVILLE, K Y .-IH D . o GO ON o X vs>o o X <0UI o x< CO -.20 <.h* Vi <0 XOS/ XUPI U<. 5 Vi X < UI > in o >w :X' -X o X. NO OT Ui o -< X mi < u. . X UI X o -J X P u. o >* X .X oo w X CO X' Ui p f**lAC0 O -J .K< Cud WittST .0 G9G7 0O 0 GO .0.0 p o incvicv o **0JNO o #06SP 6 . <0 lAlft .0 p ro PO \l O T o r^pGr Q ' GtUNCN 0 CMAl-GT O 4 o UN ** VOGT o O - IT 8>.tfM0 mCM o .o v rr* W X J ooo o OOP o .< rr> *- m h"iA0\ M ow CV QDlACO KCNftl s. O O .fM0 POO OJh- o p t- p Cv 0 D ' 0 rO - CsJ VO . . P if-OP 0n j~WvO O - m GOO. f^iAtv CyCMGT o o *" ooo ooo "O.P lpvI-.-J0f o o CO N m .00.0 OOO GT>*.0 cvh*o *- *- in o p o<0 o V) T.1-- o r- X UI .* ec o -J --' NO .X0 0 T"1 u. . O ifc X^ UI co X tr X i UI X a. OOP OOO vOvOiTk O .O *" .OOO 090 ~Al<M CV.AlGf o o :tn ep .0.00 OOO NOr-Gf O o ' cr*v .0 0.0 ooo ,OON CVlAO r" o ,o N m cv OOO .0.00 fo.00 ro ftia'is. o o if Gf CM OOO ooo <0.0 Ov CM G? O O h- OOP ooo M3 VO CM CM iAC\ o .o p <V ooo ..ooo j- OiA Al o 0o\ AJ Vfi ooo 00.0 Gf r-.ro inmov O o <0 On > '"S.UI *- WI Pj-QC P j <x i -< X >* X X-.-} Ui <fiXr 0 x< 3 4. <X* UI OS 0>O 0X o* Gras NO*GO~p. V> 1 o oo a o.o Ui o * O *M/N Z\0- mi < to- H* > *- y UI -j On X '< On O mt pc 4- OONX O < X c,<a'.x o UI *~o K p PGO XAM v> 0.o0 EOO UIO -- O o X-P^ X DVW> .UI OvS OS.O mi 1oax < O` " < cere o >*"!* > X vp<D (0 0 1 O ,0.0 p tf oo <u - o o XM3- H- py>v> B-4S * V. ] J j !; 1 \j 'i DUP040009837 TABLE B - 47 HGALLEH-PHARR-EDINBURG, TEX. o t0o4 J ? OiAifS .0vO.*rt o mSO3 <IO **# o *o" * Otfh* 6 ff -- #a .Wff ** Pi.St-0 so u 5c o % o DWO 0 c wo o *N0 <1 * o o ortMrtrot o ,ofrt * ff OlA. o fWWff rot* 0 r* * CM 6 woo m0 Xw oK X Ot*' 1 4*-0o0c0v o o .rt* CifMt(rAtrCMt .roto MiAcy oo .rt* as hi a. O IT 0rt?* ohi 1 oi .>IT* eo^M * * .* o *n4o o rot* f*:p* o mffC M: o NJpf rt* ff -- r^cwos CM >0 o* 6o rt* .1 UJ X d < ooo OO 4OtA0 o ioff OoOooO 0tff : Ort* OOO o OOO o irvos** .m $ H <MM3A ff O rt* vAOMA rt* CM y*v*- LfS ,rt* rt* frt H hi >- O lS\ .5 ,o0o0,o0 eo 04 0 - 9VN04 lA >-0 0 OOO O 0.0.0 frftrOtiOtf o ooo rOt OrtOOS ff lAlx .oo in |rt H- 1 rt ,c tf> IX X X 04 H* Ui * X 3 1 ah 0!> 40 OOO OOO o OOO o ooo o OOO o ooo o 490hi X u u. 1 e ff. -.40 rt* lA 0rtr.tWrt CM >0 CMS0.CM C*rOt 1 X m 0rt4* hi j <Urn 9 ocr :X O' OO ooo O-frtf* * .10 CM OOO o 0OM0A.b0A o04 CM rt ooo o r0t-.C0N0O rt-.frt o CsMo of hJ Q O w .0*U0I OCvt hi -J OVOS 5 o2 * ui Oosac OOVX <-J ss3 3 Xwco (3 <h0*X5' 2 40500Ig K OO MO thfOiO> a2t X - 3X.s0O0"* H * * g .2 g w 8*?o X-- os0o.0o hi O a I- Q*iA O X>X 300 0030t0oo: J as < - 3OXs0*r0itA* 8-48 DUP040009838 TABLE B* <16 MADISON, H lS . CENSUS COUNT m CHILDREN OF ALL RAGES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 hAIO ' * OVUVlt\ O . ire * :tfYOVfv> fO.iDP* ^ *-* ihmea *..P *> n4 * KNCtf.l.WO , Q. cjuvm o .0.<0r~ *-*"! * Q UOI tfVi/V *-N do <u r* 00 OOO' bvd QyaCj O.iTktfV m*-* rr *-JSTlA <yA tfvwL rO o j O 9 o < O-^.N fO - + CM H CO OS Xo UI CO ml 9 VO Xp u f" u. Q otfV p X ,r LJ XO IT XP o.oe o CVi r* fn POO lAOv <v o o JT O o *o *f"F O (V 0,0 0 0.00 WOv O Q fO r* 0.0 O SOrtW *"|A > OOP . rt fro- OOO . *- CSJ 04 OP OP NWff '* * ifY o o 00 m N ooo OOP' fOP* <0 t -JN h* OOP JO o lAlAN f"* OOP OP *-*P-- j-eo O O to ui U P0 Ova: ml < OlO ml PO ml < H*-- +X* OP*X < H- x UI o'*r*--x >O- x< *O>>v-S < Ou* V3 V> I >-<--J .wOo* O X.~ :K O </></> B~47 | DUP040009839 TABLE S~ 49 MOBILE, ALA, CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 *-- vpm \0O O O rf o o 0* ijy=f i IA 0 b .G6G0 OP- O' X*r P>0 WO O' absi oi a, 6 5 0 O* "' kaa1s.l VOi- aiwK MG 6 MM >6 p cowdcvdiirt pd - *r>o .p U"\m W o b*o 0.00 o GOMOTkOG .O0 WtfYOv to tfMfVO* liYWG O. .0 . pnN b M KYCJ o WKO o f*O-mpiOr\ /o - 0o0o.,0p oo CmO.COKt&tt GNO *-..ov O 0 p* lft$0O a .VON a r mjf a? mvoos o jr.ojr GO .o0o0.o0 o%o0 vOiACVI .&Jt Oco O' t of** Xioa-usj s P O-' GpO* *ijl tocfv *-0Cr* k1i sss o oAirJt CO0O.O0vOP0lA *-N6 oOv OOO I0fl.M0O0 0oOs m OOO . OOO irvdTM MtAO p 3 OOovOOm*\OOmw 1OofNA. ooo o a0*:0* i0n 0om OOO ooo Gf* * * .o mo SM OOKMOOOOfOO>h oo G OOO .o 0.0 0 o.*- .OV G > JUI n u ; .h- OvX OsO -J V) X GO 0 OOif o- K< h-0 <x < X C-PX >* G0> WO 0) ! O* >X o X.J kbl BOO <co--r 5<] U X Ui O * X0pvG>^*A>r " >H* 0 Ui -j < X } X OVX AO OAX oO* K -1 <W o Uf o 1-0*-*0 o </ o X BOoOo LU O A zo 30Zv0O**0l"f\ w 9>e AO OAX <0 OOCT" K *rO 'X 0>Oi0o 0,0 .J X.O0 < kJO ,o o1- 300 B-50 DUP040009840 TABLE B- J|8 MEMPHIS, TENH.-ARK.-MlS3. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1! o* < WOvO o O eg wgy p H P-*y o tsiw^r , T-fyj'C * v^ro Ov.OfM T-N.lA b oow O CO O' o ho H Z VC :ui o ** X1 uo .a. in -O' o tfS 1 UJ x a. -j .< >-- o h- pe-tyiN W(M C*0V^tf"\ 0 , inirv o.* fO ON *- eo jff o o inm.ov r>n m.njeo b Q *" 0.0oob 0X0 80 -- eg o o CO X OP,<^t niftp o >*<0 o o* oo T-vo >-<MvO o. o o -rtf'NOP GJi . o o jy .*> p flO.^vO * **iSF ,Ob- SOCOVC OOP o o o * ooo 0.0 0 lAWIP* )6n t -* oo m p* eg inn .w>CirMuff*S7 o o*" ooo ooo vr\r- f* r-invo v-tM-ir b o ro OS o O CO 1 a Z Ov Ui .oX -J Os --X .X Os o U- o1 o in Os X U1 X Xo o in z 1 UJ XX ooo ooo in to*ro o o CVI r*> 0,0.0 ooo rOlfi m*- vo O r> n ooo oo NOP o o ro- boo ooo mom <M7 o o VO VO ooo .ooo f-*- *- fTXSj f!* b* OOO 0.0.0 COSOrt .r** ' ** o o Cr*M7 ooo ooo 4Nftl CM o o rXt ooo OOP P-31"T.0^S oo jy" .jy ooo o O 0,0 p m so KM4IIS > UJ . X >s.UJ as q -J XX o OCNX < oo o *- >-u jy.X c <z < *- o H* x VO</> CO *f> t o > Z.J <-- uZ o oo 1X6 oo o* Q3Z o in Ox<bi z ZvO -- > t o ui -J X < oo -J X 0X < pz OO:**rx p o iu -- o K o %o</> </> .1 z oo . X.OO w * po .ozxr* z UJ ox CvO -j . OOVX OA <H < 043* X o X2 \o-<*/>-o f"* co <f>io -J, xo.o < wo 0*- o '*in O z> r1- D0 B-49 DUP040009841 TABLE B- 51 NASHVILLE-OAVIDSON, TENN. O to OS z 0 8 ^ -p . 0 ONWO*- 00 x n *i-iWf-*OAs O 0 X UJ XfOOv 0 On to.CQ iQ 0 0 a r* -w**-PM-p 0o f-P-lft CNJVO o OMfl --76 7 :O z< 1 w0 0 < H H* O' pr*0V 0 VS ZU NaO 0W*E-MNlf-t .0 *- if 0 *- CO x X UI o X tf> .0 Ch 00 0 NfCOMIAlAX .O o P-WM O 0 .x <*.* ..o o <*-Cf0O.lnA o 3? > -J OOO o OOO o 00.0 O > Q .0PO.0Cv0 o o NC0O M NO : OOO X P-X 0iA ^W NO *- Oil rt OOO POvNO0vMrt o iA M ' f* X < ui > lift o X O' .Orn0'rO:tv0NOO0 .Op0 OOO OOO "MAW o On OOO o Or^rOoO^r ^o MOON O zUJ V X VS UJ ' 3 si >0 5 -2 I wO oIOTN 0fO>0O0.O0ro o o mfoO P* OOO O 0.00 O WfP-\<0 '-- XOOOnfOOI-APOOT-- :pOll\n * M X X rUJ J < z0XX .oIT OOOOOO i-W*** oM1o-. OOCOOOP-OOo n Q AIAt OOOOOP N zUi X 0 UJ 58 oxxz0 a o ooW xoo0 W 1ZUI u 9>s -S.UJ cox CO J < .zUX!J- oSSE VxNo>OooxV0ooxoo *e O ua.m, Z Z\0" * 300 < ox op X* OOsX OA UoJ 0*.0*o 0.10 WO 1b Q *tf\ Xo *.i* 300 8-52 D U P040009842 TABLE B - 50 MODESTO, C A LIF. o CO on r* O .mcy.<r> b Of- Ov .Z --I < -.oo o P-fTON O .r JO H- fvcvvp o ,r~ *-evm . r-- *-tvys f-- ok .-x u Uf c AC OwA o p.!> x* a> . a o < CO .O ax o f OvQ\ 6 On -O I- B* f f i** o Q i- ,r- XI <C f- : *-> h-- < H o> VOX ,o 0N A* . ' - fO ,* . . W X .VO o *OO.iA o gVfOr- UJ & PJVO o tVCViA f-<V X p -P- w* * < Xt . w o X X in -5 LJ Xo .o X o SOXi o VN -O**s co-o tv tv te\ o f .9.0' 0 OSf 1A o o *o a> f eg ctvo o ir> o'.a . .T- w >- Xa. i <u. > ,b -- 0-00 o ooo . <h:0 <V *---' * a *- cvi*- ,oo -A0a.0eo egro.co isX 00.00.00 P-*tfVOv tOtA A p- p <IAv * ift X < w > oob . OOO bbo .1c\ *o- CO a.**s ooo tfVf-iA fo- ma i pO-.Ocvi Om cv VO ooo CV-OVOO V PfN i/i fc- X- z w ta--. XX o X NO 0v AO X Ov p OOO o 0PF>0T~.;00% om p-cg a oo o ooo . Ova eg X ob . o VO i-- CV A 9 Ul -.o < X Lu o Xui ioPi JF" --JJ < k. X X X iTt 2 0v OOO o ooo 4o? OOO ooo On^ f-- CM o eOg a boo o t0w.0o y f*-cv A .oX Uo zo* t0UzoJ > *s<CHnO-o.z.UQS4 zct<oc--XW>--<l >>- p .XIzup-<-Ji z VN>OA.CVaff>AvvOuoxXXi ZQxUJVoO*oot*f-^\ O -<HoKJ-- - . JX-<UzpJ-I z hzO- OQvvUXJ "v9U\xO>J:V9ooa> .xOo OzVHr* -J -< H- <tX0o 9vOO. o10OOatVrAoNvUOxXX;J H<tf-- ><koV-- xU_JooOAin> 3ZVO<p0- B--SI DUP040009843 TABLE B= 53 HEW HAVEHfaWEST HAVEN, CONN. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING,, 1980 *M>VW0*iITftv- OO> ^ s#ofU o --6* ^:* A0VA oo O' NO UI ucc UOLi s 2 ui _J :ph<` *-ecf.ty-if NOSO o n tfi . Ao p OooOo wvo jrmr* ioo*on-- . OA5**--8-*<sct\oii mtnjf - .o mvpjcvi ^ ^CsW-oPp OoSocrtoON *O0o0> P-.mco o . - .3* <V o cv.A o ^ 6 - C\J A .OOO OAD*r*f.OlA<ry .CrrVyJ to> 0 -GOOI 1-os T so CUOi CD .3X 0 IP i w1 f; OOO O OOO O CWfOON * OOO O OOO - MN " Oil pnp ooo ooo oo f'-PMPV Ok New^p OS OOO ooo r\C0J JT o po> A OOO O -OOO o r-A ro- OoOoOo w -pPO o ohA 0-00 omoovYo" A o A vO ooo Ao*o6 oC\ r- PO* OOO o OO O*-OA eo zr to o VAO u X 0 <-KI OvO JOP.O%XS N0V> *zs o o oo Ui OwoOpQin.f Z-- 3XNHOI~>* -<CJO oooovoozUcI Z O^K UOi zP- v'zG>*<oo*.1#-ooO0 Xuo Uoz3\i0oOp~0ipn- v<> -J <ufcp B-54 -<i DUP040009844 TABLE B- $2 NEW BRUNSWIGK-PERTH AMBOY-SAYREV 009 -J < 09 CMP o -'Wirt p O CMifY p P o i- On VOW CO W o ;c :O *;* o MM3 VO .oo 1 OIMO o 06p V* ooo 0 . OPp oo < oN m3 < z< za P O' XUi *o0 oZ . -1 Zw o \C\ 1p" tfVCO o' -CMONiAi9 $5 CM PP* o X OX0 o ,x p o O*-'CO oo Ui .xQ X >-I . . . O jp.*** coin o .zU&1i *> o MS09 6 o Wifs o p oo Xu<. > z<UI .<J otfYofolOooP 4P oCM CO YOo-OoOoCM oo **o vooCOSMooTUoo^fN .o CCMO X > -zXwOz :w POj -Q-zwzoxJ U. o1 P*1-i, 0 .0o.oC0M Oo ooPZeotfooCSM <oo0 oo0O.oP0 to o oocpoooo CMSO oCpM ooopoo p -oooO o0M.o0So0 -CM ooCM o<z .UZJ SpS _* CO < u o Xui ZXa .PUzats.i vOOo OOCCOOMM oo* -X o*o*oo^ootofv VoN OPOOOOOCM o o09 p z 5u p 2a o p .aUpa?i \awoX <z z<PzXU<-X>i. > 3 mi z< UXI p X PZUI OpO^PP*sOX; C\zUODOfCoOo1PoooioA> 3Z<OP<P -<J .o > 3 X<zUIi u X .mm Xo OPPPOZXtil ooz*z "<UVzoz3POi*ooCCoGOP%-oOCoiiOs* -J < o UI v> XCO OPPPOXZ VovQ>pctorp*eoooe: ml < o <o zOXU3oCOP*otCf^SP B-53 ' : f. ' j : :: ;J ; i '} z \ i y j; l f DUP040009845 smooot'Odna 9S-9 </><r>c V*'OvSE` m > oox r o O 1 <ft CA WOv 3 -4 o-** (/) 9%9 o > > 3n o P" n o 9 m ml u CK9fi> -*9W o OOO. 0* COU NO M-*Ov O o ooo 04 rv 8 npo NO J? -4 C0 ooo: O' ooo 0WC z -- CN2 Sfi* O o < * m' 009 OO OI </> 2 <f>& 4 o * ** PV O ?<ro z -4 >' 3*N,O O X r XNNOO m > r* o -f < vw veto ooo o poo 9 OS Vi -* PO -O-* o OO O'OO vO ce sO!V-4 O aoo o ooo KftC -n c y4i%* - `2 z >9 - o m o -> 00 9 n r z : z< O <A *4 <OOS 9 H O---- > z> O 9,9 0 r ' -4 O O' >' 3NO o 39 r n o ms. 2 NO H m< >*4 2tV-* 0 POO ON O OO OOO -4 -4 o-4w-w O ooo O OO a M CBPO-* vnwN O' OO O OOO fcs >m9 i O M* zc O2 m. 39 JN o 0 1 ml O o x; 0oS. r- o 9 m o2 -4 0 1 o 05 O' -4 9!N> ON --* NO 4 1V o OO o OOO M Ki--* NO U)'4 04 ta NO ON CO" ooo O ooo ro 4 rovouT ON CD ON PO. Q OOO' O ooo ml. o JPU-t o Oy o *nO` On On o p V 4jn-u44t :*-4*. p *4 ft? . o O'^'-O fOOO . o U 9-* VJTVJi 9 dowO \*mol v*4Vu4 p IVH s a -- o fOWON Ik- O' O vUjtUrvVi fQNj O CD On \J* S v*44in|0e0 --9 w*CO -* -slPO o P NO ' o P4^4-* || te I Cv 2 { I i O' ovr^-* o 04-^' 40^4 O CKW o ONQ45 o Cto'Vl'44 6 ONlVj-4 O' osn w o ONNJ^O 2omV9c) c nx axr > > m w 3 o 2-4 X -< m > xco w < f -< a O' X X m> w--L > 4 c tfl > 2 > am xXCrt 2 P NO TABLE B - 55 OKLAHOMA CITY, OKLA. z*86O0OfrOdncs SS-& y-tKwO2Co on POX -4 o H- > r* oOo CO to H OH > -too Ox'-p**--.' I'.O *O.0 C3O > r* OP x Pi rn ` P -- 45* bp- PPOOOP w O Jrout sji o o 0GpOo0Opi ro till o jrpui P-W OOP o OO <o<oc 2 t4jiw0x2o'- O H *PCOOonX -- 2 -4' o H O</> 4o6-o .* . am 2 H >r* 3.SO O' O so XP m X > r 2 ' < w A* aid C* op pOOoOo' v CPi hwif-s*j-o4 OOO O OOP -4 JTW m* UV-&PV3 Q o:o*o Wv--js,O0SCa2 vo.nx oo 2 m 2- XC >3--x>:. r-2 < HOHI </> </>Q\ XO4' T*O a H X > r -- -4 2> OH OP > r 3 SO OP XP o 3 H m< OoS VJtOsir CO ---- oo OpoOo ISO Vflf add -- jr otg- OOO o poo at A so rg o oJTu-4t w ooo o OOP XX m: --i - P2 O c3; PI --P X O' o ~n l o sO x *4 p r~ o X --m P2 H O 1 -- P OB a H WPO-* y (* VO Ovu a p oPOoOo a* p WGJfSJ o >4x0 (** G fgp -* o tfua o vjrvip * . p SO-4 4? * p O' OtOPi) o 4CBUI -- ui ;-- uoi OoOoUo1 o OOP A Oo' pp -- avo o OPH. o p b vnp _* oo CdT wwro o P9 os rg ro -- o Xof d: oos ooo o ooo a o ojtdiro O' y* P rg --os ad' o fU -- o Os-ff o ttpb* ' aaA o m rg -- p tgov b rg-4 -- H H > n X" X r*f. p Ui O' P UI X Om 1 X: -* o P rr 2' PH P -4 O' I p : P o 4ro* o -4UI-4 o POVJl p VJi&a p 4 SO o HH A oP xrca -- P*P -cr --yt H > om 2ceo: noco n o roXm x g rr CA 3O XCO n< >x to < I moa3 xx > tH>CHo CO > 2o >n oX Oeco o to o TABLE B - 54 MORfOLK-VIRGIHIA BEACH-PORTSMOUT smooorodna 8S-8 *4 -- OVX o Wi* o * .m > 009 r* oo O f 52 </> X -4 o --* CO O XPO > H *o > XPO r* OP XP 00C X --ox 'W!% p ^q 8 oox o -4 mm oo X rto i o> <AO -4 o-*% m o XPO X' H . > O' " -4 > XPO X r OP > XP r w-- QtX. s X u* o IQ * om o -*> POX m r*x oo X' < OI0 -4 CA -4 <f>Ov (JA X > --4. X> O XPO r QM 4 *- o PC 2> XPO r OP in m'v XP m WO--i *Oo--WCOo--MOoM-- UooOl' Pmop*oomoom-- rv> -- !S -- o *10-* o opoooo Oi C&0\ -- O 4*1 MW! o OOO o ooo o o OolVoJtOok OOP' Wl CM -- p OOi-tf p: ODD OPO o O'OP M Jr^ro aoooou o ooo wp M-- i*jr\n P wur o OOO OOO o CmMP o WMf-- Oo woiw--w-- o %--J1U4M!W-- w -- o W>U* -CD'O p P-4P Oo p0*oMp O o Cw*o o P VJ! CooM* CoOMoO--oPP Cfc OPfO--P-- o ooo o ooo OMt P--\JtW O OPO' O QOO X m I fcjo! Xe O' X -X oJ0i o-Pi 1 --o b>p X- o o X m X O VJftJfO -4 \Jif 9 o ooo. o ooo O' M o w-*Jp p-- O WppMufg * X m r [o O' If* X m Xo p. IS p 0t ---- P fPo' Pnju--j 0 h--1o 0' o oo Wr!owt-- O w o VyJ1uWgw-- P CD'PP p vi\j m P --MO P PPM >r TABLE B - *7 ORLANDO, FLA. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 6?860.00fr0dna S ZS-9 Vir. o om o0o01 9<A Ox jro S38 35 o n HOI ss s 0vHvcm* XO ' O0O0 50 Xm-_ 'OH a vt*o</v> oX--*'C*OO. oXH8 >r ZSOoO CO t r* mo me >V-- >*omSOB oOoooI >x<o/>\ xomHX' >scoo -> 5*' -? <H/> SO' * x..-es'yO&r.oOo' >f" o O' o1m(^c0s* m 500 w 4Wto HHH O OOO OOO a rao--> v o*wv* ooo 5 OOP A 01 W(N* 8o n c *h ooo o ooo: w O* jrvr O ooo O OOP to -VOI VSO*MHO** oc o o ooo 0 VI rv VI V!^9i o OOO o OOO O H * o OJ0 o ooo o ooo -* VI h n h Ov N>HH . o OOO o OOO ft* rs> V t o oo o ooo OZ V! Cs 09 m. to. 50 --sI s o 50V smro3 Ho*o mx s lo 0JaS*' Cf'a8**-H* ^ o o o o ooo NHsi vOHiOuOf-vmfO o ooo o ooo ra - r\5 ' vrannjriiNs*j o oooooo o .UiftH o CW SOVN VOlVOi O VO*Cfa9*--** O'-* o ora 0 e ' 8 \>-* CroK4Mrw-* o -JVH H-* M0 O OOP 0 VI 1 bO Os o NO'C . * o WT*ir O ' ' * O `SO o ' HPvHO O Hp --O 8 PHrr*oov*B.*' 0 HV K p PMiH OO' K-*h (ou0 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME* URBAN STATUS AND AGE OF HOUSING, 1980 ' TABLE B - 56 OMAHA, NEBR.-IOWA osseoootodna 09-3 0>C -*Z UV 0: O rn 0 0 33 oo oi -coot O --' zxr SV*OoO o30o0 -M O --I > r* m X C > v>v>c z. \--jrZO -o4 * on 0 03' -- OO z- O Vr)<O/vv- O --i -o-"** m o*4 33 0O Z-4 r>* XO'O' O .33. zo m r* <--0ze *VJI* nr --z n rS>*Tt zC3> 003 m -OooI <A z-4 03 <A Z -4 -4 o --* z<& > r- Z0->* >- x. ^oo ^o OXCPft" r* oZVoO ---4 m< 4-O OVJ3JT Oi v>vn o oo o o ooo ooo oowOoo--oorxor o NJOo?rOo'-oO W r O -4 - O O O OOO O UMttto' O' **-- O UW oo oOO --rj O !** O' O Sf-* O'. - 'y O* c* O xr-j??fsj VO -- OOP o OOO VvooJjtI V oooooo Nrooo nr oo. o -- vfii -* m --.fir O OO O OOO o yhj o roviro wo o \Mo ww O V'JOiO^ O vrtovn or-jr O 0xr o opo o ooo iji MoOi' ooo ooo voO Uoo>ooQio o i*n X CD mz 0 *on- --1 O P Z- p --r Oz' -- (Ti P Z` -4 O oo OOO poo -y *4 \jv ----VO O' 3r:-- XT' o w-&o O w uyo Pm' P tft 0 1 _ zrzor ro p p -j 0 1 pa wr&fo o ooo o O o O \0 o &ftito O' \fl O f\jN TABLE B - 39 PATERSON-CLI FTON-PASSAlC, N .J . CENSUS COUNT O f CHILDREN O f ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING* 1980 ts860oofr0dna es-a o>o> c -- OsSE V*V o * O PT 00 79' OO v/ </>0v *4 o--* o 39 4BT.O 4' * O > SVOO r O' 39 Nffm H O --t > r <flF > --1>2 SaB Vs* 0 HL * om 0 0 33 -- O'O 2 o v> O -4 o -** m P 3BXTO 2 -4 -4 > 20 P* O V3 >' 39 VO r~ m o < {iwftc mC --:CvZ 2 >2 rtVP*.. O' * om 20 --> OOP m rz oo 2< O I <f> -i </VCA 2' -- -4 -4 O -- 2> O 220 r o- -4. .*' ' O'O > 2VOO a 2W r ovo . 20 -4 m< 062 w-- 0-4 -- OOP a POP ro -- J;r VffOvftf to VP-C* o o OopPO ---- VO vira -- vO JT-4C0 o PP'O o OOP w l\9- XT Om**' o OPO o ooo -- o -4--ro 0-4-4 o POO ooo s4 O -J--* -* -A o<*rv> o o oo ov ooo ---- XT- Oxr o OO . o ooo A XT SJ o -4 XT'S o OOO o OOP VO Si|.--' o 020 o OOO o OOO' 2 2 m i mJe o2 vs- c. o 2- co m -- 2' v O o n 1 --- o- 49 2 3V rO' -- 2 m f 2' *4 O- -- o lo XT o* * CO W P XTVO vovnvr OOP " poo fv> -- M *4 X?mO o 0 0.0 o OOO o d\bl .o K 6 8 o VP XT -- VJ1U1 o 0OIN9 p Oft\0 o xrvt p 0(\)-4 o -4 -- o; CKOOV O Vi-g\Q O' S4.-- o **4 W\0 p 2"0\ o -4-* -*' - p VI N -A O' AJVffVfiJ PS v A> .o o OVOVM vs /V vs ooo OOP -- o st-fS) o -- oo o 2CKO o VU*i -- o VI --M o 02ps <-* oa -4 -- VOX?Ov p- O' W -- -4 -4 > r" hs. 2 m. i 43 Vto -- V 2 m 12 o ri 2 4 -- SI o o o' a eifo Q VO'-* VO o uvn\j --i o -si -* o MOO 0 b" ovro 0 VP 2 VO b ViCKvO H 0 --4 > f- TABLE B - 58 OXNARO-SIMI VALLEY-VENTURA, CALI CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 zs86000H)dna 29-8 -&X r4 . m. > o p* oo Old) eg X o' a-r*o* w> >H * s noo r >o x m *u-**<*O:/>iZ * m OX o O' I 0> d>Ov -** SfiO * XQ O m z-o* -- z f5 m z *+; X > r o 0--(0fr*C2 V* -Z _ II * m > r OaOoI <xs> xz*<-** 2m-f. Xr> --o 6H6 Z> T5-f ImSNtr mX` <H wUMi U.-C*1'r-j<T*OUii OO 600 - jr . 8 OOO oo oroo >1*0-4 uootoooo-* OV M* h> 0\*UCD Ul INJ JT OOO OOO 6 m -* Ovjr roftju* OVIO C*.*4JT Q sovavj' o oo oo M Mk QN dv 0.0 o -ooo * o0o*.o-04ou0i N-* 0V-* W U>ir op OO PM * g-ute M W U * mm Jr UI Otffi o urmo o ooo m o CDXr o OOO ooo 0* oo ooo X m x o -n o X GK r X --m x rmoi mt Ottur 0\ ro\er o OO O' ooo ffWN MOV MO4 OO UC*KMO o X X m i u* UI X rn ix -* m Ov 2' -I \*A4U>**OS O 4r*U O Ceg Jr NMlji o o U0It0tMJ O m* 0 U ijIQN0-M* & Cft O 0M\JQ$3Q o QWM m* 0 jrt On a US0M b MOV-- -H > P* m z c 0 1 o X o XC3 >r* r 1 m CK X 2 < 2 X < 1ro e x > c > 2 g m x o c 2 TABLE B - 61 PROVIDENCE-WARWICK-PAWTUCKET S86ooot'Odna 19-S 00C -4 -- 0*2 O v* -4 om > 0 33 r* OO 0(0 0 00 X o --* O' o 39 > -4 > .* X r OO 3P m N 0MM Wl NOW O ooo o ooo & soo J--rMwN-- ooo o ooo 0 ftOi CO fO Oi a ooo a ooo 0ge Vi. i > On 003 OO O 10 00 -4 ; O 33^0 ri * > XQ r o 30 m X o -4 -- X' o. m X -4. 30 >' r rt $ -* rnC v--*0*o2 a: ooooO0o--1*m0\ x3Om>-40 *5 - >30 5rx5' <W 50->4 &; a m-s. m w VI -- g poo o ooo 09 -- ---2 ooo ooo Ot X . 0 00t ooo ooo Vfl IV -- W Vtp ooo o ooo. VI Wal o orvo ooo ooo w raw Ow op o ooo *3IIT0T mb Jt 2c o CXD. a* 6 8 m X o o1 o Oi X r -- Xm 2 7 --ao* M Ooo.i owPJoTVooVIJloo5m*b -- o o yOi io-v*c-* o bob p 4-- OiVJi 09 c V p wfe Voo0*vooWooI- -- o W4 tOo 0 b PC&O* 09 -- aO ! -- 2 9 ; 9-0 Ofoos>i -oo4Oooro'oo*w4 o vriWwt b -4*b -- p * W -- Oa a2* o ooo -0 73 ro i -- & o o* I 39V x3Om0 s -i't--'-*4 --oo O : -pJ--. O: Sf --09 <4WO b bob O a-U'4W--- ----O WW.fr PIj *4w--o* b --OO O WV--l M-- -44r o r ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 CENSUS COUNT OF CHILDREN TABLE B - 60 PEORIA, IL L . TS86000F0dna *9-3 -4 VI*os aot O4 * on > 009 oo r O1W w ac *4 4*- w 4O ' * .O' > > r z09o 99 m WfrC Z' 4Z O' vi*. o: 4. * on 005 ai OO se O 1 </> 4 -o4 > f -*>*Os 33 jro > 20990 99 m er m S4R'9 > r* a *4 < <b(be -n C. 4*2 Vi*OOn z >9 X9 --> H O4 009 OO O 1>00v o--* 9XrO . ". O' zn 4 9 r>. ' r-Z < -- 4,/1*. z> 0*4 OC > r 290 09 99 0 1 ZO) -j * m < Cuw i ** v*r ooo o ooo -4 uo 0Os*-Noe: OOO o OOO ro oOs O *S***-* *4 ftJw O OOP 9 OOO 0 ri a^' J*' OWN) o ooo o OOP *' oJr s(tIfvNnos ooo o OOO t 0 o XT Ptf 09-4VT o OOO o OOO 0 W oICwPCro-* O o oooooo *- w~*rv t**CsPO O ooo ooo OPCs WVCO o OOO o ooo po rni - 43 Z Vc m2CJ 49 9 VO O-t* "n O 9X v` -- 9 ror 9 4 rn 9z *4 i 4ft 9 SB 1 XOsr 09 ttf ** VOOOVVII o OOO o OOO' * o ir-fr*-* o 6*0t o -4f\3-* o dsrv--* Oft ma Oa S o Ov-frO att 94 09Vlp 9 ivvru (4' OCO 6rs>iON -- -* ? U> OOO o OOO o o .frv -- O'CO o *4 044 *4 o *4IV o OJ*V) o Poo 4 car *4 POVtto o WOOO 4.fr4jr O' o frfr*f\J ooo ooo a4 oo ircw -* fr'0S9 o fr vO aft ow p Os PC O ViVO aft 0 V4U O 090 b beob 4 o4 > r "O so mt 9V O' aft9 om 4 9Cl 9m * 2 9' 4 aft 9 4 01 a>* 9 OB o\fo- o Vt<*4 <r > *. 0 M--0 < * o MIC V t*Q.fr b CBfC ah* frrcro O OWOt o Nvb 4' o4 > r TABLE B- 63 RICHMOND* VA. CENSUS COUNT OF CHILDREN OF ALL RAGES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 ss860ooi?odna 89-S 00C --4 y*i*9iZ % Om 0oO0o| 9i/y O > r tfi "4 O <-/*>*0s Zo O 9vjroo > > Z*0O f O SO ' 55 SO m SJt (* K> l\9 -o4o-1oV* o ooo mkL 09 Oaoi wjy w 44C OOO OOP .. ro o u{Oj w*r^o Po ooo POO 04C z -- OsZ o V*mo --I 069 oo mm z O 1 </> H O O!*>*0* " V o mz -4 > J'OO z f a so > P'0 m r P *3 < ** 09 JT.TF O O OO ooo Os ooo *SoO4o6-**o6* ooo QOJ-f *o4 sopoooooo --iQsZ VI* o * om OOP oo O rol lers *4 o--*_. O --1 . *. >r' zoo oo z<o rn n O' Z >Z ZO O -- >' n -35 z< -4 z > -- C/J *4 z> r 0-4= 06 o -~4 . ZM m>H < * a <Hk' u> O o tOwrO-JPVi ooo *4 Os Ora* M --q o-*s oo .o0 o6o6 vr Jo?' o <**-*-> OopooWooMi -zmio Z VI C OZ CrnO - z PVI o oi *n -sO* oX' qv -- p r* --' moz P-4 X o1 p CD O Crt l\i -* SoooO WOVJ) yiwo ooo POO o View P OOP b vpbs po Vi ta NOS rv-^cK o CKW-* W-4 O'- p fSJJr-P Vtwv>I 4. c0\--e4r-CD po OpoOpP po XI'W *4 MO o C8MO mk *oo VOvl W- U o 0-4 C4 mk OO4 ' *r4u1o0 o o mk Os VopI -JVJ1W v?ors> 0o0o6o * caxr-* p -40C b UOO jra w --K -* ^ ' o mktO-k p p vv* ijruo* rf*oo p -4 O->f r -o' zP1I O' VI O' oPVmo9O1kIt zmm3Zo5;. -4 -P4 P OOOD P osrv-* o OCKfO p giVOO O o MfO '*:4o q o *66 Ml o P VIVi so o sji(Vr -1 OH >p* o m z 6). O(ft ct- o c z -4 O n PX-- * raz* zm o *n 5rp*r >o rwn Os zzo -X4 o 4 O vn P>I Zin m < > Z. r*<-- z Oo' mz C 0>3: Z :H> <C0 >z m >o CoO TABLE B- 62 RALEIGH-DURHAM, H.C. 9S86000t'0dna 99-8 o^z o WIV O -4 *. m > 003 r* 0-0' O 9 </> CO 0ffv 2 -4 --v tft O Z 30 > -4 > ZNO o P to zto m wwc ~ov.z' *V.fl*onO 0oo03^ Q 0!Ov 4 O -** O' N6 ->4 Z. O* OO p O' 30 " z --o4 P * o p z -z4 > r o 0--0Cvz z-- mV3*omo o PCS II -4 4 OOO oo O 10 -<*A*OV 3*30O P z ri >Z P T* " w-4f ss 15 3 83 p1^ 3 3 vCMn rMg-4U1 oo o-4o6 :' o oo ro ig OvwM *o o o ov-pto oooooo ro * to O6 6w6 'O. o ooo ooo \-o4 Vzrtv-jrtvo. ooo 4oo?oo6?oom 0ov vCMnCwMto-* o oooooo VO Zig-M CM OoOoVVoO o ooo CD rw COD 4o3oo-4 o ooo VC-4fvi CJQO?MWOVOUOZtr' o o ac 4 VOZ&M CM CMVJtVJt o ooo o ooo oOoi OooDooOKooO 3? wvW 0 0o.o0 oo. 49 op S*i Oz- to pozp to z I ton* 3D NM --M*ovjr CooM 3ooP ooMoo4 &O CuMN-5*W-- O M* * O WiTM O wnOJ-4 O *4-M-* O M4Q q *mm O *4 . O OVCMVp -4VJV Oo' vWjitOgrOo O ODOM Oo VOfSMJM-4 o q to SJ!' tJot 01 zmz. tom*. o p to o *4i\j O O -4 -- CD CM P M--4 op ' NO*-* * o 0^44 O CDto~* toy** Oo' v4ne--v*4 a --q wo Oo V-*I-M*4M-- O -CD -- >r: TABLE B - 65 ROCHESTER, N .Y. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 TABLE B - 64 ROANOKE, V A , CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 o.:^' n- o OlAT*) CWCMlft i*.p.ev r-- <vr- o o m* o*m* ffi tf>*0 *-CMb O fOCM*3* ' o SO ' P: OOP > T-- f* P o p CO **-*'SO o ' ZUOzJ vf?i i ,ui .o. ,u> 9 o I0f5} 7 UJ .Mb . J* *~.CM4ft Q 6 0 ir* Wf**** CO CMP CM lA O o p POO coo !Z t --- oOCM OS OvVGlft lftftb ** f* O Q b P-* HT4 9 . NOO - m<* p o o oo vPo.Orft CM VO b0\ M.Zift r> cv.rr .~.Mb 0 b o TP bz NWO "-Oift P Op jOwPm MZ^ *!* n<o- z . X u c X-- .v*c- c ,0 IT SuXxx_C O*"f oin zp 4 Uaz.i 0.0 oo VOZCO o o o t* oo 0.0 o .i* CM CM Z 0.00 oo .:Z ift to f" o o CM CM oo oo CM Os ON eo O O 4ft .oo o tMbCbM SmT 0.00 0 0.0 svbz o C#M 0.0.0 .OP .ao*or> *-.z . b b OO oo O1"N*"Q\i3S* o VO. ooo o oo Zeo > Ui PCS VUJ mm PO .-1 wi a OOiX .< 0.0 * H- *ro <z -i < ,0.ff| ** b</> to *- </> I >z oo Z-J hJ X oo < -- o U4 * X `if\ x< z Zb*- Oh. DV>> > UJ OvX < X b OOvX -J < o > z OffK o w #- V0<ft <0 z OO zoo hJ O . O -m o Zb*- z ?>> w >z OVO OOvX O' % .< zx to **- X b</> 35 W i o oo <-6 zUJ ooA ' - *m Z\Oh f- 3>0 B-65 DUP040009857  .00 o <A :oX Ul -< "GX < <A Hr* H<* < Ul oo X C>Q cA X< .H* CO X hr* X <O o X -'p X>wU! wUl u< 0 -J XU1l -<i a u. 5U<l A x XUl IQ {A < XX o < (A X p tA cs < (A Z ul P OpfOOv trvuYgq O P VO 00 VO fOift w f*Vlft P . O CM tfY*6 m^r.ca f-- rt.tA O .o .O00 . r- 1*. .a H*" Z 30 .Ul Os P UXl 1 , CL tS\ O' "! o 1ft o Ul X X -J < H* o H* OvflOO ^ovift " .CM lA o r*r .JTlft r-ilft P Op CO M . .OlftfO Cu^T*') o > o . CviCvCO CMSTSO OS ro '- pv <m~v o - rAiA .* ? < iftlf.t< CVtftlft csi vo o * M esiiA. u\& *0*0 p O C.O eo *rs eo On cr.f-* o CM ST ** rttfVOSl O}0 n ift O L" CMOiOs <M.vO -- rnift . . * pv 8AC J r- iftm . ....G fr- S. ^- .rn O JT G . CM co O Pri X Ul X X p 1 u. P X f-- Ul eo X ,lft X 1 ui X X p NO r-fy o o c eo . - *-CSm P >0 o oc.o iftr-OO CM .0 0.0 DO fr* CO.M *~ro o .33 m , lAJXSO :* * <* > o ift m OOP CO fO\00 o a CM OO CM -roift ift ' 0.0 CO ift r*wr> o m CM oo o 00 IN* Nr- n sft Ui H SvW * OsX OsO w* a OOvX < >-030 O* L*> -i osree O <X H- -(A : .> X .J < .X >-- X u o vO<A </> 0. ,O0 xo l-r < -* p UiQ S2 -ift x< z Z>- X GV><J> > H* P Ul -J 0NX .< Os O X Os X < >- * H- X C ^r.c Q Ui -> o H- a M3V> <A 1 X CO X OO wo - X O Xarrrifi.t X 5l/!VV> Ul QvX OsO ,O.Os < - >- < ccr x O (A *<- o u- VOCA <A O O xco < Ul ' !* X ,-tft O ZVO*>U p v>y> B-68 j - f' 1 .j DUP040009358 TABLE B- 66 ROCKFORD, IL L . offftl . u\eu _J CUftft o -< ftOOJ UN SO 60 . A-to-UN . to* -- r-- o X H- v-t+ . .to* to* w UYOh- O fteo o * csj s lA O *-.6^ ft CSJfO o r-r-to* p **.0 to* z -< V) t<ho*- to* ft ftUNvO i *-ft UN SO ft V3 Z<XXX z -\o? UI o f--t X I aU-J ton ft UNfi .O' CVJto- to- >-:f*-UN o soocv CUto* XUJ o UNN ftftl- o flp to- *- ftuo CMftfO P-UN NsO eco- r* t >.-1 UXJ CM ,x< .0.0 OO OO to. ft>0 oo ey-f^ nr SO t-CSJft :N . to-m V* P O. to- o oo ft >0 ft r-ft ft ?NJ iXrt >Ul eo .ft .<0.VJ 0m..f0t .fot I -*0-v-0o..f03t mUoN om ofotocvj ftoot* v: jx- z :x 03 Z hftXUQJ T~ ^J -NfOt X f1It- 09C-*0U*-V0e9o oUUN* fot.o^O-.Nft >Uo0N .. oo to- WCJ.Cf>O f- id O it IT < X Z ft lb iad 8" z 5 *i- 0.0 0 f0- 0o-*0- ovo ft UN 9 0 o O Wf-<0 h* - nr- OJ PC ooo ft UYft *-UN ro UXJ zQUJ .ft. > to. > UJ UJ UJ to* OvX -J ftZ ftZ >vUJ X 5 ftO OftX toi < < ft -I X OftX < ft o OftX < Xo 30 to- to-O <z ,h* -- .< X OftX 1-0 AO> O to* u* o . to* z OftX O ui -1-0 to- * to- -< ftZ - W to- O X VOW tao 10 w to. > 'z Z-J w < -- o <J> zo0.o0 u . u> X oo to- -.uzooo to .1 o oo -J xoo .< U6 O % XX z< r O *.UN to. 3U>> to- UN o Zs** -z 3U>0 to" a -8 ^ ZVD-r* to- 300 B-fi'7 DUP040009859 TABLE B- 69 SANTA BARBARA-SANTA MAR IA-LOMPOC O0 Os 0 p.Njsr O h*O0 b cK irvpso a P^Osn 0 O *v m>o o Mb - M'S or* :X :oW < o psb o 0 A to 3NN O ;ps a-m p f-sO h-irco o SOsOf?* M>0 z1 < CO fO0*s H. -< n p" * 0.FF U O' Z SO 0W ~O*' ` ^MSO Q o Is o *m-smp eiM^Vjr) OO d dI Wo O. tfS os o z t0fS PPM o CTiTM o O' P *" ps"p o .<n0yo- 6 . PPP bsmovmo o b dF* 1 UJ 5 d a. $ 0.00 o ooo O OOO O > CD P** OPjy o so *-m>o -0 ooo o >0 mror\u0 m*u * ooo ^4\ o* * ` -v o a* M CO d< UJ > 00 Os OOO P OOO+O` - o SM" OOP O OOO CSJ4TM .o0 ooo O nt0n,0 O Os o M CM M ip* 0 1 fo>- Z0 UJ * XO *0 bcoi 8 ad -1 Xa wO 0 0sOs TOtfts 0 ooo o OOP r>F-tJr3** MQ SO OOO JoTo^-ou -O SO MP SO boo O oF` -- o(rAooAi o0 M d d *- Uai Xo o m z *O N* oooooo rtCOM 0 M boo oCOo*) o p* M bonsooOooiA *-M O o fi7t z wtr > Z: P O lu > w u . w zo O o CO co z UJ 0 *vU# WE 30 . -P <z H` CO > zu <--: od.s< Ou. u -J <d z UJ O z -- Osd OvO OOsX o- s-d ,** <s/O> <i/Vo ,d .ooo- UaJ o-u n 'Zn o *t 300 _I < b~ O- -J Osd u<dzUJ p 0\,O oooa^sex; v*o--o o <J-- ou- oo z oo zoo t- wO o*ifsa o SsO* z 300 Osd ON.O -J C<O oOOo'.J-ovTzd. .*- o <1o frU z CO vN>O</> p -J oo d oo <u* wo O o H* ZSOF- B-70 / DUP040CI09860 .0 CO Ov o' 2? CO P O X u. p w 0 * .z < to X CO < .p W 0 0 > -J < > CO X < w > lA O <" to X +z .0 P < CO Pw 0 *< 2: X W a -J aw 0< >* h- 0 O .z w ui X 0 < -J i X 0 W < u. tti b w to z \i p b {0 CC1 CO p a_l CO e? z -< 14 .0 fOr*\0 b a ** * < SO tn 0 .0 *-totrs 0 0 h- -SO NO CO > vdfOOv CVjvO b 0 0 a ODrfYvO CM VO O O c so .On 1 C fr* ,0n r* -W- os Z SC W Ov O *- X .1 WC C. 4A 0\ P iA -ON UJ X X - .* CVf>CM CM iA 0 b .0 r a.fMtA CM.CO Ov c\smn O . 0 Z7 -T- lA *-.aa *- fOA 0 0 0 bo 0 coo 0 < CM.lA. r* -- XT SO try CA 0 r* CM fr* CM a . * aHA c\ir- 0 0 0 co ** vO P CO r*- CM VC p b 0 dr b co .A<rs.C PO sO 0 .0 0 00.6 OOO h- *- CM-CO 0 0 CO a r pmco inopo CM A- O n 0 COO CM Ov|* - CM un 0 0 -0 CM ov.a POtfX b 0 0 obo 00 *- r0\ n 0 lA O a O CC Ov r* 1 O f- Z Ov UJ *" X a -J .o n -- -vo X Ov 0 *" 1 wC O lA Ov a: - U4 (0 .C P lA Z Os Tf 1 UJ X a. O .CP .cco 0*- to .-- -- im 0 0 O' a T- O CO coo f^CvO "CM m O O SO h* OOO oco jAiACM O CM <0 T-- OOO 00.3 dT CM 09 m dTAj *- lA O O a O A* ooc POO 09 0-09 cnO CM *" CM O O -D P" m obo 00:0 drtAtA CM 6 - b 0 a- OOO OOO aiAiA 0 0 PO vh r* 000 .C P 0 m<n <0 p O 30 OOO 00.0 OVOIS. O O CM > UJ H- ,OvX >vW * OVO -J tox O O Os < p0 * ' +" h'U ax O <z < *--O h- p* - X vOSO CO > z <0 0 .00 Z --J .W xcc < O wo* X O *CA X < z Z\0 *-- P fa PCO.CO > w w -Os X < OsO X OOsX -< H* O * w z ax 0 w *--o w a sO</> <y> z OO ** x 0 wo* w 0 *lA 0 Z >C w z Ui ovx P.O OOsZ 0* -1 < W < oax Vi *ir- O -w \D</> w <r> 0 00 w x 00 < wo * H" 0 *IA O ZsC*>* O </></> 6-69 DUP040009861 TABLE B- 71 SOUTH BEND, I NO. CENSUS COUNT O f CHILDREN OF A L L RACES 6 MONTHS TO 5 YEARS BY FA K iLY INCOME, URBAN STATUS AND ACE O f HOUSING, 1980 -J <OH O lA*0 --n o0 H .OO<0' 1 o ;Xw eUoCLcJ. \ooo 1 o ,oifon id Xa. < O rth CyiOJT o. o o o moi*- - oo. CMCMtA P m-amOfslOf of Co0v.o0tto0X mCM f? rTJW .* * *\l P roo* O h. O o 9 stCM.* r c--$u&t o - Oo. O --( oo** fOooOOofP ooo . f rtO t*f>" O r* p iOfOCMOAO o 0 lAfOCM. .<M.J** O. o o*>! Jj'.in o pf" Nino o C*M-0v.u0r\ ** o*oo*3ooo03mooT0P iNoonCM o< i nXo id ox6 o -x >oc p u. o XUi iooTnt" X3to in X o** i Id XX oortJdoTooiA .C0M OoOoOo f-N*-COM *n OOOOOO o o o*0o4<tn* *0 so 9>>7* Ui s ec 'vld OO -J (AS 9i-.0P <X-- .03 P -J < X J-- OX o oxx Af O ov> </> I o < - o- X->/ <^- XUi P 0-0 soo wo * jCQX X< 3<M X -- O *IA ZM3</></> OOftiOONOOr* 0ohX <ooMoorp-oofOn o m jf OooOoO oo NOcsi1**> m > - u Id J ox < oo -J X oox -.< o * H- XUI o.x.x * u </> o XMM oo xUJ oQoA *o :X oXM3*m*9>3 0iOn.OC0MO0CM r~-mT o o Oms OOO o oOCoCMMotOfA o o Os ooo VOOO'DrOS' AooD fj'fl CM ui OX oo -1 oox o *> < H- <V) o*#^- so o H* XV) \0<r> 4/> oo -J -xoo* < aUJG*>m* o x*3V>> 8-72 DUP040009862 TABLE B - 70 SHREVEPORT, LA; Sh .z X g P w 0C SC ' *. Iw-- < GO CC ' W i 0 > >a, 0X < ui > s AO 0w < Z -1 1oH<- ONn , fctJuC<Vol<Tnv o a- ; r-f^Oataf\ or* 0.00 OOM p-r-fS MOO 2H U O*-n X wo fl. iT 0 O l/N rt Uxl CL VOlftOv OlfN/n cycvjm p 0,0 0mr0-.m0 a a o o On T~ 0 XU) O' xo -4 O' --ox --SorO>-1 1 6 ). o O tfN 0 uX * ** ffl X X jft Z ON ooCO oo .OtiTVVO O to m ooo ooo *-vOJf\ ftJft/lA o o --* 0 ooo 0.0 0 **"*"* o ion a' O ONCN v-ma *rf-. cMoOroO.fyv . ooo ooo *-a MO *** o o in ** 0o0o,o0 ft/ON - m oo rh- o0o0.0 roa oo ro <0 ooo oo : .{CM On o m ta-N f^ONtO t-jNtfS Osft'- . ft*- O yO *** p ftlNO O f0f0*0 ooo 0.00 n o *~m NOn -O " CSJ o :PJ M OOoOo *- a n o *-cu O r.fti ooooo .On NO rOiTvON oo m 0-0 0 oo mom CM CM ft/ o -QJ Xo U> o 'MN.XW >H* o Ul OOVX .OftX -J < U UJ _j osx < On O CC O On X < UJ On Z o ox -J < 00 <90 Jtf> Wo >- o J oa*.x <H --z M < sc H- NDV> o <f> o *Hoi- Z->J z u < --j o o zUJoOo x<X w z -- zo</>>*<m/-> 1- O * Ul u az NO,V> v> S/S' z ooo Ulp % H* o *m Oz z<*x*/-> lr* O t<fi Xi/5 a* z \V*>" o 0i o HOH- J < oo zUJoo. o O z*- 300 B-71 DUP040009863 TABLE B- 73 SPRINGF IELD-CH t COPEE-HOLYOKE o 0 0 0 & u O ur O < Q ,<x 0 0 UJ z: o o ar w X ><,6 ' CO 3 CO id X 0 UJ SC Q X u X X o u UJ O m* CHNiA o >< * OOP .6 01 .o.X o o *- OJNiA POO 01 .f O O y^.PcA lA lAP *" C4.CA 0 O P c o O' *" o f0 * * - H* 0 XUJ AO p 0^ X1 Ut o fi. tTN Os o IT8 0 . ur X X J ><-- o t- XiACSJ ** PUMA r- fOX o o p ** A.iA : . or-p fMA o o * ND4PAO cjp^ -^ 8 .x P o vo 2002.20 PflOtA ro*np o AJ P * pfjp Iftw O 1-0 0 0 O r-f*OJ ~<v 1-- P p CO POP **miA p p OOO OOP opevi ^*0J f* o o M r^ P-C4A" OOP P O P -*"P0 (UOh ^Nvp p o P * jrpAPOP r- fOX p b p OOP OOO iftmN iAPi-- CJ O o lA P M .0 -0 1 o fX Pi Ui Tec UA -r p -T 'O XP p * ' U. O a> p X UJ V Xo x ir XP * * i UJ X a. ooo o 0.00 NO<-iT o ooo ooo tAOCVI *01 o h* ooo ooo 06 *>^ o X AJ w OOO .o/o--^o 8^ o o 0 ooo ooo SO 00 M o X A ooo ooo >0*~f-26 o p lA OOO ooo O OP f* WAO o O p p 0.00 Or-pOjrP* n* * ^ Q P OOP OOO MN mtfVO o lA * > UJ " N*U1 pgs P -J wz p OpZ < SO >-o <z -J < O oxx -*- o .H* X ov> CO </> 1 > X--l X w . 0.0 eoo < -- Q UIO CxD<Z pu. X -- *(A x *p ~ v></> u UJ J PX < 0 -J X OPZ -< k o * U* X XX O UJ H- a NOP to o X 0,0 xoo Ld o * u* O %cA o xvo*- z 3V>V> UJ PX PO OPZ < O' < XX o CO hz </> CO <r> i o OP xoo < UlO O (A o ZsOi3V>V> B-74 DUP040009864 TABLE B- 72 SPOKANE, WASH. 0o<8 000 0.I0E COtfsH- olosf^ ^ OJ lfl . O so 00 r- r- c o p-fllf**. pi-ffvd CJVO o oo Q Uoi 0 *.** tf\ O ht-M 0 Ifspvvo o ` P '! . ffias 0co *0,0 0 *-40 o o1 * * \CP-\C O pp Okf 0 ' r-.fp* . <r* t*. r/3 wQ < CC S3 UJ X 18 vOwr* CVISOt- 0 o OOP CfeJj.tO^ 0 '.oO * * , ' * lfYcfOvir* o oo * OJfftlft p-VOiTHflO n .6 3* 0 O o Ops** 0*6 to CM- 0 0 j* `NOlfl O 6 -,po* 5 -< CCt .0 0.0 Oos-oiTAo CO 0 0 0 JT 000 OOO " i- rowT"" o 0 .C*O oooto oooCOooo(VI CM o oorO 03 -X< w > CO T0-- 1 ooo o ooo f-NO oto 0 ooo ooo f^cp *-.co o tof\ pop ooo ooo dr co n o p- CM O T" o CoO -p0p .0) ro- 7 Ul .0 .c :x 0ouul .0 0 X 0 0P ooo o *.0-.O0 f0p-.CM tooo ooo 0 o0to-rl*Tot>r o oJT\ oooooo u>*-ey o o 0 CM MO 0 0 UJ X U. o 0 X irs 0p u CD < X o IT X0 ooo o ooo p*5`W p-CU-rO oe so OOO .0 OO O f*o\ SO CM ooo ooo r-p-CM 0 0 UJ but Xa. X o > o bw O >*UI " >H- Ul 0X 0.0 UJ -1 0.X 00 -J UJ 00OX 8 uo 3m 03 O0:OXl 0 OM o < 1- 1^0 v<-X~ 0 *<C-C *rx *p o %ov> </> o .>- Z. >-J <r* o0SUx<. Xui o X -- OO x.o o XUo<\iQ/o>*<tp/f>p\ X i- 0 0X o> < W XUl .O0X h0- 0 \o. v> o `X--* u OO WOxoOo.iA* .oX X3i0/>T</-> O..0X <n X OOJC'. P-O >o</> 0 V> I o -J <hou* OO xUJoOo.3 0X0- B-73 DUP040009865 ) CoO 0\ o -J o.*M o >jfM0*..O* -< t*.*t CSI o f**T O <0 `'.f* O " CM >0, :-:3o u. UI < .o ,0*0 iK o P fOV\pO 6 MOn Ov 4 R \OlAN* *".1* P O :.* *V N*I.>- o o o .<z .</> .59 H<- CO z ** m as 3 w ,zuZoi Ua.I #> o I | :IT O MPa* o 99t!i p n-Po . aO 9A9 40$KM " IS p O P 8 OvS O ? - N8Ar * O CVICOJT o tfsp* p.* w mz *- CSI >P o oo -r* <|Af* p.PtfS * *n O o *o* .<X > BQ PofO-OoSf*T*OoCS oolrA-t PpoO.Po 01 OlA OOO 'cOOvCiOioJ-MnP*'oHo oOO JTA (0 2 > o ooo o CO OP o *-w rt 1 ooo o QoNoAoA M*- .-o(9Sf9Tt POOOCWOiPf~\ r- 000 -Z p <0 z Zui Z o X *0 Uot<oi .,p---zJm xp. u o VO f oIT as UI opPoPoMoor^ ooOMN POOOPP s 0*!* *C0K 0 0V0* * oo0jco0oio0rv *-MO 0 0 z1#1 \* p -ox z ON t OoOpOo Oow Vo" OOOOOP fTlRAWA0V z a . 0OoOpP 0 0 z*-istvA0 A" Mar z uo&si > xu > Ui Ui 1*1 u- AK .-J AC AC 8 5 63 *N,UI (OS 00 1<N-z--0* . to 0 -J < OhS- QOAvOX OO.9999*tC0 %ov> ; <0*0 -J < IOU < AO ZK ^I O S< ZUI ozc R*0 O p ^0O0IO AO ^| < p *. 0< 5X5 ozc 00*0tIOo ,O~ C(0O :Z uoi > ZJ o< x-- Zo.-w< zUI 0 z C.P ZuOoO.* O .iA Zo<voO<~o ' 5 zoOoO H- UI 0 OtfN O Z 3*00* OO H.<1- uzOioOoIA Oh- Zvo*^ 900 B-76 DUP040009866 TABLE B- 75 SYRACUSE, N.Y. TABLE B - ?!* STOCKTON, CALIF e . on 4CM*0t O TOfO.X 0 F'fONO , XOvtn XMt o sex so OJvtft P i*- *o m r-Mcn 9 O L. O u 4fprt s0 co Os Os O os ^T-sp O O 1CMN** .o Q *-C\|Ap O <X 1 f- CO O' 9 tops O H CO H> O' X OF-TO CM O' CVJWX - IfS r- fO O .*-,coifs o *-.0N o <\JMX O XI Li O X CL m .9' .rO-' LI PF-t -* o .jf;irey o fOF* o p ac O m ` ** o 7 8` - -- 6 o f^ocvi p o CJ CV.iTv o > L *- .fO UA o F* CSiCWlfS o i u > -1 CC .a. I CO .o ooo o 0.0.0 C Un -i ooo o .< *-. .ooo f*m*~* o O' ooo P F*<M r* o ffl> F* iM.a >0 O S'* csno o w~ _* SO Os Os ifs * <o F* CO X fi > j ooo o ooo o ooo O Ift ooo o 0.00 o 0 0.0 o O H- .s ffF*SO i-* X to 1 0X0 .N0 *- *- S' so (Mm TO r -O CO -x X O' .F* Li r- XX J: Q -J O' ooo o OOO ooo O -- AO ooo OOP . ooo o AO X O' t Os AO t - po Os TO .*-. Os f- W NO :*-ca F* roXVp TO so ! W" LJ u. o O tt\ < v , X r- ki -J a -J x ooo . ooo O OOO o < 9 lf> 00.0 o ooo o OOO o L. X O' 'r 1 som os L CM xx- o *-.0J ;x SOO O' in T- cj m f* LJ sx Li a. fiC J > 9 *- , O u. >. LJ LJ Ui >* . OX -J OsX OsX NwWJ 0:0 .-J < O' i Os -j F* cor O OOvZ < X oor .< 09sZ < X 9 o* F- F* * H- O* F" 9 H J OJjK o <X < *- o X .XX O LJ O f- < oxx O to F> o H* > X \o<o (0 H- </> i o </> t o r sOV> so </> t o to 9 to X Li ,1 .> X-J -<--- or x9L<. X oo Li xoo LJ O * O X x>o~ 9V></> X* do <n xoo Li o . Ft- O *lA O :x\a*- X 9</>V> oo -J X 0 .0 < F* UC piA o XtOr* - 9 *oo> B-75 DUP040009867 TABLE 8= 11 TUCSON, A R iZ . CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1989 J o.# o * - F <If- x--rjffvnoxNr P P e .* . lA^OO CM o o o o CD Ow>' ro- :wwoOcr 4OTN Uca*.. f*.Pi4r 0NW*-fljOf\ mm 0N-*.lA \0 vfl P .* tvxr --9 o P oPm 00.0 F-.CoO o00 p t*. cv* Qsittt* iftdssO o *o NOOA P *" P xrari 0 poo oo .x t n o o p POO ooo op .O' opom -fimfv ooi O' r- cZaw O' o> TO ;O*"*' u. io1r ,XUCXQJ *o"> iP zo oo OO'O *- NOAO o to fm oo . ooo o frljWuvio* N .O 00.0 ooo p ** o o CM CM ooo ooo df o n o ooo o 0.00 jOMn o so "CM Of OOO o op o CM*?5 tn o .t-esi'b oo .Ovpvr- o NOn.tfSf* oQ .xrf^-p- o o CMXP eo CM.ym M xpm mm 00.0 POP .OSOiB) *" CM p 1 oo .0,0.0 i>^AlT>Oi isfft o >-0? CM OOO ooo 0*-ON o 00 ** ooo o OCOM OON o r CM > > *N.W H -* op ox a *<-.zo .mi < 00 t-- Z.--> 1 ;WZ ,<cocU.2<x.1Jj : u ---z w OiSC 9vO O.CVX o* 090 v\O>*V1>- o o zwooooo* zO*-i*f-t v>tf> mj < +o- w OiOO ,:<c On ,OOn X J < H Z OOXT K o w o*vr>*o0 H _ zw zoooo .1*10 . tA o z o7SvS>v> Ui OP Pn O Os X O- -< " <W O.v?00 a o XV3 \0V> V> o -J <- oo coo .W * o O>-- z>o.** PV>> B-78 T t .T DUP040009868 ` TABLE 8 - ( 6 TAcOMA, WASH. CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AHO ACE OF HOUSING, T980 <-J *.-0s.* * its 0 P H O rr to its .O1-- H- <OMO .wm O o 0. CMCOtfV OWft- rriiA O o J* ec o fs *-- h:~z & 0 ui Os u tc 1 iu a. 4f\ Os ** Q ifN Os VUi aat. .J < I-- ,Ho QWls OJTiA CVl.p 6 o I?* mtn ir CUSO.CM mco^o OJsO if* oo ooo r- --03 cum >0 *-- CDPOO. CSJVO p o O . P'S CM O 0*fS i r- mm --: CSJlfs o f-- oo o CQ.2T.iO .CM CO CM TO .JTPo.c\ * tV|N) P * so *- to *- .<0 i O Qs J0V<OCM cusp o o oo vmso mi> CM O CO .3* i OS I :Z .o> Ui DC O -J so X P 1 a. o Om X UJ so Xo m z i w DC a. oo o p-c^us*o m to OO o o f3fs\ *-Z O >0 so oo oo f-*T1~ *~ M o o ooo .0.0 0 iucvio sr m . o .0.0 0 0? CM r- cu m o f* f!S ooo oo mcu ^ -- ro m its > o OOP .CM cum --; r* . i-- cu .oOoOoO fs Ov s-- p^ r* OOO OOP --< m r-- to OQ o cu to r- V.UI MX juOi NW<* z> > Z<.~*-f az zov< >p- O -J < X fZrr iou z oowoxc 0\uzOZ0<s.oo9o/MO>1-<o0*omoo/> J J<-- Ho -J <JOuC Z Uui ' z-- +o z o.o1zsSaS-Ufo0xslJ VUzz3><lo0/1>.*om0o** -J f<O- Ui . O9ssX -J O OsX. 0< a* x(0 M 0.1oO <H* iOs- -i * CUJOO.Om oF-- 0zs0o*0- B*77 DUP040009869 TABLE B- UTICA-ROHE, K .Y . I I* .9<90. 1 S 3! .9 9 9 o d o NJrm p* $ S p.tAit* P P*- g 0 1 - I 99 9 >-* z g AC fc* 9 Z 1C UAUK9.ll *9OiIr- 9 POP 6.* CoMpP'dM p Ul Q IT nM r o 9CCMVdTI**"* g I S 0O0O.O0 fiwja-ro o99 9fig >UI tn o IV:Igf* 9 9040 O 9.9 dr 049 .* o CV9*?* oo 9*0.9 o *>*N-fCS o *o"> N rtO o ftlWfi* o OOOOOO ^x .9oo* 9O0OO0 *-N O O h X Jft#*- o Cr.MwlACifMt o o o <F*tfoO;oX o p 019.0 p pmvO : CMlArt p ,*0-.^*.o* oo .OOOO**OOdr ** roCM-A OOP O**O9P9 o W9 s .9 9O0.9O09O0 o99 0OCM-O99O0a0- *OOi-n OOP o P9Of-vOO *" Snist to Ui 3te t < c oop IT OOO 9 iftdT.O t* r*CM ** 9 OOO OOO a* CslW 1*1 9 OOO OOO itunfM ivam . oo CM 1 wtc > ..c.9O 19'wWa0s> ,0 s*N>Wi > il Obi $ 5 < ->x Uoi X 99.0t9il gi* .2g 09V1>0 2UO19f 0.00o.*0t*9f* < O- 5 <XiXU**l p X* J t- *. z 1*iOzU0O9o*d00Io.i999T~14*Oo109o*UOi0SA. *i -:o-N<--J1 <X9W '-O<10J-- 0D0O0UOQ1Ei9Ip0999oO00OO*0*XU02o0otSO*rIt bH-<OI" B-BO' DUP040009870 t ^ q M[ q 78 t u Ms ^ , o K M^ .- o \Q *- *0 :. to 0to p too.uS O s: 3 < .~eb O -to O 050:0 0 --.ftl Vp .0 .00.0 p *- to 0 0 f* rr H 1C u. p W mr-O ,0 9 . . fOfOCT 0 * fO.to 0 4 O < toa CO ', eo O 0 to r> O .to toQfo CM to 0 0 f!-- tr0J3: ** it- O O to 2: t < 0 to .0 9 ft rTM to< to to>- (V O .0 ,1 * to r--0 0 . ' * f^cy O . W X VO mO\to O to to to 0 O 0u 0 n*t*St O w.fOZ 0 f- to.J? -P Z f* *t to .0< cc 1 ca UJ c; to m .0 to 0 0a:UJ fOfO.fO O fo-fr to fo- to O *> .. 0 00tfs to CO O tf\0 O p JTto0 O 0a .0 OJ to P f- cT c? t-ro rr P * t' ** *- ** UJ > tc -j CL x 000 0 00< u. OOO O -J o O 0 0.0 p bob P cO 0> ,C3 < w for-'-oj PO0CO CM r- to f"-to.*** WCr *- CM 0 ococo *-00 - tr? T-- to to to .CO C < w :> 0 0 000 0OOO O OOO 0 .0ifft CO OOO OOO OOO p .0 Mhtf- r-- CM0*~ CM tntofu to 0p to 1 f- to 0 . -r- fO CT 0 r- *- 50 CM CM 3to to : X0 H* UJ Z tc 0O 00X -I .an 0 vO oob O OOO O OOO OOO .0.0 0 O OOO O 0VO -x .0 CNJ to VO .to tototo to <CQ0CM .0 r- CMAOto to -foja- 0 to 0 .CM tTV to w.0 0 .0I U_ tf*N to r- CM <0 as cc .1-- UJ CD toX . OOO O OOO .0 0 0.0 O < u X X0 00 0 00 to ft fO O O to OOO 0toJ3* CU.CM 0 0 m 0 0.0 N fO0 *" -T UTV O 0to p1 UJ =X a: 6 CL Z 0 4 > X to 0 P u. > UJ UJ UJ 0 to V.UJ -- 0Z 00 aj ,0Z < 00 .--J 0X 00 1-- to O 00s < X 0.0 X < O0X < X z> 0 0* to to .0 * u- 0 > " to 0 toO -j O O z a.cTcc 0 < O-JZX O .0 <z < 0 to UJ too to to 0 - -- z \C<S> p to to X toto to to </> 1 0 to m 0 to to 1 0 to > Z .0.0 X- UJ zoo .. z-- 00 KC 0 bo nJ zoo to <" 0 UJ O * UJO < UJO - X as O -to to .0 t.m ft- 0 -in UJ z < ,X . Zvo'to O z to fp' 0 Zto^- 0 X u. to to Z toto r-- toto DB_-779Q DUP040009871 CENSUS COUNT O f CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF NoUSiNG, 1980 NOVB o Y-CV'O .o r*w 0 pjr tfM^OV O OS"J*t"-|sSt* p P nh* o 4rM*T<N0 NiO O f-W*-.O oo mru p *- oo J- O' hZi *O0' O we oi a. jn 0 CJ*-m O'Off o 0*"*c4wrv~p po ^rovp o o ON O ooo o VO *-N O Ppm o rrO* tfN<^8 (VO ON o cucvm o ^y\p o ooo o n0*" 0tf~fi.s.m0o o OooOoP oo ON- Ovh- rft OoOo.op oQ 0cvcv<isnr ros CO O' 0I zhi O-' OX ---J SOO' -uz .*O1-' tO 10 O' uzj m z oIT -z O' UIi z 90w0.0w0 *Oo -0oJf.tor0noo0v .oo!> oo4oo-lofoN ioopn* OoOoOo oo jf OcvOOmmo fmooS 0OO9O0 OoomJ OOOOOP JP iJoOff\t' roO^-oOcooO4^Tr oSomt oo0t-0oo^4ioon* ooN '><19v--LzZ--QoJ zox9C-<xk--Ji >o - Uo<xMz--I zw .08U9Zz_O:IHO0O1o0CQOtPfk*nn-.s*OoKXuoOO0X-k\ -o<HHJ UZ-*Xg<J-I z.mm oz OZ 098zzo0Uo*I4o!00oOS1-*.oo<0ZO2~>n ui <^. OOOO*nKOI 00.0 .-Ho-<*I Z 80r-0 ** MJ<, VZU>JO0Ol .O0> thO z90r0- B-82 DUP040009872 o .0 CaPr 15 aos . O w (P < IaPs *Z 9 -3 <C **9 as c c: 3 W g ;[ > mi I5EE 15 49 c: ><LcJ <3 49 :: U. aOa:: O< A < -Umuf<zoitJm..i 0mm <UUo13.l <>1 :V9 4Wpo9e: .<j iot. aLc-J9::i ao: II. 0 o0 01 Kapr 0q P C/J U 0 -< =(/)) zu; o lOf*0 o mi <H *O- r- .8 --B--C *-CU>0 0 O *** lAb** 0.'QoQ -tf% 9 f- 09 O >?* @.--A o. tfiqCtj Gf **fl0 0 ' NON 0 - o ,o CM * o 0 Orjp O P P.rO-,00 op P X v LJ O 01 :UI P JO O' I. :ui oc CL .J wp\0 N.Or r- fO.fcPV o o noi.o 'w0m9j0if .P ooo 0:0,0 CM-Ov CM iff CM 0 T-fOSO crK CM \ O 0 -r* w-evns. p *T--CCMV>56 o o 0 0,0 ooo mvc r* 0 0 90 *- STtQSQ S'CO'iQ cy .ur\ 0 AAN** OOP ^ C915 CMsOr- CM O O 0 *) 0o0 1 o 2 0> Ui - 0o mi So 0VO*O-v U. .0U0zXJ 0t*or.-n U<i 0 ft o*O *oO0foO1"'A* VhO* oo aoo-moocy oo P OPO-4OO*A"*PPC-M* oo*9 >>PsZ<I<"s--.oXz>--UoJi z2<f1t] >l-f O mi <GC whz- 0 z oomC.mcoOrN*nvevuXzi .UOz3zJ\oOo>OVvOooPA- mi < of--- iOO^lAOOvOOSOO COoM oofO ooOMooCAM oo 0^o-.C0oVJ.Vo0O o0o >> p .-<1 sHzUc,i p ioz OOVZSOUzO.Oi*v4O0O0Z0f>>-*lOO.XO0iU0-foA-i -<HoJ- ooCMoo*^*roocCoJ .ow0 ooi*s-iW*ooirSooi>O- oo0 OOcoOOh-OO.CrJ- ..CmooM .X< V) .;-o<?J- %oO0UOZO0VJ*o00O0^0>OA^-O00XO0..U8Ao' rI -<j .o1-- B-81 DUP040009873 TABLE B= 83 W iC filT A , KANS o OtoV oV) o se Q UJ -w9 < w '< ,--GXOi UJ . ,03 .o z > 1 u. > to to s<c UJ > ITS O' Hw X z0 s p V5 UJ O< sc u. o z w X0 X P w p h oZo y to 9 C/J z UJ O J.'OG JTOSAiO f^WtfS . o -:0 O'; O.1 H* On z SC UoJ O*-S x WX otfN OS LTV OS UJ X X w < H o H- o t-,OsOs r* h- p PtfVVD p p SOlACO r- nsy o .o pr" .OOOP PO tom *rm p o rP<\j 0 to On l Qr- z UxJ ,Pr~ o J O' -s NO os o u. p 1 o in x o> <r UJ p .X O 9z tn os ** UJ X X ooo OOO p o PO z ooo oGOo-.*" o*** .w-Zf* o o n ooo ooo h- o r-fltn o o ST o f" > UJ h~ OSX >s,UJ . : On O -J 30 f<-Oz I* "* P < X o px oozx \OU*"> o < o c/5 > Z-i <-- G X< p.vUj -- z UJ o z rx<Aoo1 ooo Ua Oins ZovN>Q<*/>- ? tnsp P o o *-op,- P ooo O r.c?SO O .to**IZ.GVI car-- . .6 O Zm.to \0p3tf*S 6: o 0sO*> 3r>n o 9 P in *-.9 Ours 3" p top dlA toJ- o o jf.N t*o-t8oD-sESr p o O ** OOP 0.0 0 w*Tm 30v o o .6F 90 0 ooo wmo ztosn *-M oO n> r* J9- opo ooo top *"*?? o oso so oOoOoP i^oto top a O O ooo 0O On to -to o o z OooOoP o o .>c-osoowQV ooOoP com to o o to to ooo OOP '*"- mffim** fo-- rrj > H- p UJ -J OvX < OsO X Hz UJ OoO n o ^z*-xo < J- o p S0V> z 0JooO xUJ ooo w o *<n zo Z3N.0O0i- UJ On X On O J o pz < OV fc- < (O 03Ko o z S0<0 u 01O _J OO XOO '<Uo wo o *sn ZNO*- >- 300 B-84 \\ ;- DUP040009874 TABLE B- 82 WEST PALM BEACH-BOCA RATON CpO Z m3O toOto O < to o CMtoCM o * to to to OP 9 **.9 r-CJto o o .o to to SO toCJto P o o SC 1J OOP o WCSIto o CSIPto P a o eo ..to O' ps f-to pto ..to f to o totof- to T-ft!o-.Pto o oto o 3M to St to .iJtf.to .. O n* o OP P HK2 z to UJ O' o to CC I wo a ir> O' to.80Gst.ojf O p *" to toto o ^ey to too to to o. *-.Wto O UJ MCSIto c ON o to to to o Xo 8 to O* ' NcvCcNvJjttoo o o Ot9ottoo p too 0*t0o.t9o o o . UJ - aa.: ooo o OOO o 0 0.0 o < coo -oq to.. 9 ooo to 9to --oH ooo o ftOh P to O & to ^rtoco ov eg 4r.co<y .to eg to to to < >UJ o POO o ooo ooo o 60 ooo p *O *' 99 wr f?* eg i ooo f^-toto oto to.CMto to to OtoO*P* w cw to eg to r- tt;xXoox . z to o> UJ ** tic Q -6 a OOO o OOO o OOO o two to to X O' O - 1 to ooo o CM CM to CM trot1 ooo 9 eg eg <y wh o e CtoM oto.ocuo6 I cg-srp o CM >o to 3 ir O to O' os UJ -i A < Xo . to X OTs* 0.0 0 oeg o--J oto o OH oop >oooto o totoo OOO OOO csttocw o o CM CM U1J t&c.. ior .ux .>to txXo oU -WOt . >to -- Si U K<.2a 3ttZ<oooo:_>--<Ur"! -J < tzUotcJ o -z Ur OVtiS 0.0 00'S o* 0--,9 aos V\o></l> o zwoooo; -ooto- zto- -J ,< too to O ur -J < oto QtO -J x ,tUZoJ p .z to zo 0oo 0p-'Stoo t\oo</i> o tUoJ 0oo.o0o -to Ozttoo^to* <ttooo UJ ova: CKO mJ OOvX < <^ tx(o0 0O9%0 0to%v1>-oo: to too .<-J, twmo 6ooo H O -to tOo 33E0to0~ B-83 DUP040009875 TABLE B - 85 YOUNGSTOWN-WARREN, OHIO CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, URBAN STATUS AND AGE OF HOUSING, 1980 Hint** -J * A < oo mr* o 1 N NX o !*!*** X.09 i--h* P O o NOP *-NP O .09 o 9> XwU .\000 AcUcf O S -tOf9N' I ooo o P 0,00 .P 9X o *- o m.NX *.p N00 p ddd d NWJ -<hoJ* 4o0m<.om0nho0r* oO0X w mm * *-.<o o 0 (A9-N O NNmIflAO d P xtft*- o f^Os.-Np oo oooooo r>m.Qs ** 8AMN Oo9m -N -.h* o mmf-*<-p o 0 f>* ** N O X*POv PO NiT p h-OX oo OoSuOroO\MPoOOfO Oo as .2X POnI XW .fO*Is. Xo J On --z0 VO 0 u. o| O -8.0K :Ul f a XOx oIoTNj uai X oooo CM ooN OOP OO NOm* -Oom oo N 9 OOO 00.0 XNOS WWW o o if> flO oxOpoOYm-OoO ooXN OOO OOO f--p** P SNO oooooo NO,*.O-9v P*O* 0 OOO .OOO NNOv o m X ooo ooo f- 00 NlA Oo tTS o> ooo ooo .*m- mift0p0 o o CO ip* > Ul H 0X .3MX OiQ *4 09n { < 30 O ' -H sHO 1<--X * V> X->J < --1 COX z< <i F-- wX p X OMX* KO </ 01 O oo ZuOoO* XO-*Yif*t O H1 O.u- 300 > w 1 0OS < 0.0 X I* OOn X o* 1-- XUJ oxz *-o Oh- o 00 00 .X oo |m o UKJOoO..a aXpmtft X 300 W 0CC 0O J O0X o <H' <V) >*X *Xo O I 00 v> </> OO -J zoo < Ui o % h* O *iA O Z0* h* B-86 DUP040009876 zz860oo*odna :Y *' ij. ft. i's j'i if sf l | p` *; V 1 V J- 1 f; ?; J* ;; j 1 SS-8 <*e -- CvZ v* o * om 0 0:3 oo O 1 <J> -4 O --1 o aco -+ r o > I'flO r OP m '8 o --t- > r- w x >- VX/VC z- -- <AZ o HA* O -4 ' On OOP m oo at. 0(0 <AQV o -4 o-**. PI O ato X H o --4 > zoo 3 r OP 3VD > r rn o -4 < <A<AC -- nc wZ Z >3 VJ!. O 2D -o m o -- > OOP m rz oo z -< O 1 </> H- <OOH x ---4 -4 o -' * 3> Z> O 3P r- Or-4 -4 * o OC > ZVOO o z . r OP H m< * w gprs 4? O wO -P*P O OOP 0* r* . o P4T0H o OOO o POO a VJS-* HO ^twv< O' OOP p cop a wro P-*AA O OOO o OOP w (S> IS) p o oo o OOP VA P-* P ov-*ig O ooo O O O' -4 W fHJ -4 O' vaoui o ooo o poo (Hi m* O\0\C\ o OOP o ooo M VAfHJ W o OOO o poo -e 3 m r mjt A o O A o i -* P os p -* P *4 Of 1 Ml P P o, z c z m 3: o -n p X ~ f*o 3 m z r\y milt O' (Jiffvw u XrO> -* a OOO OOP m* o HJ1W-* pi? - o V>oio' m+ o 9 os os wPO o-* p 4WO M>. ' ^ ; OP' HJI 0 0-4' O ooo 0 0,0 M* o HJI fO Ptf CO Os'3-P` o OOO o ooo m* o HAW o H 0ISJ -4 o 4TCB03 o' HjifHJW o 3 -- o PPP Ml P 4M o HJHSAO p OOP o HAWfO o o -4 o -4. > r*" 3 3 ri P Ml O <5 01 M P m r3ov P z' P -4 po uo^ o 'oaw Oo *4 --a* w O' O'pP o vnrpw o opo POP --L \6 - o roui-* CHOP O Osi\) o voyijp O -4 0SVJ1 Q U*-1UMtPW0 o 1* z c o o c z -4' o *n o X -- ro* 3' m z o > f* r* 3 > O m OH 2 o z -4 X' *4 o HA '< m > 3 Ui a < *n : f < z Of o z n e 3 9 > X' `-4 > -cCif<l.: > za > ma O' rt OcCA O NaoO TABLE B- 84 WORCESTER, MASS. . c 8Z86000H)dna 2-3 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND AGE OF HOUSING, 1980 iftWC *v--o**c0cv3rmEa oc O MIO<6M >0ipmH'- . a1 O-- 30VX` `O0 r XO30'f^^S1io cm -4 *V^0OO:.'*90w-O6^*I'W2*03 0 ^>|H9mO"I s *.* * Mi 3m0 >r sOMO tO-ooVoOS*Co0B Uol 6w><vAiw <--/KOAisCe ->i *Vg*ovOmo rm9 -t Oe-<I*00* oI s *.* ,, P 33n0:V20 ^>" i 3O0 w mkmfwf V Oo4 0OoUoO!MoO * *oV--0oJ0ioo0*o3meZO0 ->rm4 O'0iOifyi OI -O-44 r> o3XD-V>**2oO*T*OO to 30 vo w? S2 m* \ooJf oooooo HO>4 *Vvoo--OOa2. .i.vKoo0<o-rOff02tPoGo0Cm3O!0* >-4 mrmO_I r oso>o $ i2m*i nx Ctoootf o0.o0o0 Pq jrwa CooB oooooo Noo-- *' Goo*oo4oo& -Ooo4B W-oo*OWooVoo'>-4i 4OOoB*' tPOOorOOV*OO-- vCooDi wtooo-oo--4oo* VI Vi W-- v--OV OOP ooo &-- o to-- 2r\n to OOP o ooo O 4s o Mto --1* -4 OOP o OOP V* CUi' -- VoI ---Mto OOO o ooo to Jk- to viKjiSr oo o oo ooo ,UoJ0o--ooo--0o-114*i*'ZxnOxom3xo--oCxnrD O' OoB OoOoB VVooOIOoo(MUooI too: o9oO-woO4oPVO -eoo4h 4tooo4oo6 QUooR PooN 0OOOOOO--OO2P? *oo4 0WOo0ofOjaSoPO ->r1 o w.prto 9 pop 0 O'Uvt o CKtii o jroo p ooo o toJTM o -40 to O bvib O' U* O o WOO o W40 o p VWi*Mr U b o VIW * O ttt.sr'to O *4W O' OVttfO O W2r -- O V Q0.C* r 0 sr?-* O p\o O O2^0v OO 0WW-4 o .p --VI o o oo41 r0 --o00<*-3n3a460- O' otto-* o p vOdw O WiOCDi2 O ttOVVO Oa 0*4-4 o o*4Vf O U01--W--M O" 4T0Q oO \VOIMN--tt O o CoO o ro>uw OO* UO lWW* O*> O OP o 2oTtojr*-4* o io o e Vt -- W O . 0 0* (*4 O CBwsd v-4*WwCB o oijr 6Z86000t'Odna 1-3 )} `3PU3JMBq pUB `S)i cE>f9d0J_ XI *<asBuv UB$ PSq `xi `puBiptw av `unia stud TUq `av `X3a MW' qqaaN-xaaa amn XO *P1U3 PUB `xo `UO^MB-1 XI `q XY^8 ^ PUB `XI `opsaei NW `aaqsaqdoa pus `ift `ass o u q &q ON `udqBuLtJng pue `on *quj,od (6B8 ' pufi `uraies uoqsuLrt `cuoqsuaaag 11 `*q.i3 BuiBUBd pile `il `qaeag uoqjBM Pd VH `piajisqqtd Pq `VW `aaq.su iwoaq-fianqqdqy WN `saanao seq puB `xi `Z[q 6 6 6 VI `Aqto BMOi pus `vi ` anbnqng JLW *sL|_B3 qeeag pue `Aft `aadseo Xi `uosLuaQ-UBuuaqs pus *xi `uetqeqs aBauoo-ueAug 13 `uapusw PUB `13 `toqsiag AX `oaoqsuaMg pue `\8 `uoqBuitoooig ON `sxaoj puBao pud `o n `spaeuisig 3W `uanqnv-uoqsLMaq pus `3W `udBueg : sated aqq aoj. uoqs aq uea Apo sa[qi?q a [Buis pue `adeq eqep aqq ud pauiquitfa uaaq peq svSMS Bu M]^[ [_6. aqi *AN * Bat13 qqtM pauiquioo si uotqBindod siqi Aquno;] eBotl aoj. uotqeindod aqq qnoqqtM UMoqs si `Vd-AN `uoqdweqBuig uaAtB si qiun letquaptsaa qo aBe pue auioDut A(.LUiBq Aq uoiqnqtaqstQ -sapea LI id saeaA g oq sqquow 9 paBe uaupiup 4BA03 pue suotqeaawnua snsuao *'0 0861 J-d sadeq moaq aiuBD BqBp aqi 'VSWS BUi Oq auneu sqt saAiB' qeqq Aqp aqq Aq uapao IBatqaqBqdtB ut UMoqs aue Aaqi ,,'Aqt3 [Buquaq uj qoN,, pue ,,Aqt3 [Buquao uj,, sauioBaqBD teiquaptsea aqq woqs qou pip adeq BqBp snsuao aqq eaaqM `aM`Mw x aapun sudLqej.ndod [Bqoq qqtM SVSWS S6I apnpuL xipuaddv stqq ui saiqeq aqi 3WOONI A1IWV3 0NV SNISfiQH HI3H1 30 39V 3Hi A8 H3X01IH3 9NH0A 30 Sa38WflN 9NIM0HS. OOO'OOS NVHI SS31 30 SNOIlVindOd HUM SVSWS Q39X3W ONV iVnaiAiaNI 30 S318VI 3 XIQN3ddV CENSUS COUNT OP CHI EONEN OF M i . NACES NONIUS TO S YEANS "BY FAHTLY F H C W t. STATUS ANO AGE OF HOUSING. ,0 0 0 0886000fr0dna ft~3 trxncz i -- OvJS > vr* 03 ^ om r* oo ;o m O'O o i <n a COCK 8 4 o -- X PO w> 4 < o vn > svo r* O'O xvo m PI >*ri r PI 39 :K- <f>> c -- OvX vW Opi OO X oo O 1 </> </>Q\ H o-** a XPO -4 4 Of > XV o r %0 Xv PI H >03 rb*8 o 0 -*81' w > X 2o X X m *i ro OS <IOsW* X, O O OOO OOO 0-- X QCMv' CCMK O'* --* O O O' P OOO wto moot a o oo: o- ooo f-04 o ---- tOvrOacM ooo 2 </3 H O z: 1 > c 03 o X' </></> <z c-- OsX UT ^ 8 g 0 0 30 m oo 0O 8 <ft c* </> v I -4' O-V o. 94TO 4 . o > r X'OO 0*0 d.59*0 8 o O <0 a --We -- -- . wt\jo CA o ooo a o ooo * CM *v -- o OW4 o ooo o ooo </t(AC H -kC\2 > *Voo0jn-o0*<iA3O0fOv8 r0f38: aI *4 O -*' O-4 3*^0 10 > xoo r o30 >_ PI H O r 10 -- po OpOoOo <-- M 4 VO VI o- OOO o OOO <--ftoWs aC: Vl O * om 2,0.59 oo O <tAO<Js> O-** O X-P' I- X0v3O 3 PI 5 X O> *4 OJrcu OO OOOOOP -- w(g----g V8 p OP P o OO t0 -4 os jar P ooo O ooo X Pi ro ov -- bscoro o OOO o OOP CM 44 -O4hV--iI OB O OOO o ooo VI Sf--1 44W o OOO OOO- V--I --MWCM-M o OO o 00.0 Os OS o O v 4SISJ 00es-c0* ooo 2 OoOs' OoC0KOoJ0?cOo*--a oCoooM V--ooOoo--CooCMM --CM soo VVooOI oo--Woo--w v--oopO VXoOt-r'-O4oormO--o': o 4? w -- o C*Cr>4 --J PO --* o V*W -- w-w o WWf\) o: vttChJ* PPM O VK>^ o --pro o uiro -- O w-sj OO V-4I.tU01---4 O -- `Vt o pp-- PP-* O' PP -- O PP -- Ospui OSM -- O VlifOlO o vi w -- o os--to -- -o ic OO 0WVfvW; --r O O PJf 0> / p VJlKl -- O .POP o O 9W O -- 0*4 O V* W -- PP-* o cMVi to o: vi --j O VHC9VI O P W -- v0vo -- pO OroS --rou O VPWCM o 0vl0 o oroso O P--VPi-C*M O 10--si o pu -- o *OvW O VT^JP & r> ? tioat. o i5 (So fO "H .1 1--0. Kox |S:5 X v P tsz i p *V 59 m --i fS-o Ip PI 1 X' Mto.POI feyX Kb *4 i -- tn x w. 8 X 0 ax m x. >. frT~ i mw Sor X. CA < PI > X w 5 5. oo X PI w H> MC CO I o PI o PI o ct CO VO P .03 o V I886000tf)dna $-3 V-*I*PomX *: o i </> --* 33.CT O' 2'flO OO XO m I eI* w<oo * OpoOoO 0 1 3: Cft eft 9 ww-- \* \P4i-i o Poo poo ^ft2C *VoV mO 88* <lft<P* O^ X2 0 > xop f w'fl. 39O m ->I CrO " ai s--o 9 -- n r s- Cft I*OOV4 2OorfOotafOo--* 2 r*! W O povv O OOO o ooo <--/*<P/>2c Von OooQoi3<Sa 3O0J--TO i o OO XO m ~>4 r9* m n 1 -- 9 m x. 2-or X' 5 9 oomi- UoofVoIoV<oo4 OX' X 5 p Wtt V WVT-4 o OOO o ooo 00C -H V--P*PXQ, poOoo<x0 >rm o <ftCN -- XJ* r -f Z'OO OO XmO m p 1 WM0O oo--IV oo--oo-* 1 r ---- P: JS-N o o o oo 00C 'Vo--0Jolo0-P nX<3ft o <--/**P ' z %tooo OO XO m H > mr o l -* 9 9 ^ o < 4 X *roo4v OOO at'vOOftOOw oX w IV p fOPP o oo poo 9 ww Vt W-4V* o OOO o OOO Vf mat ,o o w *IV1 OOO pop s -J-4W OO W P OOO o OOO PM -4 CD 0 9 -- o O O O' o poo w SN o OOO op M.. VI --4VUV w worv o o o oo w <v p Jsr*4-vft o oo o pop Vi -- p OOP o o ooo ST wVi wvt4 o o ooo o ill -- -- p -- OP ooo o ooo WflV v -- to b VOP o V** o -- Jr W b 02-4 o v--w b --b-4 s` p --yirv b tobo -o p b vtw -- WOP bbb -- p VJIW -- 090 b 9 Vi 9 o vtp p ---* b Cobb -1 -- o P W o uiw o jr-ww p uuy-- o OPP 4 OO' MWM O diM : p Pwyroi-- obro . *o' .SeP"NWi*--ff S02 o Pw o vi --W o Pw -- o 9-- . o SNO b bbb p P ----: p PO w b< *44TO -- po -yro P0 ro-4 o WP -- o VIM -- oo -- b 4* Wp -- - p -- -- o o ^Sl.pp o w ---- o W --VJ1 w --p O-- P M* -- p i-aoaui O O'O-I MoJkICz92- -- mx 43 9 o-n 1 --o OX p->c'r a X -- m. 02 Si 1 m*,- o 9 lo ; H o; H >P" X X m f o: ur 0 Jtx m. 1X --o on bvz 0-4 mi o o o 9 o m 5SftfCtX >-4 O9 >s2x mr * o ftp . | <*- ? 90 0 9 9 rxt ir* PI > > rf !8 3 30 > x s pi r 1p f n T o I 3 2 -4 X 9. --4 yi < 5 X CA 9 < > X p. --' J1 D p 2t i m1 eft H > c Cft 1 s* & m X X o Cft 5 to 9 O CENSUS COUNT OF CHILDREN OF A LL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND ACE 0 f HOUSING, I9 6 0 z8860oow)dna 8-3 vxftcs %u0--o*0o*Pt <am92/> > --rmo_q* viP r 9*0-4 -*' S v U--k r>- I'OsoO _ m9sO om ? 9 * CM * mp p O O'O O OOO 9o ** Q * 0-*O9VXC >-4 UT* CD *o <oo*/><m9p/y mr* or -4 0-~> OH 9..** 0' *--l ' >r Xm9s*v0Oo o>_ 9CreA' 9' uCMi -s*in.M OO O OOO 1O o 9' v<UmooAlo<Oo'i/V\rvo9ZeC* Hri>e". a -4 '0**O i I O 9*' W -->4 X,. N* OO CM f- VO _ 9re SO O> X * OWN *O -COOm'OPU'O* m* to OOO o OOP > i-: * CM-* r" CM O O CM, OO Cft OOO *X4 -' to so *Ossd o OOP o OOO *cOo C0pM6poto SCooOM SPOOOtOO--o*OOCM s*Oo OOsOIoS)OoOs 0WC >umtrQo.s Zore ooo0< 009V -4- 0-*v ->r4 9.ir9>ve*si.oo0. H >pr~ re as CCMO m 9r a XO' too too o CM -* mT HOiflB o OOO OP U*ooS CoCOMM.oOtoMO -*'0UmoS0oOoo' s.CrZo9e ->prr4e- o i vi a H 0<m/>%p I O-4 9' **0 P *' >r* 5O9reS'^OO0 99 i .f t*o -W--Moo* o rree -0>4 X u to to so SOHCM o OOO oo X 9 r9e. wo4t -- . *o*oM' *O-OM-*OOt>o PP as'i OO'' *---OO*UOO--TOPp C*-oo4M twCOOoM*OOy*OO* SpoO POOMtOOPoOOO 0: *oo4 p*osoO*o-oH OX' X 0 1 9f*1 O9o-oJO*IOxXm9"9_H 1 - ox Os -- *5 tonxs Or->4' to CM CM b HOsOs *WmHO O vp-o o U-4*9to*-4* bbb o OOsO*O b bbb U*vln* b top 9*--Mm -^ CKUISO SP0tCoM-H P CM O o *MJSC)MP SOSO CM m-*to O' *S0Ut O p*p oO s*o*usut 0 o9-oP1*.nnX9o9' OH O so O-*S * O s**ttoo CM toPto o a * IS) os P coo* P o Cm4NPO O *C4M-p*| P **ICM oo vo*o\ o ' toOSCM PPitSoO CM ' V--q b osto-4 o ->CMU1 P *P*tHo P b P-MCM o PCmMu* b bbb o0 -oH E886000t'0dna 4-3 m-vvcr --4- *osz > V**' p- * o n r- 0-0 X m OP O 1 </> o </*On I <-- o --* 3 30 --n >o p :voo r* 0*0 5n0 O X o X in < rr** rn 9 x. xr -- ro > ij o\rjo 39 ooo op Z o m z in -- x t v p--. > Z XrOOv o o OOP OOP 0m3 z: H OXAC -- OvZ v*v O03n o O' o </> 0>Cn -9 o --. O 3-r H *o > ZVOO I- NO 3*0 m H > f" rn o ro NO to 3 o o 7Z H o < > (A 3 rvs -- 3- OO* o OP o OOP --o MOvca ooo o POP 4-- \o0 o 3XT-- -*o o OooOoP JH>f:l ; w OQN CD 3f\s ooo O OOP </></> a -4 -4 2 > v p** a * on r~ 003 rn oo o i <n o <n& i H o --* O fvj H *o o > Z'OQ r O' zvo m3 ih H O r o -9. VP CM -- > Z 3 Uivo o o OOO o ooo: X rn 3 -- o m 3 45* ro -- >4 o co -- ro ooo a-9 P ooo -4 ---OiZ > w* o % on ooz 1oo O v> <AON r m O 1: --9 o ** O zee- INS H o -4 > X'OO 1" oo NO - rn 3 rn X rn 3 -H O vZ- > PS C* O vr-jxr OOP X O ooo N-- CM MOto O oooo ooo fMO --t Cb --p -- O ooo ooo >do *--4.---4 *4- oQ ooo OOO' </></> c -- CNZ VJt'-* . * On 003 po OI0 </>Ov -4 > F*. n C5 1 H o -**. o 34^0 O; INS ON > XPO r- 0*0 33*0 n3 > o zn 4 o z * n -- r Vt ----- 3> O OOP o ooo Cm O-- O ooo P poo PCD' CroNV--J1 -4 O ooo o ooo W OoNv O--W-- JrT O o ooo --fc ro4' o W-* Oru OO--q OOO it OM O--wOCMOW-- OOP 4 C054 NCOKO>'--J? o ooo OOP p -VP CM -- vjl W O CM O ooo o ooo O *-* p ZCn O 0 O -- 0 PP -- 0 QUIO* 0 O VP VP O" CM'P--' O -4 VP -4 b bbxr O C* w -- O VP ON 00 O VP xr ris O ,O O ON ---- PON *JVP 4 P 4-- P z-* O O OS CM O Of\3 O ON XT 0 (Mp 0 -- 0 CM -- VP b CM -- CK 0 06 -- p --:M3 b Ovvn 0- vn rj -- 0 -4 own O' 4 NO c* -- vn --r -- 0 fVJ XTO6 * *t O wo -- 0 4-- 0 VD'K)-4 * * O XT NO 0 WON O n o *vn O P-4P 0 --l:-- -- 0 O CM OSi ' O: p Cm *4 -- O VI CM -- O' jr --^ - . O INS Cm Ov O CM X? -- O VP ON O Pvt \P O osw -- O -4 -- 0 O Cb\PH d On ---- 0 N3 vO -- d ro -4 -- O 4 -- -- O H0 d O -- d VP CM -- 0 XT-- CM 0 -4 0 *4: n > mXm r* < "* z o S' x. rn 3- : r1n -- PZ NPC OX --n3 So 1O'-n --O k*nOopN ar--z* -- 3n 1lV* iac4AO>` Z' H O>rH*-- "3m0 NO VP 0 <o SJ1 3 on 3 --O on C7N'-Z OH *0 <4 ov 1 O O H O --9 > F" nm z ccCnft o oe:. d x m Z- > 'r- r* x>awm x 2 XW O vp -r>n` < *>Xn 5 >HC-I in x>O' > a rn n xCCoA: CENSUS COUNT OF CHILDREN O f ALL RACES fi MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND AGE OF HOUSING, 1980 meooorodna 01-3 --l "s-n*cop omxz >wrm* a O I v o </>< I -O44 OX%f^ir'o vir* r> XoXA>to0OO C7 m 3X* a zz \> fir'fir-* O' OO oo Ctf o-** fir * O OO <f>V>C -- C\Z vi- *. m so at </> <4 -<*/>* ->t Xxtf*oi::?,O r* Xtto0 n T* > m r* m, o. 8 ffii?r O 5 0{AC 'v-0o**o0oion9Za H ->4 '! oXX. V*Vf0i*Or%0OO. r- sotxoo m H tm>ro* o 9 JMr . so 9 0e9 X X X 4? o re tore-* oo 1 o o ac $ to or w re to o re vt re oo * OOP "9 ITt fSJ o 00N ooo VI 9VIM o firWO o OO 00e H v-*i*as >. * n r* so m ooo0l 00 of -4 O -- -O4 xf*ir Mfir > X'O r* to S'fl o m or e x m 0e9 > 01 re 009 POO >r Q ppo > Vrei VtfirrV to O oo oo 00C v-*0v 2 *o.oGstsn. oOo09I00% fi? >w; rr m rt > XvO O r NO SO VO a m Xm X o4` fi^re oPOoO o* or O roea> oo o fir fir tO Osw. fO O oo o oo -* *4 fir oo o GO o VIU* re tO firto POO OOP fir.-* o* -* VG C^ > OOO o po c 0-H> to w re o OOO o o1 X. X m i 02 JC X m 9o'S0O I ox --or* o X omz 4 o o X I -* 10'-- fir -4*0 C* oooo -4 0* M -* vivto* OO POO Vi *4 re vi -*0*0* oo oo re o tOCM to 2?-Si o oo oo to vi re-* firvt GO oo oo fCi*tfOi*iu o fiTlS) M v*co O fNirUurlett fv>U*KJ VI V* oo o CK0O**0 o PcK--i-ro fir-fir'--* or Vr0*'Vl 0 v-fifwiT-fi*F W0-^ o fir o* re VO o Voi vu o o tuorefir tch* / o *t0*lO-`tO* UON0tUO O fir Q fiVrcfiur-*4^ O N9 ViCri O iJW0 0r W 0 oUl Cfiorlfi?i gCmKoo*o* l*re O V*0 ON# o o* o -* fir fir O M-4* l\> q>-* O' -4-*W sO' 68 m ix -n om x -+ O T o CO -J On ** < H* * . H o X Sfi a o C O 0 u. o * Wo o f*- < o 6 t* o x < lX- O'ON eft WSh .a o X1 < .uw. ion (A ON % * * W . O OIT 0as o T w > d Xft. r U<. i < H 0 (A O H X <w > Ol in o * i o <0 N- Xh- vw8 .w**'* XX oo x wo -* NO o (ft X p o*--1? Ui o Lb p m < X or- W .0 < u. ax If* X O*- o I' w XUi x ft. X o m* J 'X p u ow +* Xa :0 x Xp p I---* (ft -CaA >m"J. XUI O X<u. mn o m eftPP p b o iftlAp ONNob CMP O o *O " MOP o bob b Xlft o tfV O>Np* MPO o b O r- bbo 1f\.to o b oV- cft.X.X Pma* p o " iftt*fr* Ml** O o TP -h*M . . * *-.XX p o .0r* i" h-.CVl . . o e o 'TP V,-mC\srvr: oeftp o o** lASOO o '`ftl'O o PJTp t/NMCM mto 0 o o1-- POP opo tfMft P o o*- \Qr-tO M Mioeil *- **>,m p o o TP bop Nbn* ION o p o XlfN*f*pj rh o o T* in pin p MinCU o r- eg so O M r-f*. CM*- p p o o T" C4ro& WrtJf p o Of- fr-ONJf i^pth o o oT* POO 0 J0T.0 -\M.P o o ON e* g" ooo ooo eOgNOlft p TP CM ooo V0O.N0O0M Csito o mo NO OOO ePftOpmO rftltO pJ o1- ooo oeft oPMo o o .eft .jr tr ooo ooo XNOO\ --u o rOov w -J -_*i* ooo ooo *- ro eOiNi . O to NO a o i- X < X 1. 0.0.0 P Xc OOP CMlAO o h* -.< CM CM 0 X a i X p < .x<x. w o On X OvO W to O.v X ><- to O t toco o O *ft o UI POoOo w wo .0 O lA iiC- xno -- o</></> ooo O ooo O pf-<*- NO ooo ooo a-tojT CMX Po ** < ooo o > OOP o 3C POO t-T pX X o (A w -J X < X w p ONX ONp w > to % p w pox o.**x xo NinOWi o -oo xoo < o H w uo % CO o *m <H- DWW ooo ooo TP *-- o oNO to ooo o oo o oT"o.T" o CM >< ooo U Ik ooo MV-p w > M UI o o On wo X 1 Ui p ONX On O -J p .OOvX o^ < to o.xx O 1 NOW H pwo w w oo xoo wo s < O D2NVO>W*- OOO oCftofN*orWo oCM Jf OOP o ooo o Wlflft J* rW POO o ooo o p-pp p u. Zi < a Po Xw o Otr>n ONX On O OOO nX OPX J <1o- 1 p wN1O1Wa ^o0 -H* w-J 0< h XOOOO oUIOAir*\ XP*3v>0 0 0.0 o opeootofN o NO eft eft K > X1 X X w ooo o >- ooo ^ irun JT to TP m WJ w 5 eft X X X POO ooo *-ON o o to xo TP w ww > p X X 5w o o g? On X On Q OoO*n Z OPX w -< for- .! O 1u 1 NOW o wi o OO w XO mJ w o 0 o *>in < XP** H 3WW C-9 DUP040009885 fr V CENSUS COUNT OF CHSLUNCH OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND ACE OF HOUSiNCi 1080 oootvi o . .c ffrr*8 ^0--xP . f*r.-*c.fa*raa* oo pppl 0 fKrYmtfVpP P tf\f*P N*~.0--zO8 ^ 9 CVJPOt o a> ac-9aaa* op. .o o o p fJsUOOfrtUS--eJ*OI9OOaT-'' oIfUTIrs *wOSo^ So II ti fUiC! oi- a *5S w z fr-o>iA, . mJplmA Oo pap o lA* frm4 O CMfr* P fcr-aCPMm*^tA"p* 0Oo- OK O pa-frmp o9 m.mm CMfr* 0O 1 # Poo phJO 0 p*a*.* o- frfr> P p.iA.iA P * 0 lrA-.!m*-Kp pP lAfrp c.am. p o: r- a p poa o OMwTValA oo o QPiA Q\ Olfh O *C-klJACCMUlA a\m CM p P--yc0afrp* op (M..UVt.t o a*-<.mMi~A o **frjp O ptmAiaA oo OGMoOoOOfroPPO aO(ft Oa00fOr,O0fr aoo 0Oor0NoO10oP1 pmoofr ooCMooCooCfMr fmOor O0on ?aO0.pP0 P5mop* *Oo-OoaOo ofmr oof*r-0oom\oo aom OOPoOOoCM POCi OOolOomAcOofor ,oom OoCUOoA-4Oo'lAT aPr- 9o oOofr0oop1oofNr pp fr S s a oo0fr*e0fr oOP 5 X w OsZ IA oO o4, <K 0aaoi o' Ui (COO _tni Upi o%t>f\ fr* OUMO oooooo m po--o{ ooo ooo CMP OS O o lA IA 0 X w <MA 0\OoOA<1Oo0PPA*i.i0XXWQX50. < >o- KOO UJ P * *O9J0H%*IA aootfoofvrooo*v* Pooo OOO ooo mFAiAiPt-Afj p Hoi IA 2 i Ul OiOSCUl mIA 1ooO^0Pfg0-QOSf fforc- O 0* O OO Ui fl-OO _a<frJ WoseOa*(A- 900 POoOoOt.OoOfrt ooTcOu X i 900 o 0 CO O0OfO* T- CMP o oeo >was zz .X omooo*oor- 'OCOHMI <Xa * OOP o mOmO%OF- p fr* CM 0 u. pA 9i f<fl o00o0POo0o1%^iXUiCoop;ii rtwofOoo<%Oo>m- f<VOr-- 900 ifr llAA POOOOXPw J< Oi <0/>0l O O OO Wwm< wXazaoO~Om~ fr 900 C-12 DUP040009S86 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND ACE OF HOUSING, 1980 "<foymr- o rffiO . mr-jnrmot -oo 0v'oos) sh.r .O. **.*-se ' p plAfiO O f|S- O <o0 IAvjtO P SO #fUriSt\ o PS0 NN4 OO ' mOVin P0 OO-tfs o ?" p JK0 ,UOOxSI*oIf JtuUrICnh o PPm o o .pPOf- Omp O --| win p w *-mCM p no* Jtso --C|tf oO J-OvO l^onj o *' P PPSO o xwop<^va^rr . P omm oi4g o p or V*O^*GfOvSoO o :0 > V o X.O UI o so O If* XCN 1 1" w a CL U > .X .< POO OOP o o VO o 00.0 OOO JMPJ ,CMf-VO O o ps ifmn .00.0 OOO M*1N o os OOO . OOO cum^r ` o o Gs OOO OOO GDin ."`Ctf 0 SO .sr 0 0.0 OOO CWOvff CMm o .o o VO OOO OOO M VO Pooo Pm* CM . os St PCO4OCOVOOO o p OOO OOO m\0O *-mcv o <6v OOO O --| m CM o h CM < . I* fe 00.0 OOP -p*Ov o o st .0 0.0 OOO T 0o2 m < > Ui wi -J > r < o 1U0I OvO , J OX < so o * *-> OJTX o **: 1 VO0 o v> i O oo ai OOO w o . a 'Ain < JBJkOf* h- 2 OOP o Urn OOO o ovcm CM -x CM o < Ui S3 i > < UJ a free frQ J OfrX < O* sr OJK o o t seen P </> i .0.0 UI XO.Q w uo ffi o -*m < *- </></> OOP OOO mom f-f-CM O o o m .j * > L tc o .. s< o Ui a 0 JT I O Ui w S3 < .w Ui OS OsO OCX O* o^f ce *r* O 0 V> O OO eoo Uf O o D00 -6 < H- O H- 6 OOO o OOO o o fDfrff% o :Z m in < < : Ui o cr o CD o o Ov .. st i O Ui CO -< u free frO QCVX o* os-te r O 1O0 v> | o oo KOO UIQ Q Mf> Kifli" 900 < H* O V) 5 Ui fl 3 O o < ui o in i p Ui w fi < c-n UNDER $ 6 ,0 0 0 $ 6 ,0 0 0 -$ l4 ,9 9 9 $ 1 5 ,0 0 0 OR MORE TOTAL 300 1100 2700 4100 MOO 1100 500 2000 300 1000 3200 4500 1000 3200 6400 T0600 7 .3 2 6 .8 6 5 .9 100,0 2 0 .0 5 5 .0 2 5 .0 100.0 6 .7 2 2 .2 71,1 100.0 9 .4 63 00 ..24 1 0 0 .0 DUP040009887 . <& < to H as S3 Xo P u> 9 1 f" ui o X3 r* < *Q C < xp P U4.0> a Ofh i < UJO a. tr Wa ui d Si a: .r* | UJ > -4 A> 1 ,u. -1 < >K 03 O 0C0O H -< Ul :> O . .03 b > 1 V) X Zff H* Ul>2 .00 su 4J --p N0 X on 9 i .Ul U-o y OlTV < 00 f- Ui -J CD l X < in X u. oi Ul as .00 Ul Ou 00 Q J X p u. o Ul I- -X Xo o X o v> > p .a-- X .x Ul < p -u. *"r- ar CMfv O b o r~ t-.af tMOf*-.arat o o. o r-CVJh. 4 PNr rrtiTi O * o o ppm .000 T-.arar O o o np 0*^ at f-ariar Q P O *-- .0.^4 * isrr^f^ O / o p c\iAi TO VO p mojcvi (Nif-O o p *-- CVih-T* '. . WfNpk o o * PPfA ' m>Ap fom o o o (owtn .m o b o * ounP * . * .ar in T-iNin o . o o .! %o * ,* r-in.** P o o w- C0WC0M o o P - h-P OJTX o o o Pf XPP in t o -- coin o o ** pop OOP p o f" m\o a n*<w (*704(O o o o 4-- OOO o.mih t-- (*7 o o o *-* P P ** -.CM o p t* oo :o N cO N .(*7 p p .ir- 00:0 OOO p-*r-pA f*iAp O p 3 * OOO 0.0 OfO cum o o o p POO OOO <g o o p o ,CS1 00.00.00 (*>0(0 i-crr o o NO 0.00 OOO ar. .wNO . j*P P OOO OOO o?np-W o o to oo OOO T-ir m *---} o o ar o -J OOO o q OOO o p . .f* CO X 3 -1 8 h QO O Ul u. oo -J 0X < O^ >6 oar a; .H i <i> P </> % o OO Ul 00.00 -s Ul s o -.m < SOf f- 3V>< < U. * J < -.00 . O Ul <u y< i 10 00 Ui OO o u m p yi Ui -i eo '< OOO OOO 0 0*0 CM$M o o p in OOP OO xar o o p Ul O 00 O A\ o p * A* \o</> : </> a OO OO ui . o ^ ZvOr DV><4 -J < >- o J- Pop OOO inar*- f*7|A o o o -J u. OO . OOP >* p H 10 .mm P o h OOO OOO ncuo ff-M o o * ar V* < Xo OOO o OOO o X . ar < % X H s JC 4mC < OOP ft OOO o >0*0 P i-arw -x < -J u. .x OOO q OOP < NtAf Ui CD o o o CM '.X O H-1 g o ui u. o -j ox < p .O ^ h- p oar O ** O J- 1 </> p H O OO Ul OO o-J up ^ O A < h- 300 O Ul .li O J ox < ar o 1- V) oar o *A O 1-- y1 00 <f> t O OO Ul OO -i UJO A CD O A .< xvo -- 300 OOO 0 0.0 CM **7. r- CM o o o X OOP OOO pmo t-- o o CM OOO o OOO o arp r CM < -2 -< X Ui o w q < Ul P o -J 0X < OA V- V3 oar o *t-- o y1 *o</> V> l o OO Ui OO mJ -UJO A m o >m -< x*o^ H- 300 C-14 DUP040009888 Csh -J -h< . * 1p- x 35 Xo o Ik .BOO' o ui : < , .pOIN*' -ox < wIp< fXupVi.CcOhh .uXa- -otiop1r* ut -..x a> .X M > -rO** UXU1J* up 1 m> <h1" V) -~f><t6 *n l <00* *o* 1 XXtHXoo' xU--XJJoVnt>oO*. to -up<i --<JI Lk yuX.,tioi XUmJiO--n' xX.oiOpn> o XUJ &XU1J XQ_I Xo u. ou -Xhox* -x X XCO >mJ XU(OJ p mm X <Cw jr# a* eon tp 0 .* p0O** "' h*W totfvm p9'jr . op* N*"0 IfYCOVO Wtf> .o r **40 .-Sflft w-ap o .o.op If0.tOCM3.*tVNoO .Po6" . XrZ~f!trPo-,VC*totMf0\ O po.- wtoto Vjpp CMN O toWBO On p p * CM VO o P" o ipnrotitAo -9p* VOvO to*"0 P h-rvOJ VO.r'CM p-vpcvj P o toNto CM. p*-Wto 6 p . CM. : tf\W N p -80 o fp 0WlA VOjfOv P- '-StiO- p- p *"N p* N>lAN K?.lA . O f* |f\MP .to n .-- 8 to in O p wto . VOlTsf* WlA o Poo mm CM-vp o o o p- o oo O IA CJ o o p 0o-o0-o0 CiTMvNrrjtOov ,p O m GO CM oo ooo <M p * CVJ CM tom O O lA .* p OOO OOP to CM <VJ..W JT B o OO OOO .X NOflpO % UJ a* tvj s H -h UI > <u. UJ X oo toX VO o IA XX ` p 'O 1 pv> o <S i o o UJ xoo mJ .UI O V CD O -K< . xo-- ;30V> <ml b<o h- OO ooo flO.P'O lA IA in p* OO OmrO** CVJ-JP o a Mp* OO o .X -.< 0fi0P-S0 CM Wm 0 Ui .J < p 3 Xp> Xa. i oo oo p* Pf* o r*4 w 6 J *- , * w >< bk UJ 0VX Ov _J OvS < p* * H IA OJT..X *K-- 1 vOV> P w 01 oo xUoio.ok ffl ,Q *tf\ JC_r- 500 O 0.00 *-CJ o CpM < X % o do O mJ .ooo UkJ u. CVJ/^fO cvi CM V5 H- H a. X -< OO OO .O0 < CVJ X X Ui V- 1/i Xk OOO Oa-OnOiv O o X so ow kJ 1 X X X X o hk-> Ik UJ X OvO -J ox < *. H tn t O-.is*rx 0.0 O H p 01p Ui xooo Cq JO < UIO * aSB sok*i-n. H* 300 OO 090 fP*" ff*o vfpt o a <0 OOO OO vo---in**^ O o m m OO o 0.0 0 f^ph* 0o oo OOO CM < ij < A UI Xo Ui X o mJ u. UJ X . mJ ox < O k >" in OJC o -- O h00 P 0 , UUJJ .0.0 XuiQoO^ p o kin < X0P H- O00 ooo ooo \p0**m-Vm0 o w .v-- oo oo Op t- OM o 0v o o oo 0 0sr CM :^-CM X 0.0 wOmOO-- o 0 tft UJ .9 X UI X o UJ .u, QsX ' .-J ox < o .**- VO .^.X o AP f 00 p V> 1 o Ui o xuooo* < Z0' kpin J-- 300 C-13 DUP040009889  CO ox J9o o u. ,co o W .r< . ZQ < m e iCsO ZwwvoC pw wX oI 0.1OT >-J [ 5 -<woJ m > S o CoO .was xWW a: D WO V3 W w .X -J < WOX .--xO wf I WO Oin UXiof s:'PXXo fwmXaPi.j u u. ' o uxooX p C9O > CO Xb<j .t -*WmvoQ WiOO O .CM. (0m0s.0a o P COQOlA wCCMMcPo O h- OOP . CMW lAr-W p CJW CM fw , .*m*cM* * ^ wo a *-p p CfNO wW O f- o f CJIft ca p a om o (A o vow CM O COW tWoyof.vsot a Wrt rtfOM p *- o *- CMAO o lA P fnfO,6if* o POOOO .PAWN>0 *w0f Poo O PO ujf>in CM q . Of OwOto -- w ** l*Ar> CM OOO OOfO5 cow w o vo in o. OOO o tPfNOCMP o o 'O :ao. x H .X OOO o OOO com `of -v in s $ SO a sXWo mOOOOinOOin omn XtXwpoXoCwo1O wf pt ..wfw<fi vwV3oxOx>Q*<ioooCf-ff.^*t>wtXooX8XUooo0A-I -w<woj OOP WO.OlftAOfO o CM CM OOO .OOO i-CfMfw CM Xa,* 0Or.vO0ocO0w3 OoCCMO UVXXowXoX<-)IA wCM p1 U<wwCQI .ooOW^*OKXUxoI oXwZxo. 3vo<oo/O>o<oom/f>* wwH<o DO OrOoeO- -o.VO fw OOO O _ op .0 ** ssoo X o wwOooJ w0Ow.^OO0rc.OC0vMi O W X -XowJ XX< nw ot wpw<w <:x9o>ooowX/o>oo<.vop/.>ro<oXUooox*x/->I% -wwoJ< OOOOOO mow\fcloo o w OOO OOO co*ow * ** o m <A.. SWOoOoO*4Q*OWh .* VXsP) 'x.XX< .Jjh** P Www<0 AVW&ooxooX>O<-ooO.aoPp*<-OooUXpoxxofAI wwow< C-16 TABLE C- 75 HICKORY* H.C. UNDER $6,000 $6,000-514,999 $15,000 OR MORE 200 1000 700 200 1100 1800 3100 0 800 4400 5200 400 2900 6900 10200 TO.5 52.6 36.8 100.0 6.5 35.5 58.1 100.0 0.0 15.4 84.6 100.0 3.9 28.4\ 67.6 100.0 TOTAL 1900 DUP040009890  00 0< H O A t-- o 2 n s o Xo 00 u. 0 O p" .1 hi o o n* <0 f* p X MC t-c* 2 VO CO hi0 o Or 2t < hi +T A. m so .p0" hi 2E 0 O in p0 2 t-- hi V2 .J CL 1 u. J < > 1" ao W x < u > q m CO 0 uro-- 'T o !f> fvS 20 K hi^* 22 O Q X JO vO X.0 p* CO 1 hi o h-tOin <0 2 tfr u -J .2 -J zo < m 20 U. 0 i; UJ 22 UJ .2 2 O J x' o u. p hi .K X .2 o oz p CO > o CO 2 i hJ Pw 4TVOO miA0 r-.CW.m O o p ** PAVOVO , *"0 -Aim # o o r- 0CM0 r4 O o o r* 2fA0 * Oj*-m M P: P O evia o p a (Omi!) CM a o o ** iftfr ojcvnn o o f* ah-m O.h-.*w vO o in eo so A-n- . P O * 02fA Nfiift r-wm P o o f*ma .2 20 MW.il? p o p CM 00 evaP WMM P o o in *-2 00.0! com p . o p* mmdv .22 0 *-<Mm o o o ? * OJfA0 cvia 0 P o r* 2M<M *-a.o *^a o o o *A woo * 2 p.m -- * O O ; O ih aao t - U\<M ,f.W o o o*h pop OOP m.m o o o f-- 00.9 PCM CO f-forn o o o f- POO 0.00 00.0 J rtvo o h* OOO 0.00 CVi-fACM o p n* ooo OOP 2 20 T-fr2 .o p 2 0 poo POO MOM 2a o o a CM OOP 0.00 pfM *-2*" o o 2 a -* * OOP OOP *-Mv .CM<5T o o m |^ . OP OOP MOW **2 o m m POO OOO .2FA.fr'. o -O a r* POO OOP woo csim o o CM f!A OOO 00.0 rMN r- m o o :fA POP ooo r~ o 0 0 CM POP O < OOO o J 2*a m u- A UJ J -- hi .2 < hi o 02 0O .J O0X < VO v *- VO 022 o Af-O *1 *&</> o0O 0.0 hi 200 .J hi O a o Ain < 2S0j~ f- 300 OOO ooo o cum rX *^2 vo hi h > f* 5 0 5C u *- 1 2 O h CO U >5 -i < pVO 9 P hi J a < i- OOO OOO ** hi .02 00 O0X OA 022 A1~0 VO0 V> l o oo 20 0 hio A o Ain 2vO*D00 0 2 J < H O h OOP OOO M CO** ? O O i-- cv OOO > ooo a 0a 2 f-N A a .-i j < h. o p in in a 2 WJ ^ J hi P 02 00 -j O0X < a OA a 022 O **- O H i VO0 . p 01 O 0.0 hi 2.00 -J a pUJQAin^ < Z^Op H 3.00 ooo ooo flACO -J* o o .2 CM Pop o oo o . mA m*> o m O -J o p A .-1 UJ hi 2 hi O 02 0O -J O0Z < 0 OA vp 022 O A*-0 Vfi0 p 01 O oo hi 200 ..i hio A a o A.m < - S2 ooo 00.0 m<- n- t-cy o o ro 2 OOO ooo * invo0 a r- cy 5c o o o m >* < a 2 hi hi 2 hi O 02 0O O0X < O OA fr- 0.22 O -A*^ O h 1 O0 P OlO oo hi 200 --1 UIO A -a o Ain .< zah 300 C-15 DUPQ4O0O9891 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO $ YEARS BY FAMILY INCOME, STATUS AND AGE OF MOUSING, 1980 w .< H O >- o CO . T of WX*0 o*wf a. if' r" .0 IT . _w z ft. w H O H O <0 *-- O *UXirir 0 JO( -ZX2 PT wo om Z O*HN UI 0 x 3tfS 20 U1 I cac. u 50 0 X .* > w UX<. CMW0 W WlA 4 ' 0 0 jr* rpft orm ^s t j t p f 0 0 F mm wb O O Ot" 000 mm *~iOm 0 0 0T* M0 P O O*-- poo 00m0m 0 4 p *0-- O OP* *F--.MNV) O OF m0 AIW> .0 O O .Pr* *-o0 O<oOso O O OT"> Oi9h .4 omz ' .P O b 0 > * P'". comm - h* 60 -- 0zo O)0 p p. 6 O' if^ 0 r- r*o p **0-4r 0 / w^r*- O b *" jfiT 0 . * .!.^ mw w O Pi-P O P i j '5 '1 \ i j|! 4 \ } j OON <\JI**P i-W0 9 p *p ppm *o.snf .t-ziar 0 f00 Wrttf W.rt2 P O 0-- tfApO P mom OO POP PJOO .f-jCjPJt P PrO OOP 000 O0 * 0 m0 JT W 000000 SO W CM win O O OO POO OOP *i--a0fift 0 pf-- 0O.O0 P0 ftlh'Pf-- 0 0 0 CM OOP o OP 0 0. 0 *-W.0 0 OOP 0 POO 000 *- CM .t0o 0 000 000 0 O O St O V* OOP P *O-CP0 P 000 OOP rCM *- Os O O P *0 CM OOP rO> OPo *-m.m O C*--M 000 O 000 O flO1--O1if- w tn 000 0 0.0 p WCSI w OOP O nPOwPo w ffa**T POO p0 ^0 w O CM OOP lO- OCM P0 St to O P W 0 < 000 'r0C- 0f>f?*0<pp O nO r*o SB 5O W W .X X 0 > UI Z O -I > 0 AX < -CO zz O **-0 #-- 1 NOO> g </ .1 0 .00 UI ZOO 0< 0uXNioOti*n-A h- 3VW> OOP 0-0 0 OS!"!. cvw 0 m 0 4 2X * z 3 a. 0 n Ui X 0 w OOiZ 0 .A' < 0 0As*!r-t0e 0 Oi AO</> <0 i 0 00 U-iI zuiooo. 0< h- Z0O/>|,<*m/> poo O POO 0.WJALf0fA NWOO -1 J h W Ui x < 2 z X< UI 0tK O -J to 0X 0 */ <u> 0 O.JK %*-o 0 h 1 a <0/></1>0. Ui 00 Uzi oOo 0 O Mf\ < X0r 3</>V> - 0 0,0 mO*P-OCM W 5 % <" X M O UXi Ui 0.X X \Q OPX P -^ ' P ozz A.- 1 P UI </> 1 0 ' OP zoo --1 wo % 0 0 -.m ZNO- <A0 . XUi b . 1^- 0 0 m ui w a. XUi ' -H- C .X UI UJ w -UJa .X j < >- m 0 .0 .K 1 0 w w 0< K 0 OP Oto OCM.P>O- UI z 0 ox OA QA>Z- ZO v> 1 0 00 wZOoO oZPAwm* ss </></> O P m CM w< * 0J- i .; C-18 DUP040009892 CHILDREN OF ALL RACES 6 MONTHS TO $ YEARS BY FAMILY INCOME* STATUS AND AGE OF HOUSING, T9S0 .< H O o CoO> o or* ia-evOoi W9 wXcwoinI Q* o IOT' xw H<O Oj $ xXWPr- a *->SQ X,CK I ir X rwCD x9 oirt XO 1 w X 8 r-r-p O odd o WM.tfV h-TO.O o iASO o OOCJ PUCTSU.P 9 * o o *-- TOOvcO O Wt-Os O cuso o WWtf o tfVJtf- p NON sot o oo Oi?P O o. . _ O JW.IV m<9ft O ptAP O TOy^P o t-mu> p Ivf*P P rfl'W O FifilW' O *OPvJf O r-ty tf\ O ooo POcuPr- Oo iS-OkP y-Py- O OP # O Ofir Os o0 OVflO>--^ WY-r- p irv*eo o estcw^r p 0*0 otrwr o r-CUP p OOP O OmiOs* PTO Op t o t o .^* o 8 ^ o*- o p WNlAri Oo .O0m9s>Or00-mO0r0" otcruo\ OOP*TO0t Oo,Oo0O* ow o8OY^-oO^r-coOous .oor3* ooinoowr-ooo^ ,o0wow OU2O3*tO2^W,YO2i?-- lOA eooooo p5 P-t o y - :Yp*Wlft Os XI OOO OOO W0 r-Wif O O Os r- oX < X<CXOhIO OOO oWT\oOoPIA Ooirn 9x oseUc! OsO sro- OOo^.xO-%VxX o o 400I O u-<h0j xwXpOo0oP>^o98^A> OOO O O- OwOo 0t o ooo ooo *-ino\ o olA w X roo-popfoo- o SSoOT o .OX9 o ^3 OOsvOX -J fA. oo9osA^tcxc A#-0 IS oK Oa w OI OO- Uwl wxoooA CQ O Aift h< 3XWPVr>- 4o0t.Qp0io0t* :pIA 00.0 o OOO o ooo to iuts\ d X P0TO.Oi0fOT0O 9oO* A O CXO o 3 00 N 1 OstC OOCsKXO. O OApY--Ox 00 J oH* 0I O Ui i xwoOooO O >iA xO.p0y0- sss s WlAfWV ,f9ef ooo OO t ow TO p o kf\ TO CO s A Jh wwAoWI ooo T0O.YO0-sT0iOA O .f9* 8 w CKX OSO w .h9 OOOSA X o^TsOrOx 00 $ o -H w-0<hI xWOx3MoOp0OAOoO*0lO*A. ooo o v> oprotho* r* X i-v-OMA y- ffi Y- I 2 CD XAO* X1 090 OYO*vOWOvOTiTO o ow p X 8 OMK Dn Q PO | ox O^ OAYff-tOf 00 JS or- 0t O OO XOO WO A OZP>IA^ >- 300 CENSUS COUNT o r C-17 DUP040009893 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND AGE OF HOUSING, *9 8 0 hO-<J> ac o 1-0* xU*0o* .0 tXWOI Aotr o oil hat,-: 0 .0r1 -O Z9 Wr aop --0 XOPr1 wo oir fla*-* u 0 xtof zo h1i 0a. u s -ox >-J 1 w OCJfi ddd *-**3 o o o . m o'm*. rr**CtoMm 0A o o sf* tf\3tM o **-*3**3m p 0F*M o t>l>d r*st*> oor- ooo POO Jffirt nso9r--- 0 P f* CM CM g f"-*- O* H*-,W3 0 sim r-<yi*0 o d r- f-30* o . ***"3 o <m3* o ' -*--- R . R *> .33 o ,* 0 O 9.iN' .* o . NrC-f0- O O NACO . . > f-H-3 (F-fFJi# 9. o0*>" rvfir *o*0 o .^ 0A 0'* P POP f-CM o or- pa*o m r-POv MP7CJ o o9o" ---* --*--m ? *"33 *-33 o o P <M3 o vd-CoMvId*} 9oo-- POO o CoMdindcy 0Q 0.03 O r.*h-OVv0Nvm* d P* * OOO 000 03*0 wr CM o 0 0 ooo *P-O0iPA UY0H- 0 i9n-- CM POO P0O 0r0h0i O O 0*-- ggg s 3>* e *-0 OOP O0OineO* g * rmrt O POO O ooo p w-CMl!CM0 o p >- ovp .mf-h* &IX> o y y V3 0 * * ' tWr-'O o Wh P wiTMft OM0T4uVTO* O- Oo 9-- CU*0CM o dccvoldp .odr- OOP OmOCOM r- P to-- O t--s OOP *P-O*O0 0 ofU r.W 3 f | 5 * c OOO OOP I-I9W 0. . *O0 U. ^w*m 0 OOP o OOO o :P0 f*- r-'lft i- -A X W >< = ooo WX OOP *0*i--0 C--M to H- X OOOOOO oo A<. OJTCM 3* CMinp ,0r 5 k a o X hi .'7 J h0 < W0 X< hi 5 hi OiZ . OvO -1 J 00*X0 OPS O' .< f-- p 1 ozz *o9*--> 0 o 1- CM P ooi o 03* ee < 'H O 1 ++-o h*O0 o > o . O 01 o W zo.0o.0 -J :W h-Ji zoooo wo . .m< O tift Z*0r- 0 .< Za 0r i-- 3>0 *- 900 OOO 0 X OOP 03**0 0 0 CM in CM 0 2 Z o p > OOP OOP P O 0CSIO 0 X0 CM y- 3 X li* p Okl 15 J hl 0X 0*0 -I OOvI < 0 Os o03'1* X r- O I Q 0*00 o H o *- oo h-Ji CQ .xaUoO*>o^A < Z*Or H D00 pop o OOP 033 fo!- r- X p 0 X Ui POO 0.00 o o oX !*0<M to so 3 < X o .z o 1fe UI OvX 0\0 J oo*s '< 3 O A H 0 g O 03 X 0*O0lrOo OO OJ-- Ui 1 xwooo* aO < Z*Or 900 OPOOOP in 3r-*0 0O*f* OOO jOrOOO o oIT* 0V 0w X o X 3 w o*x 0>O W Orv\ O.OvX O'.'* 0VO3<r/>O <H* gOh o hi mJ 01O OO hXiOOO> 0 o -*m < xvo*- 1- P<^<0 ! ? S C-20 DUP040009894 CENSUS COUNT O f CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND ACE OF HOUSING, I9 6 0 < o V- <3 <0 TII o h He* acrp UJCM o * ice i wo sm <* 9-- O tn i Ul S -CM < 1o K O :<o o XOn Wi fi: o JOv *-P SPO8N- U-O OifN ON St** Ui CO so o in SON w OS A. w z p o2E > w 5 u$. 100.0 irs -- M.Oh> *-\CWp o o o rr* --t iftT-fl CM*- o O i-- P Ovh* f* *--T-p p o O f-- f>r*CM pi-.CM COP o o o *-- ppp -- T-CVIJA 100.0 TOO.O i-.PlA r* (O P o o TP CM (A f-.P r1** o. o T-- f-oidA .* hOf* CMI> 0 O o T" n -CMP* r-NP *-<MP O o On *-- p Per o n CMp r-pr*> r*tAP CM AO p o ppp OCMfp COP P o o o p..o CM COO CM *" P o o. T- PtfV*A Q I'--.CM P o o . T" P p--t-- pr*pN coN p o o MftO h>Of CMh* o o p ffOP h*ON TT T~ p o o T* i-PlA o n per .mm o o o r* PPON p*- t -p p ooo OOG rtf-O *- CM Is* o o p ofT" OOO 0.0 0 00 fO fO t * *-- p o a iA 0,0.0 ooo CM t - i-- CMT*--- o o a Tp-- OPO OOO poop CMP O O On ooo 0.0.0 f- O CM CUP.0N 100.0 16900 5800 7000 ,4 1 0 0 ooo 0 0.0 to CM .CM CM o !> CM OOP o 8ooo o os . V-tA p ooo ooo Ovtf\ T-p o o! ON OOO OOO po o p CM .o o p .00.0 ooo p -p t -p OOO 0.0 0 CO ONO * * CM o o On cc OOO ooo r*-ONCM CM O oto tO o SB O ox z o Ul X. On S ON.O O.On Z mi .< p p Oo V ao: O A.-0 H- p</> o *r> o oo Ui soo mi uo * <CD 1- ZO r 3</>0 xae s* ooo op p ui lAr* p i--. *-- to p w w z os o ooo o .z ooo < 00 so CM ON 5 W O ec p < Ui ONflC On O O.On Z < m O > oaec o - i p <p/>pI o OO w OS 0.0 ml wo * to -< 1" OZpT*iiA LA ooo ooo N-OsO *- o o p lA OOO P OOO o pp1* MJ CM w w <>* u. Ui JO\CC On O OOn Z O A* < 1 OsTK -k--o o P p v> o oo w mj cWoooA aQ < k* ZD>T0 O * OOP o ' 0.0 o 4k CM O t - CM .CCMO W H- *w > <w < OOO O W OOO o CM CO CM CM H* T- CM 0} Ul * UJ UJ <> u. .3< w o*cc On O mi OOn X < On O - .H OPS O -*- P pp 0 o OO W so mi wo % to O *iA < >- 3ZP0-T0- ooo ooo t*<*a 1-- f--TT3 9 OOO <-J OOO Pf>0 T** .% CO w .msi O W ac < -J w &CC On O OOn Z o P >' .1ON PP*-So 00: o 0lo oo w s oo mi wo % m < - O (A sso300 TOTAL C-l 9 DUP040009895 I CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND ACE OF HOUSING, 1980 j<j H O H O 00 P9" .1 JO .--9O"' amr\Ooo' Of OUuS.iOmi O*"' o m o Ui a: & -J < tHO-* oCO o9-- o1 pZUCifNas -qjTd'q XU TONU. o pXmOt-n Ul ZXCDO:tf> 20 rU*I Xa. Ui 2Xoo > X .< u. Y-oo P t-O-f`OCmJ o o mOMin O CM.ON CO r CM tft o cyo o CO co rs o o 0 p^mvb CM NO o o o1M* N* 0N4? a . v-.cn^r -p -- -s t mt r- On On CM M fO p oofU f0fi) wsrth p o or-- bbO'CooOooON o pVO OJNO9O-- o04 boo i0n0-.0in o r-.af NO tf h*CM O'C0M4 NCOO o oo *" boo ooo *Y5 CM 9" ffJNO o NO o*!" ooo .04?-.*m00* 40n? po9" in 0**04? 99-- PCMOP o o pV" NO** ' o o o OOP O Cr-M.eNOoCtnM o o NO-.-OO o ifnr4ti*n0 oo r" ooo Nf0Ol.*P0Jy Cy0p" o o JT eh *T" 0.P0.0 fO>OvO o ion **? MX P-lAP* o CM omrj o r-CMVO o to NO f" o >r co.iv f-CM.in -p p rt:l>0 ^rPON -Yf *-NQ o o ot-- to.CMin G9-wvfo o oo*- ooo 9oto- oC^VroiNnO o o CM o1-- POO oto oNOoCM o o9^* 9-- CM CMP*--Y p9--.cOgition P O.oIT* -V y 0 4? NO o p-4p.m CM CM iCV ofof On NO in o CM ONO r* *o in o o9** Off tCoM croo <to0 o oo9-- ooo coo CCMM tSoO VCOO o oCO C9"V OOO . ooo o o n --in m 9- CM zr ooo .rc-oo-mo .N9"O T~ 0O.O0 O0 p*- >to- rn o mo fj o0.o0o0 fj.ONrt o moCM v:oeoro*oOooN CM oC4M? ..0o,o0 oo oo gp Cr*MCtoN MCM3 ooo o s of- oT--OoON oCh CM Xw fr-- .-- ad oo CCDO 9 W OOnnXO -J o -9- 1 O>OOo\--O<9^/--.>*nf'iXOS <Jr* H o UI a < V? 0I .-0O XUZaNIOoO-oi*n-9 </>-</> OOO O oCMoifuo;TtPN* oCM CM < > k O ac aa X o .2 > UI On OS .0*0 04 U u O On X O* G.srec M3<l> o V> l o .< Jo-- frf U-4i UCD4o0 o.0- < O -lA Z \Of 3V>0 X. 0.0 0 oO.CoM.CoM *-- CM *"3 o 2VoO z * XUJ *-- CO UI Xo z .< X ONCUi TO o 1' NOOoO-Oc.Oj9on9Va-OX0 -8-<y . o O UI _J CQ < H- V> 1 . Uxi ooo oo* aZoN<oO</"> o ooo ooo *T '--f SCMT ,oot0on X' o a UMVI u. <b z -<.x 9o" i o ui UJ .On 'X OOOnvOX O04?^<C <>`io>cr/*-> O o xoooo -J <uoV-- CO < ZUa4\Qf-lmf*. ,u 2tf>U> c 0.0 O ionoopoca Pt-- CM uoi X o -- a .as ou. UQI X UJ CvX OO in o OOQ.*.p'49vT-- SOX <Ik* .G i !0 UI <x/-->oiofi>ooo mo * IS q -m .< ZQr >-- C-22 DUP040009896 I CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND ACE OF HOUSING, 1980 .w *< .d 0 0-- 1 I0H 6* XJWo-M*.003 xwflu oi o ior wt .X.a. J < 1 0 Oi-- o f* X0 W f: O JO> xa Or* f U. o m . .0 Ki" W 0' to 9 in Z9 1 W Ka. w X O O >w $U<. o m\o '1o+ . M o s-miA o 2 .arm in p f^l*i0 p0 \OtfS0 ' 0o t>- lA <x*nni nj9ico JArWos*o" o .o9" lA Cvl-if rOY-- lA cy so Po 0.m 4 <yp"0 0 p *oo" A 0 crMymr-he*s. POO OCOVPI0 ,OMO dfltO-KlA o or* ftp# fOOJfO T*" PO in o or* 0.9*e fj r- *- t> o of* 00f o pMOl o NCMp o 0 i*pir O0.CS 0 o rO-cOoi.iOA .0* lA0m i-istar o o -o.* IA01O Oicor .o* V3 Y-r* o rOft rOof-tll.OoPClJOoOP o o0 0 OOP ooo ps dsstto o -or3-- OoOoOo tPQM ^ ' ^ .** oo to m ooo oOnoV)o.h0 o o m#* OOO oWtnorf-tol0r ooo ooo C4 3- O o M3 is. ooo ooo fO0fO n o a St St . ooo ooo T* .to X < .% u. u. o OOP w ooo 0 00rr- co W X . o o . .lA o o .0 m ooo O ooo o 0 * i~N st 0 o UI .X k X J o o X Ui -J 0000 w O0X < 0 OM 0 o "* -. b* 0<K> O u V> 1 O 0 oooo J0 WO " a m :< \e^ 500 X < ooo o 0 0.0 o X lAN-iA <m X o o X Ui w H w -1 .00O0 P0* Oo 0X o-flf az O 01 0*0*Oo b w w0 oo wepo o -m < X0#Y- 500 00.0 ooo o in 0 O O P o *" OOO o OOO o X 0X0 0 *-csm A* U X X < o. > a 0,00 o 3 OOO o 0 0.0 0 m 0 r-50 0 < f .X o X < X 0 O X oW w 00XO -j 0 Oo 0*X -< i-- 9k exx o 1 00 o H* -O 0 1 o w .0w oo cwcooo* o >in < Zr 300 00.0 ooo h"0W 4r o o i0n ooo ooo 0f^m r fO o o , wX H* % w OOO O w OOO .< POO St X to w* CM X < X 1 X ui > a X o w 00UXOi -J 00 1 o O0X aOst"er: 10O"i0- o o < O K oo Ui xoo 0w up * a .ir\ < X0*" av></> 0 0.0 0.0 f>0 CJ ob 009 inmp ' sr :X poo ooo X 0 0CJ t r- -a" 0 0 < X J J w oc o UI w 00X o o OOO P0"XX' ;* l 1O0 o 0Io oo Ui xoo -0J WO s p < ZlO'l- C-21 TOTAL 6900 5600 3500 T6O0O 100.0 100.0 100.0 100,0 DUP040009897 -O co Am ch $<-- -A G fe- oX so 9 o X u ,4o0 *&"* Ul O o h* <& P' X < so wfe6-oO -a h* XS ^1 < f(0- aw. ion T>" % XId c IT XO' On >-J Iad. 1 ml <I-- sq o .X 2- > lA . CO 9i g <0 . aN X fe- -XId'Pi** X fie :oc aWONOl: \0 Xu*P- Li uo IP .cC; 91 '*- Id .j < fao8 w .X0N P A.8d a: X .ul 0. a: Ci 3' O OMm h" .9X' cS' so ato X .Id Q IXd o u X *-- . >. ml .mm j5* * .* O floNssAyfl O m* p#lff;l maf"ohs o 6*o aovK P rN-OTcOvOimN O -oh* {M. A P mm cwh* O' 4 o o*-- o..ar o OrN*ffl 6 or* . ap*ffl O Pma " CM NO o 9kh a* 0(0 0 o *> co o '4m.*m. o Ciftlh o mm P Oh" pop O omm o Nh pop omm *-ffl P o or- ao*m O mmt^vmo f~ OSSQmf Pffl *-aa o o o*-- OCSIO o d o CUN- o t-Npa Cwsi--cvia . o offt P Tr-- iCyiffl ,or WoodoI^Oodn Oo *~al mrft X o X ft <0 Xhr ooO0So9Pft o NO P wa Mi X X o 5 SiXdO oiofVooSUooi- o oco a x8 1- m 7 (0 Id X O X CO ooo o o5 foftoieo*cym o aNO X oX :X O o Id X CO X2 Id OiX On -J OPnX < * | OaA x ftp"Q nO<A h* OK o 01 O Id 00 O J Iod OAin < *3N0O0r OOO o omoamo ao- r-fh 9s ooo O omoahow* NaoO ooOo0 o ao M (VI ooooo h hr* * X X ft < .9 X SO .<X Id OOntX OOn X M* O ft . osrc *-0 1 u0 oo Id W. xIdoOoft J<CD- O ft(A X^O** 900 o ao sy w < hOh* ooMS.ooMopO (NJfOflO o ao *-- OOiAOOhOOh cv o hfO* OOomomPi-ft o po w ID SO OOP OOO o o X< h*N.O f.Wrt Q as oam. id OQ X d Id X ONX OOOnvQ n ,o ^ ml < fed 6 q oax oi8 0*04-0 0IO h oo Id .ffJl cUelooft o *m 1<- 900 OOmOOoOOo o om ffl 0.0 0 oo o o M ,0,0 O r O.OnOp*--i OoON CJ "X .X o p OOO ooo afflSaVI o o NmO SB <fed X ffl Id Ul X POnn XO OPn X w < .a! Ofatx 0 \ft-ift fm J 00 Q0 OO Id ml Xuiooo <ffl XP.p.fthd*S fe- 900 C-24 TABLE C-115 NEW LONOON-NORWICH, C O N N .-R .I. UNDER $6,000 $6,000-$i4,999 $15,000 OR MORE 1400 2400 3700 500 2000 5100 1200 2200 2900 6300 3100 6600 11700 21400 IB. 7 32.0 49.3 100.0 6.6 26.3 67.1 100.0 19.0 34.9 46.0 100.0 14.5 30.8 54.7 100.0 TOTAL 7500 7600 DUP040009898 .oaa p< H G 4- 0z O o XO 0 W O' 0 1 Ui -O 0 < On -oz < 4-- cs Z so wo S' o** H- . i < wo W w tn SO a A W X- : o to oP .:Z f > aUJ: -J A. x < u. < >- 4- 09 ,o H- {0 .< w > O! to p?" " I o (0 :r*- X ZOv 4- w *-- zK oO X Ja *~ XOn V3 o *** 4 W Wp .c? lA < On . K-t- -1 Lu CD -J XO < OtA u. Zi*p-* p1 Q W X a u. O w KX Zo oo oz p > o V) zX w .< o U- o3 .C0,C4 P ertf\ P o o TP 3CN OSr CJvO O o o r* OVCOro f-MY *~rt3 . . o J"- .m r- <0 3 o o o *- vow -:3 p- ,IA o 6 o " OOP . p o o 1" 04 0 CO .0*0*0 "(OlA o .o f** r*3 CM CO.On 04 rJS O o o *" ONflNO C\J p o o r- tno N-f^tfN r-CMjft o 6 O ONO.ff) : --" On 0* o o r- .-- 8 ^ -- On 3 8<-- 3 6 oTT pv. m CM3 o o o tA* .O* K. On CM o o o Or-3 3^K " CMtA o o pr-- tom K -- <5*0 o o o 1-- roosr** !>-** r- <5 lA o o T" e.wp lArV** t-vOCSI o O o *** OK 9 33"*3 CM O o o r* tACM CM On IA8A .3 3 p o*- ooo POO 3f-3 IA0 o ift K OOO OOO m\ co r-iTOs o o On lft " ooo ooo 3 CM CM 3 NO o o 3 p*'' OOO 0.00 CTN.ON 3 OT-- o o o 3 CM OOO 0 0.0 h-o r- o o 0 r- ooo ooo 8 ^.--\13 CM 3 o oT*K 0.0.0 0.0 0 p?P-VO 04 o o >rot < J w ooo O Ok < o 0.0.0 Ov On O CVJ lA OCO CO p o p w1 _J -1 -- ooo O > oo O </> o NO p ,r" H X h- > OOO ooo O O o ON COP- 3" -J CMlA On u oz < z < <0 OOO $ 0.0 0 o zo ff5 *" lA --f-- ON CM < OOO OOP p-f--lft i* r*rt o o NO OOO .00:0 O.CMO *C4K O o o r-- OOO 0 0.0 OOirt r- - P4 O o C4 tA OOO ooo On 3 0\ p-,3 04 o o CM On OOO o OOO o <rW4T On * OOO O * ooo o < --o rJ *"04*^ .3 < OOO OO CM lA3 r-- o NorCM OOO 0.0 0 r> f> *-<M O .o 3 0.0 o 0.0 0 3.pr*Nf0- O o 3 z X o o CD -J w Ui X OX .0*0 OOvX <c o- w o 03.X o 1 .**- o \o</> o V> O oo w zoo -j UO - o tr\ 1< z*- - 3V><0 o z Z) o Ui X ON On O O OvX fV o o 03 8w >** o NOW u v> o - oo u oo w wo * O -tA 1< z~ - DWW -J < o w A u o z ow X On OO OOn X -< o -. 4-- o 03 O O >- I NOW ow o oo Ui K.O O w wo - o Ain < z<r 4- OWW Ui X o o h- z o Ui X On OvO mJ OOn X < On O * k~ O 03 o * ---o hr. t </> oo oo Ui OO w Ui O A o Ain < ZN-- H 3WW A w r-p o z o UJ X ON On O W OOn X < o OA ;4- r~ 03. o p At- H* 4 o o0O OO -1Ui oo WO A O MA < Z.r* h* C-23 DUP040009899 CENSUS COUNT OF CHILDREN OF ALL RACES S MONTHS TO 5 YEARS BY FAMILY INCOME* STATUS AND ACE OF HOUSINO, 1980 * O> CV*pI.rtJ*T g *0(0*0 p * > > 0OvMm0 0 OK o *m-o4e0 0o iAr<viom.*iho o* 9-CMM3 O *-*? o *-mmm oo O**" o 0CMCM p* sCM4Tm m*-0 *rN N%0 o - 2 r-jrov o CMtfV**-40 9P !*mCoM o p hff Si a.1r O 0Ioti til 1 -I < NOOV*QO* gO OV0VCM O O\m 0 0jo <M irter* o . M*-COM00 00 0*0 *-i~0 CM O mjmfCiMn o I-OVJO *<Io*#,, N OO 888 s 388 5 OO o 00IT-M0A 888 8 0m.ih*. *<*y OCh 0 r*80C^ M 0 osroo**oom r- fO0 O r-O CMI^.b CM {V IA O O o oooooo oo jmov in OOP (AiA CM.CMtA o o o o|ooIooA . 0\ *-.5*1*. CM cII* Z9 U e- ec -So ia :w0etf otr Wa xsacicroj --uKri 2 888 8 *Sc5 5 888 8 mm*.4f JwB OOO O O0<OAOr O Jfr r oooooo oo o sNoon0 m to ooo o ooo SO^Ti^Or ooc OJTQ0<< CM O0OO0 mS_ i # ui -< is u-s4i ic0nod* t- *$* 888 0 0 r- 88 UI 8 Ui < CM 0* IN> *" g ^io ? O <A 000 OOO i" o O a* N OOO O o*-.or*o0 0 $ l J Ui O oVi*5 -J m--" OO*vZ *** o < u'o 4 8?o w ccoo f-lJg wOco%^tf*\ ' I, OOO 0 < > ooo >Ofl0CM o 0 m MT . 7 flC 888 O O 90 oI 0w AUCI *08 i. N*gI- 00O0oJi*T*ooK oJ-- wJ cwooo.% 0<H* *00A^0lft OOO (0 ooo 00* 0 *CM X % . o00 OOOOPP r- r- CM JOo* 3I 5 8 s 0 < ui o. cqvc\e0 --I 0-- I OozOr*vcXc 00 O <Ho* H o 01 o o ui oo J0 WQ Ov < h .3 00 C-Z6 DUP040009900 . .J CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND ACE OF NCOSINC, 1960 -J < 5 H oflC O' c1 fo- a: so UuocK>.JqiH&4r os --t9n 1 UJ KBC. -J < 1 i 9 N--c1--UX0-XJJ 9O10rC0** u. o4 0X09-- Uf0Saflci.O--ior uaai.: u s zo -J 5 u N-90S o ; 2--f.0<4.WCWif\ P Ops P 1A--9 . CM*N 0r- -r.n cw iAN tfVAOO -- **.9 p p* --01?-08W0^*4--JA. O 6o-- cw --C--MN** oT* JAsOCO o ICWW --fVfllOA --o iM-lOG--tfA-- p -- tnesjiA ----990 P--O 9(04*** P eoN* --:*NlA .--o OW.* N O OPi^ o\ Vo0- mco :90fNN O ` star G-- #APi IA 6W O' kA0O . P-- PON 9-- 0i--A p or* .tf.lftlP 0 ' ' -- CM SO Oo-- ,o.p,o M-- OO0 0 ^ -- PO*T|-- 0A 99** P* G00490 0 G-- ' sCOWU*Y*C>O0 P :O-- iA9-- p -- 04A -- 99 o p ,--m--oNo* --oo doo GO I--Af*W*t9A cow !** ooo OOP -- AOCW -- 9 AO O Pv p* CW 00..00G0 N i--OS 9--9 *o- OOO -OOO 9CW9 -- CW o o AO a OOP OOP OOsN- m 9o f- 888 8 0*0C0W :w9 pgoo s -- lA SO OOOOOO NW# oofoNs 888 s * CW twxro I--A gg 1 ------ .C--M OO--.OO--*-OO*r ** owo cw 888 8 AO--sOCfOW m 9 O Xo X* $ ,2X 0 jp|B o U-JJ O9P0SXU4 S-9X <V/^>O--ift o zUJoOoO* -<HOHJ- a< 0 *iA O0P . > coowoou vzooin * O OClAW JBA Q yh 0 fOoNOoPAOAop C4AO COoW O 5i XX0 fj X IN -- PC9ChKXuOZ o0:.3**%OS. -J #<O 4 0 -UJJ o<h- VaUSZ>JsGtOoOiO--poA> >< OIOANOO*OOSO CWIAO 8 A--O0 X -ZXOhX<1 OOOOtf\AOOO oOc9w Q Z sXf- 2 z APOUJ 0 1 i* O-SNfO.X < o 8p UI 0UcOoO oOOA OZ3A0O^ 0A-- OO0-- OO9--OO--9 oAOn B< z><J .zX>zU0I O0cOwAOOOoOO--O -- 99oocw 0X <Itl XHXOz OK -- .1 p U-Ji ..0< H* Ui V1Xo0oZUoA>OSJov9OP--OoOO10^sx*sXi,OI:OXOo--zo0AA <.J o ooWooCWooCOM oICAM A z0zo o10A.oA0Ooc00w Nwo aX4B $ zoX oc--w 8 p UC-1Oi <H UJ OsX OOPOZ 0\0xUZ3O--AJV9OO0I!>B*XooOo--l0AA J <4wo- C-25 DUP040009901 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INGGME, STATUS AND ACE OF HOUSING, T980 Nfr* p OOO O XXA M TMROjilnh p PM P N O. *-P PM (AlAO M P O P ,QWVlA O MX X o - QlAlA inwftl r-fX O P tAOX .0*iA-A ' -* rOr lAO lAO iA 0 PO I * uiw 0X i wx.*oOr UxI < ci zu. iax AC J0 --sfl xI O oIT KU-r*Xsssro aUx.l UI X o as >J; Xu2. PM XW o WON p MO X O lAX o x.*~ O lAO P M O *- o UYVO P oo o *- VStfO r^f" rA o lAO p Mo o --p >0 O M OMfl o\ X M O o*o o M. P OooOoP m *x- mwo O*0 .. sss x-.x<A oOMoMPxo S f- . * 8 cr-\jMx .MX gg 8 AN $ OooOoO -MMX g xn M ggg MO 5 fXIA oooooo Xo>. XoiA POO o 0MP0,C0SI IlOAA o0ooooXo oooo oxoooooox oo o ooxpooooo IoA :ooMooooiMA *P ootooAoo ox to .X X a OOoOOoOo "M * XUi Xoa o > oXx OXUI * 1 OoAoX O0,M*AXO v> o V> o Ud ml <X oo zWOSoO*oXiA^ 9V>0 Oo IA ml <X O h OOOlOAOO O O 5 o-6 Umi Xa Ui OX OO M x pooAo*-xxO i *o</> O Ui 0 o1 oo xUi ooo O IA < X X90s0- O oM ml X< p X ooo ooo 1AXOIIAA Xooo - u X o < Ui X OopX ..ml X I o Ui oox ooA**AOx 0xooi>ooo X< Xo OUIOI>A <X x900 rooM(ooIOINooO ooo *M < X A o Q u Ui X OX op ml 1 oO oAx o0A0T-xO < X o ;X a Ui 0xooooo -6 < X UOXIOOAXlAA 900 X .oooo oo o -i < o 0-A ae QQ Ui Ui X ox op -J iA *1 O Ui mCOl X< 0o0OoA0oo1*A-oxxO0 xUJ ooo aZ0^f8-^ 900 X< oX C-28 DUP040009902 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS fcV FAMILY INCOME, STATUS AND AGE OF HOUSING, 19S0 VA. < 1o 1- D 1 o *" X.VD uo oXl :U)0 x*n T0 uni x X J < H 0 CN c Cf IH Xi Ui ras o 40t S-S XO* Or1 ue O r,o*< ufftl l6 *S> xcs .1"1 UJ x CM. .UJ x o a x > z: < M ,ii\tf\ ONf'rfO O ,6 o OQN OuAiA CM 0 o 0 f-- moo WN0!i :T"OVJlO O .OsirifS coiA O o o OviAtA (VSO .cvovin *nits o o o ip^- CM *-SO *~<p 0 o -p*" OfOpv jra* rft| o o oo-t ifSriyr^ p o o rm 10>0 csir- CMlfNCM cvjrm p o rO- Ovoscg o o 0 r" f* tr r* fvl SO P O tfvrs *of^ *ntA O 6 p r- otApr *-CJsO WOO! * uyo v8 ^ a--- -- p o c* ocyr A !* -r-jfriSr o p *" OJOpv so^-in r-<y;U> o o o !T" fOFO iA IftfSh r- PO JJ- O ,o C-0.0S r-CMiA .0o.o0o0 f- fcj.flo *fPSO o -O <33 F -- o00o.o0 OfU.rr.WN o o CO p oob ooo OTO^T r-co o O f" ir o0.o0o0 r-Oven o co rr r" op o ooo CM (A CMtfSrO T-- ooo ooo FO.Ov r* jf-iC o o o eu f* ooo ooo c\i4f >-- 6 t m O o f*. os ooo o ooo 3-Cvc oY" < r* N) u. k <-J o o < so X UJ .Ul a. ox oo -J oox .< so o s H* -- o.tf.e o *.r- O H- 1 vov> 0 v> o O W -J SCO kiO * o *.tf% < X%0*- H- ooo ooo *-JA if -J m X W /X Ui a. O X1 ooo o Jp ooo n -8 ^ M^ IS ;X *"CM 4T UJ X -J .< .00.0 O X ooo J WNJB fs** o o t o X -fofi V3 X Ui r 0U UJ . ox avo -J OOiX < .** o * *- -- orx O f" 1 *- >- o V 1 o oo UJ xoo mJ UJ o a o sm .< XOr- </></ 00.0 OOP AT -- 6 o fi- 00.00.00 o J7O0J VO ev eo ooo o ooo o UJ r-0\ X -- r* r* ,ff) vp o X J X o UJ ..OtX Os J OAX < 43 O * u> -- OJ7X o t* H* 1 <00 a0 O OO UJ xoo 6 UiO a O -m -< XO-> 900 ooo .Ul ooo o r* l>* (SI *1 .< X x X * '. oo ooo X -o.in Ul r* j- *toT Ul X o o X1 OOO X ooo UJ OvCV > (vi.cy o o X o o so CM O O Os tf\ -o o X v> X oft. Ui OsX AO -J OOsX -< Os O s' -U N .000! a * s*"0 ' - > <O0 P 001 .O0 Ul xoo mJ UJO * m O stn < XOr- h- 900 OOO OOP rO r- lf\ .0.0 OOO PtAOO .r- rO > OO OOP X N>0\jr ir ^ J* UJ 0 X UJ Ui Jt X o o o Ui X OsX Os Q OOs 1fM0 OtfX %r- 00 o 01O . UJ XOO .-J wo A CD O stPk .< XO*r t" 900 G-27 TOTAL 7600 5900 7200 20700 100.0 100.0 100.0 100.0 DUP040009903 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS ANO ACE OF MOUSING, 1 9 BQ -J p 'At* 00S0 O O POCM . P < fOtnbi 0 h- 0 O r* e 0 . <U*-0 O *-piA O OtfviS* O T-W0 O H O CO s Y 0 p9s r- h9 3 SO UI.OS O *" E1 UJO Q- lA Os O Os * W (K &. ,<J < hO H- OvOS*-* <0 P O Q *! BY fT)>0 Y-inm 0tf\ 0 0 0 r* WT* rwtfN O O O * 00s0 mpiTk y- r-. O O O Q<ST0 " (p O O O 004" IfINh Wr-iA c 0 0 *-- l-lAP WOP >OlA O OO OMA0 O W0 O 6 0 .f*" m\o Q O O *-- SOP NO ID0h r- W lA p 0 0 *-- *>0 WWiA O O Of-- fO0CSI 0OVttf n*n p 0 0 T" OOO OOO cncoin Y-tO O O SO f!* OOP OOO (OOO Pip *9 0 0 a* J? CM OOO OOO P0Z "iT P O O P CP f-- OOO 0 0.0 0f?*iA O O P z 1" O 0 Oil .1 O !i EOi Ui *" as 0 -40s *-0 X.Os P*-* u,.o O to E rp Ui m. x.o :oin ZOI rF 1 W as a. ui X 0 0 z > ..J '5 < U. 000 OOO * *"\0> O O i*-- T* OOP OOO wovtn rnsi) O O * OOO OOO 0 P CM ' r-.p O O 0 (A OOO OOO m 0 p iA ZT OOO 00 .sr*o--t O O M .CM OOO O ' OOO O CM O w*.CM X X k X a. Ui to 0 . K" CO 5 f.1 p ui 4 CO < w ON . OvO OOn X O* OJC *-- 0 SO</> 00 00 KOO Ui-> 0 *A Z0<~ </></> mi < O f- OOO QOO Tfs--CSYJOs O O <0 0 OOO OOO pfr-.ir n-rt O 0 Os iA O Ui X 0 s -J < Ui 0 OvX Os -J OOsX < IN 0 V h* .4 O JT0S O "0 1 so<i> O .0 O OO w POO --4 UO * O0 .< tsflf h 300 OOO OOO * lAr^ r* W O O I* :<n O as 0 OOO 0 X OOO p 0 IA p f *-.0 IA X 0 0 1 >as 3 P to I6 < Ui ostf .Os mi n OsX < O % -1- .1X-- o-r-x .!" O 0 H 1 sow: P </> i 0 - 00 Ui coo J Ui % 0 Q *iA < Z\Or H* 300 OOO OOO 044 lA 1-0 O O IA lA u. 00b O OOO b -J 0OV0 p < ,"W p * N P X O .< h- Z <U P 9\X OO OOvX < z O '-w H O ST 02 O O H* 1 SO0 . 0 V> O OO :Ui xoo UJ O P 0 tA < 2\flr t- 300 C-30 TABLE C-145 SANTA ROSA, CALIF. UNDER $6,000 $6,000-$14,999 $15,000 OR MORE 900 1600 3500 700 1900 7300 9900 600 1500 8300 10400 2200 5000 19100 26300 15.0 26.7 58.3 100.0 7.1 19.2 73.7 100.0 5.8 14.4 79.8 100.0 8.0 19.0 72.6 100.0 TOTAL 6000 DUP040009904 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND AGE OF HOUSING, 19fl0 COy -CV cor-c\ CUS0 o o K 6 -- ^ OOP tOVD O O P o < 8 o o OiAirt IfYiACh <ir* 40 o o o <*pflC-h P9 CY"h HO ur o P*- up P P P t. Id EL. < H* . O'* p ' .Z O' -Wy ios - mJ.O\ r-sc :tC\ O*- l up mo* CC *" Id psto*on X0I 1" 1 UJ 0 .& -u O O Z > _l U<. rtNO O (AOmfA-- o P4 .Wmhjf dV** O' . drop ro* ' ptnsd o Nr^r-fC^M p P OHfO OltAOfi\T0 .p OUMft o y -8 oo .JftPift win -- y -CSI.P O .Oy- Nrh p **0-<oNii% .ob ' *> pppmo o .. p dJCmMCdM? .o 0\QS3 tfM-- CM Y-.cn.in O 6o ' .IA V>0A* 'u--ncsi*" o p* OaowOo8ooPch6 woCO 0ior.o1*h0R.oT0r>" p in sro- 0O.O0P0 oo NNcvd3r ' p iO*}jOT P&i fo.cY>m ooowCM ooo .0.00 iTinr^ Y-m o VO ooooo <r.rCVJSO O o c% ooo 0.0.0 csijwo * CM oo CM df oOoOoO OO CO CMA CM -3* >0 OOP 0,0 lAhT-CU . w 4T oooooo oo y -vO--O in YA -o > Ul z A Z yX sO tn 1 Id -J 3 < *- Id Ov OO OOv O* O.ZK FYY O \o</> oo fIoldC.OA.m Z'O*</></> -J < o H X (A 3: oooop o n p* dr ooA r-.f*S m w < ft. 1 s p `5 OOP OOO y - t-.OV oo Id C" M Z X id X oz1 -<J X u Ul K Chx chO Ch < .' W OOdKo O p1 Id _l CO 01zIod-0o1o0ooO*v < 1- 3ZO0-Y0* oooooo oo CM^7 0 o ,T- n0o>.o0oo0o P to' * oo p Y* w X Xo o Ul X Ostc OiO -J o3 OoO*VX .< t-- YY OdrT-oX 1 O u 0tft0ooOoo mJ CO Uoi OAin < Z^ O't - 300 OOO OOO CVIM9VO y - in o jr f- oooooo oo ffJONCV dr . wr*ift to o E A <z 5 < Ul w eio: OvO -d OOn X < Ov to Oo^rvce .H O r1 *rO 00 H p 0|O OO U2 ZOO U CD oUitfAt < ZM?y - P 300 a zz X .A a oo I6 o~ a H v> o ,ir fN* 1 P w S1-J .< C-29 UNDER $6,000 "$$6 ,104 ,0909 9 $15,000 OR MORE 500 1200 2900 4600 100 700 2000 2800 200 2400 7100 9700 BOO 4300 12000 17100 10.9 26.1 63.0 TOO.O 3.6 25.0 71.4 100.0 2.1 24.7 73.2 100.0 4.7 25.1 70.2 100.0 TOTAL DUP040009905 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND ACE OF HOUSING, < f"* o h s 1 . VwMq* UJO n O' . UJ a53 H< OH q 40 Or*' .tUz.l*o* 3o 1-va 3o5pIbO o.in o g1,0 ro T UJ :0O5k >-J < N POS O* o ' a Ovvpp CVMO o VOJf ,*w01rt4h0 o * . o >050 IA p . P OvOON r-CMin o o *-f-C* M.* PiCM o: O * ,p-f-jt-in.* h*** r* *-CO o *oo opq Meoo r*pp p or- ooo 0ou0n9w Aivo vooo Q\ 00.0 o ooo o PO*-Ort p P 40CMO ,0n ** 40 o o *" m vp.tn pA nancy o i-CMvO o WA >-vOA SOTO o CM -- in o OOO 0r~.m0'0O o CoM ooo ocvno>o.p o w JT m O \0 ,mC*VIIoS . P4T A* pin p o o r" Ovi^ O OVTOV TvO o o .009 oooov .o *-A0 0!V 0:00 OO o o *-jA CfMM* 9 o* 0040 o CM CM in o .^40.^ o bvvo.<P0 o o pvo**-* o movin CM CMP o o 0,00 Co0M9oOcM1o3p o JT p OOO o ooo o VOVO*K-- Ov CM 0.00 oWfoOCoM o :h> CM CM OOO o ooo inotn o * <* -- p OOOOO o a a Cvjro i4n0 ooo o opfoofU o .p p X :<Q A V) ooo ooo <1NQ 0O m CM Jf ooo ooo o o mi "** Pi-4t-0rf*t 05 so A wO -i mi UJ <u. w o X* 3 -<.om0* ui ova OAS. UJ 0 OOS 0V -nJ OsO mi r" lsAU oosx oP*X **- o <> o H* 1 Vfi</ PX < -- O .% m p o ^ > ti 00 O <J> o o0o u <J8 < oo oUi ooA O2>0*m*- 300 JUI - -460 < >- oo KOO M o O*m^ XMD*-* 300 0.0 0 POO o o O tn*s*o VO s CM ** p p X* boo .Co0or-0oJ o o s- o i-cy pv ,A a o. % muii u ui u. tk P :# X 5X CtoU ui Ov.flS Ov mi fi. 0 UI CMOS ON -J 0 OoO.%VX -K < ` X OOONA X .K< in 1 a-os r* O 00 oK P0 in f" P.Q .% o O1- 1 00 U 4i> .t o _o Ui KOO Ui ccoooo a< oUJOA.m* ZAO 300 ui o a <h ax3v0oA.0i^n C-32 TABLE C-155 STAMFORD, CONN. UNDER $6,000" $6,000 $18,999 $15,000 OR MORE 600 1300 5200 400 900 8300 5600 0 600 1800 2400 lOOO 2800 11308 15100 8.5 18.3 73.2 100.0 7.1 16.1 76.8 100.0 0 .0 25.0 75.0 100.0 6.6 18.5 74.8 100.0 TOTAL 7100 D U P0400Q9906 CENSUS COUNT OF CHILDREN OF ALL RACES 6 MONTHS TO 5 YEARS BY FAMILY INCOME, STATUS AND AGE OF HOUSING, 1900 O Ov 1 N Os h-O' z ;cUoeuc-I*iPiO~ni ' .o v o> UJ ec a. -i < o H* UZ.IQoOtOhTS"1s*" O--P-SUJ.O0msoor>1os' eUeoeI .x9xos ,KaU1.i. UJ .X --1 X<u. !k*fter p JOtAoftmih o m*reoocfof o mvO p 0I6D>.oQJ p p ffevr- P *5ihic-5 oP , OOM Osf-ro ff.Cvlff VO|t tom O OSWOs * S0> t - CM sc op .pop o Poo o mm 0.00 OOP co.pm torn o w p\ OOO .pop f-W fopf- AI.PI* *-. r- fO|A o p - NSON mcy.ff Nh> o o t-pCh lACTO *- f>m o o o t!*0 ff Pm pA po p* , .eo r* *3 prey o p p fomw -.-efyf.yfcf p o 0 -*' ooo OOO ftr-Ao ff CO** o fpf w .o0o.0o0 po 9~ into y *-N.K ooo o0\oeffyoff*f Oo oeo o0i-K0o.mo0evi o o ptftf* f*fcl ear-* o - Oo !-- ppff .*- jot* Pp 0S P Oo ** ?IAP -* * m-s?* rF*h so pm mm cyso p ' oo ffvOOs r-r->0 oooooo eoi-.ff evjyc o CO 0 OOO 0<rr-0O.\.00J *-* ooo oVo*O!"* eocyy ooo OoOov CM 0IoT.\o>e0--So0C0M Oo f<fv .u<0. 0 Mo0.oN0 fof -><o(<Ar <(ft OsfUlJ so ff o1 U<-CHJOI OC0\M0 OOff*a: 4VKUoZfC<tJOKo/>f*tM<OomO/>-* < Ho poO.voOoo.Pff VO 0off.o0oJ0CM oo 00.0 oo . CVJ p.p0*.o0-mo0 foof m < 0 * .X<XX ><(ft oOseUOi ff 1.f> p Uil C<D oOO<OfrfssOX c <K\UaXoft<lOPOo./l>*^O.ootfrv P<ft4ft <fo1-- opofooVf.tSooffSf omo 0 <CL XoX<z(A. as -rf1*f p UUJI OOOpOPff ov*XUeOcci <PxUf*t4oIorlOf-tooo0 < o o< XaOPOXmf-t 0 f0Of.tO0ff Pf0> o m.ff -5: X o>0CUXwDI fpf 1 p U_C<uJDJ- .oUcI O. .OOsvOX OOf'-f14' PcUoOXfSt4CloSOO'SffOttC-oOoOm--ft <J o1- fOcfoOoO sCcD X -Xo< IOO^OOOOOeffo .mm . + >H p 9Xp v5 OOOPviXUXOI m0op1" -U-C.J<DI 4poOaof%<t:60f0f5ft-...O0O DzV>r C-31 TOTAL 4900 2600 3700 1T200 TOO.O 100.0 100.0 100,0 DUP040009907 6 48 to < i* o z CO O 3j> U* 0o 9 Q ui o o < toi a z < H69 ZSO w a UoJ>.to- Xi < > * L0-U.mO wP r ui Zo ,m p Z tro" UJ > ..aos. 1..u -J < .>ar hO h- ui x < > -lT> .CqO to oH- i (0 o n X fr- ZWtTo- Xo X X --O1 to >0 ---SOi X cv CO oi- UJ p O4-OiTVl <X X to- -1 2UmJ 0 < mi U. zto O z UJ i UJ Xflu X -oJ mm* X p u. o .UJ H* -z o p o p z-- CO X > CO UzJ u x u< WM.Jt toOiA r- WVO p, o .o** <0.40 to W1-ftJ'tAoOo oo1" r- 0 O f*0CV o *-cv?o o .^00 O iAOrt O' ^niA p t-^m *to Q eon o CVP o vo to* f*in h q o or covovb o p . tocvcv 0 CV.f* o. o oo o to p OCSiO p mop p rtjh o ON o co m vs CVV3 o p 0*tvo0*<*0 o o O*CVJflO* toUMA ?-- CV lA o o o *r" 00 90,00 Aim toP *-*-to oo *p" 0,3 CV*~. CQtoCV O 0 -ftim ;Q to*- O O -pm o OooOoO f**J>*to oCO rr * h..f.*i.* o Z***W*.t\ofl o o to.tot- p t-- 03 to o AJCV.Z o o0 o0.o0 p vos w P".4 V34f^* *-toP :.GJr*m o poIf* ooo ooo toto.cv p p o r* Poo ooo ooo Mtof* o o o r*t* ,-toiA p tocvp o' CVfA o tocv m rnpco o o ** OOO OQiOncOo o op .cv ooo toofo'-ro*- ev.cr*v o o f- .ooo O ooo Ptom o <v *-AT OOO o Do VcSv Acv poo o oop to mo pto cvto p ooo o oto-o!M AoJ oCO to OOOOOO CCVVPf-JO*O* O o to CM * ' .X OOO O . to-- o* *oto o X'1 * CpV o X o <* o o UJ J QW .H to 09 toO -j O to-X H<- *- o -o O - i \o</>: v> o U--0JJ < oo zoo UJO % zO*o-*rig-\ *- w X OOO .0.0.0 O0 totocA 03 -.<V AT UJ u zUJ x Z J< o OOO lOAtOoJOT O o 03 CV z < X > X< UflJ. o UJ H* tox too -J CV p 1 o OtoX ooz%x 0>0(0 . *<-- oh UJ oo zoo .J UJO s CO O Mfy -< z- 300 O0.O0O0 o o *"cvevv\ m A- 0O0O.O0 o o t3To* *3 Z A z o H- zUJ ec UJ >* tox toO mJ *> \o OOO'ttoo^XX u* o i *!P-0 .H\o</> Q <J> 1 o UJ mJ CO OO UOxJoO*oiA^ < ZVS*" 300 OOP OOtOoAO- oo >3 r- CV to OOO ooo o o < POP m < * < w Q S-J <3 M o UJ h tox toO -j to Oo toX <Uf o OtoX o i 0.0r"0 P UJ 0 < VS- f o oo xUoZJvoOo>o*m-A K 300 opo o ooo p :CV-*0 to --19 to OOP o ooo o to,trvo- VO CV XUJ H X UJ > UJ H* tox too mJ m OtoX OA J<- p OtoX o1- i AOU> . P <j> 1 oo UJ CD UxoJoO*om < ZP>- 300 C-34 DUP040009908 o o .j-- m. o x 3) o 'X u. u < x < 02 H< -K CO UJ X o ,o .>-J f (U >* m U3 X '< UJ :> ^A 0 Ih- Vi :ixiu x O X 'JO .in ,8 6 o < . .4 uu O z 14 tfC O .4 p IX p 1x :q o o in s<n :e p _-j < fOr* H 0O0 O' o fl* p h* OS x*o UIO !! .X*ri wo : .fiw0iA *" Iop. or1^ 14 XA. -J <{ *" +O- o J0SO V1* . ohzUlo*~ a: a J--On o so 10x-0*1J ov> xvo-\ U! 03 -xd OlAf : x oj 1' UJ Xa.! w X o a XJq > - Xu<. I^Ovrt ON*-.00 COlA P 1o- M0tS- O V0lA 0 o ^>*0 O WOvh* o o *>!* ft 9 f *-- r- MIA p o p eutoin O C0*>hl3A oo poo cecbcr JT& O o ** 0.3 0 *-AUA p o *O " ,ooo o OOP *--- r- O0 POP o POP O 04 wcr ^*!>Q *6*10 * .0 o o .*! 8 *^#t >. V-6r^ fo- 0 0 P 6 o A f*b> 0 o oil"* OOP OOO CU*5 0 *-^ 8 o o CP -.w* 0>0<A. PrWO o O o f-- r-'CPVfN f^PO W*-so 0 0 O .* * fO.tfNfO 0 0 O o1" 000 OOP *> 4T ^-CP0 o tA sr CACAO C4W4A P-. o ooo OtfSiA P O or* ICr MlNh o o Jo-- lAlAO NO <*5 0 3,iA o o o T~ IAOIA 0 0fO00 o T* O0O OOO OiNhr-.iAO 0 .o0 A1--O nffito 0 ttlAiA : ^3 4T P OO0.sO0r-OO0 o o o AC ooo O OOP iTi r* <p CM ooo POO w 8 ^ 0 o f*-- m <a. ooo ooo O o * \Of* <vt O to UJ O UJ -J oo UJ - .< W ui iO OX og -1 eox < 90 *- *8 *^ .OJTK **- o H i o UJ <sz/G><ao/l>o mi UJ o CO J<-- XOP>4T-N ooo o OOO o IA n J3* < > X1 jomm ooo ooo s t n o w o 0o *> X0 X O h mXm UJ ooo ooo lA*-U\ o o X *-jr NO i UJ mi m i > X -U00J UJ >-- UJ 0 OX ofQti < h m* o* O.-0X 4**0 9* o h- i 0 o 0o oo UJ xo mi a< UoJOtn> X *i- P D00 ooo ooo ONP.NO o o CJtfN ON OOO o ooo Mn O0 M *> *3 u. tO0* O*0O-.Oi0Tv o 0o UJ u 0CO .< X < 3 -J < UJ On X 0 I*A 005^X2 O0^0. -J X HO H 0 o 01O ur 40 ><- OO 0OO UJO X0PM'*A900 POOOOO oo 4AO*P w o -3- OOO o OOO P6JAO oif to 0 0.0 o O .Xn OOP *IA 3o0" A UJ .H0 < X w X X ut UJ H On X oo mi 0 OOvZ < IA O* 04TX Ho 1 O * 000 O: UJ zoooo m0i < UJ O * O %IA Z\0* J-- 300 OOO O0OO-NOO o o o cw J* X X .< * X< 0o.o0o0 o WCM o NoO -3 <2 X jr UJ *J o0Cv.o0j*-o0r- o ao* X r* <NJ UJ >- * .< X < 2 K x y UJ H* . OX oo C oox o* -K< P**1 OX*-Xo 00 OU* o 4> 1 O UJ 4 OO XUJOOO .<10-- O *V\ XNOr300 C-.3.3 DUP040009909 CENSUS COUNT OF CHILDREN OF A L L RACES: S MONTHS TO S YEARS B Y E M I LY INCOME, STATUS: AND ACE OF HOtiSINQ, IfS O *>- 0 or-Nddp 1 o *riftM6 ^ .60 -o o 1 PCM 0 F-JNNP TdO" rt o tsi .fTM Sa O CM<lMArf*- O -NH* T--* NpVO OO' * *rM O rO p r-.** OO O*W N O* ' `Oft 8 **. o POP oo I ZOUHUA.Mll9Ii1f- OOt -MOO.ONP. p- oO MflO o' T**mop 0o O* P*-i CM^- o pof-- aiwe* too0 - trAtA.Tin-ji.r* O oow 1* w.* .M. ttf-HCPM Viffll s Cj o T*--MlTk o A<nNtfpV 0O O rW~M 0N\A0,* "CMMN 0 i OF` -vl4ftMrA.siAAe ooo1* >-j i ] j \ \ ft. g 8or0w^0o*.op0 Jf OOP *0W0O.0P oMo ` *JMA r- ooo6o-oo6 op iiOOrft\wOOpiPCPAM OOP OOP o PCU:NC*M fwU sss g *-f-N o6OeP Oo P:OO*O*-OP` - !oCM OoO*oOf*-..oO01 opCM oPn-<OoowOo o *OoooO>oOcs-i oOn 88 8 SSS s OmsNrosf ** 8 pSNSSNp SWp ppg 2 t ** S | UU5l Ul! -j OOvX < Pw* Srt*fO* *o t P V>OI0 b-Jl u0aioiri ?5 <& oOa*oO**oON * P0QUl (V 8^* *JVT>"CC0 io- 0I " 9 OueSo>oift POP p <b onmowo o f! nfil 1- t ooo ooo e 0 Ui o a-w ACMi paUsl p 6 J< t 5.2g S A 0V ^ U-1l S ! * I O Nlft sXX S 1 * O04if5i a i X*?- 3 g s< UOiO,t S&l SSS s CMO M * * =li lh*f-\ 00.v*o>I.* oo U-il uiooo *<* OxOV*Xt**A-> H" C-36 DUP040009910 O 0 0 0 X 5 oaos UJ s? :0<ae *- XU*IQ 5 0U0o.I:iOf1"t <A ieJ I 0 te\ * ui faig. .1 < 0 .00 >25 *A .0 0 I 0 <0 f**1 X x UI a: SgM p X Or w1 UI U-C ..IT X 0*" J UI ^0 -J -< .'OXSlOA U X0 UJ 0 0 o u 0 o o 03 V) fU0igl hWO O pm d0 PXP O wpJK d0 fi.ttt P o!m a .jrpiAmx op . . *lA0fc * . * lAtfVO CMp x*r;iA o0 *-X *A O K 8mAtnA O N~*CM piA O C*M. tAm. .& g IP Pf- OKW Mf> POMA a <-xx a 0 01-p 0 XCMXMX dp OOC M .0 . Or .IAX 8 m-.*mtA 0. - OOP 8 POP e df-CdMdP 8 ?uj? <yw o *< fifirt CM m m NrPiwA< O' g * . '. . NOW O mmt x' m?v o CM O 00r'O..0r0tOif0fvt Xr- x8*--m*8rr8x XN sl*A-PsfvfswV mglA 888 8 J58 S MSNoi) p CM fv O 00.0 COO cum -- CM O o fv CM 0 OuO\mO Xh 0 K CM lSJAJOC^<O-OCmOM moo mm OOOOO O N*- m z OOO O 0 fi OtAOPOO r-.CM Om X 1 00 iL .j > OOO COMOf-PlA X X XI x 5 UJ X--> AKui o p ox: a i M5<A 8 ^ oo >U-<oJ-I u*3KaCAiOM6*OiO^r^ -<J 0 A UJ -J OOO .irA0.l0Altf0fv -J P OfA O ui u0 8hr-8CM8CM 1P 5 <* > U0I 1I5* 0-%X^mA3g.0O ,*H * 6 uO<kJ-I 3.cUQXO. SCJ0ooAY-ComoIoAAA poo POXOOO meg 88! rwCM.CCM l U0I 81 --<I 0 %* P<A <A I g tad 08S UIO A p AlA 8 UI i; s: W .it 8 -o1 *g8 UI K< I i NiAm i- CM 5> C8M X8n M 5 1 1 UI ?8p!j -<J ^5 8 I ip^-CAr % C-35 DUP040009911 (continued on follow ing page) pp (0 0O000O 00If) 0 0 r* r* m c1->1 V3 V23I oz 0013 (Tl 03 O rl oJ cd VI xi o (Hft'!! ;: rH ;rH O x: o0>0 H ll' + Ol in CTt fH UJ aQn., as * LU 1 ~4 ,, 00 i 5' NH <, 2gf 1 [IviSt '. 1 ' |!<:. (sA- 01 a"5UU#.i: OS-1O' OrH Oto :l!' 1 ft ia -- ooco ta -- <8 <n '' C2I*"#l: 2LU! ? X [NI >'Ovf: lun M> $ 1 V) . 1 j PH ! j fc. i a. : fa ow w VJ w. ><U.I m 3' <i! VJ;1 2<:1'! 1 (A Hi+C |: O ' : to i 0OO3'J 1- c ! .j 003 OP0%' rH 1i'0-,O00'0-0OG0OO E .en to ci ' ^ m <si 3 l!i. 01 vi : S. QTass' S< I1 f%| 10 2LU: oC--sli 2**S4 VI iff a 3 u. 4X.1 en IiI!I10-C : .' jeSt-: aB3s iOi'. Ml <rH71 OVorHn* t ::i 1 0O000rH 00GO O0 CM CmrHM GmO- OO03 OO01 <OO71 U, < O OLUtl as Cs2OO!:j <m XVI GD a-4: U2CarSl:t <K W L-03O JUC0H 0X I <VI Vs:I -_Jr; Of au. CM CM O --HT ftOo m r- * +4O0* O0 O0 . 0*0)* x*Or-if VCI -+.V4) 1-4 3 O . Cl u. 0 LU z Oss' <1o-n 0WX0-4 *X0-< be VI ausi: a. #4*: 'a < Cl < VI 2 4<40 44 1 VS 2as s ^ 1 a >s CO AX ! 0t. >- zOf 000 OCO OCOOin --00 to 03 p--* m0 ci r-t Lfl O CM 40* CO <N <*} P* 00 iH tVOH Cl CM *T --.r.>.0. mor stoo (-- GO0O 0OCO0OCM GrcHOi Cr*M4 rVCHOM OUOO OOCO OO<71 03 <n HCMNMH- .OtOo OHOOO<t r(HM> HroH*Oco 1** . moo OOO -OO -4O1 f-- ( HVC-) 0-.VP3I O * O OS .j^mu.a O OOO Om OCTiO4C <n in f> .PS to 0--0 CO <n 01 ff> to 0)0 10 HHH to 00 CO CM6 8t0LtnO cn a 0. to C? CM to Cl *C CM 0.0 .00.00 a* w Cl <TI O CM tO OOO OP% OIS.O0 CO tCn> C.0) pH --0CM MOO OOSOOO Lfl CM O CCMM CfHM OpH n0 0u u0 fr" 4) "p0-- IBiH vi vi >e- 0+3> u< -e Om aOnf -V0e01jI ' 4f 3O1f C VI -o OOcp OtQn OOci fH 1-4 O Pw Cl 1ft: fO rt .CSI to CM to HCM lfl OO O H 00 C--| .iCnM Ctnl t-1*. vo to 0to1 CCll .c00i 050 0m0 000 to Cl r*. OOO 0OO0 O0 ffl Cl to fpHH Cl GO OOtn OrO>O0O CM H O rf*s4 cn co 1-- . (QUO 0 00 +-- p -<a0 VI C-H 4V34I a r z <1 a. m a -4af pm?-- -*a#C. 0 00 Oq o Oci Otn lfl Kp r-4 PO. rfHH .C1M0 yOOH OO00 OO(* to PrH* i0n 0 rHHf O 4f Cl Ci CM Cl CM O .rH rH rH W'vo vd rH pH ci 5 tn <d eS* NO M CM OpHl CitM 03' SO* (S*i rC>l*ctoo wCM PaOH* b t<oM pUs" mos 0 00 OOi OGO OrH 00-00 .00 GO4 CM tO Ol CM P. 03 03 CHMP CM CCMM OOO O Ocn OrH 4.4tj'd-- ppHH rH rH OcOn OGO OOfH 0Hr to cmi- On01 On to O-- Cl rH 00 Cl HrHt .P^ tO WOOOO50 OOVO orpHHtCsM nGO moo HO* OX41Ir O*X4rJ1- VCI 4V4I *- 03 * a 4m4 oa oa pOr O 401 O 4f XJ Ve> l-- VI 0*36 1--1 x X< 44 40L4 O41 0c 44 V0I on 0OO0 O0 CM tO 40 pH W -tO lfl 3rH O prHH r tn tn M lfl ^ pH rH m i-ieo WCl .OOiCOl H. lfalP. un to m- .00 00 000.0001 0pH3 r-l VrHp OOO OrH OiffOs vCnM O' rl O0Cl O0CIOO0 Ooo --SI in 4o4 ujt u.* OOO H 4f *Ur X*4--Jf C(A 4V4) PH 03 22S 4 4U4 s s as OOO OOOO OrH Cl ;trnH SSI m r00H GO 01 CM in pH Cl rH CM rH Cl *t Lfl .Cl rH rt (M ^ rH .a 0> tO a cn r m if PM 0 00 OCM OO OCM 4T rH Cl CM CM OOpi.*OOcirOO*r.-- Cl CM pH rOOH OOtOOVOI tPnK 0C1| iCnl f-- 4m4 oa oa O O CJ X4HIf *X4r3f .e01 4,v4 N4 03 -0x > -XJ .c rm-- 4>411 O C 1 P-4 - CM cs 44* tn to fs* 50 OS i D-2 DUP040009913  CO J a% < K O K o X 5 so .40 u. o TO-' u jhJ <a fo X < I-- ON .10 Ui0> . Q*h XI < UI0 9- a. tr> V) .ON -Nr* W xO o IT u X Or- iL >X -J a- :r W< -J < > *ip O m X < W > i lA .40 O O>rn >- b .:c aeo *- w*- ;e X O .Q ;[ --ION -- NO *D X0> Or- 40 1 UI W q Ocr < c: CCO.r-sj Ui -i reoo -< 3-lA xo u. r- 0 ar 1 UI ce UJ lb a: Cl i > x p U. UI KX X ox U o Xmtm C/I > X CO XX us < Q u, O'*-. Q eoraro O *-rtlA O * KOf NONOf!- cvno QA o P W4a ; ONtAlA o o 0 I4ON40 ihwo r-fOlA P o o r- Alps On it CM CM JRIP* o o P jr <vp fcTVJj- o o p 0vr- 0r-O o\o b o r* zrzr.- OVXN0 coin o o P CA4r.*^ OOP o ob r- 0\ ' . N00 r-rttA P0 oO 0-0 0 OOP AHA CO o O >0 NO .* * ooo 0 0.0 9iOO CW? oo On --^ OooOoO r-<V) O Q tA -O' f-bf* *a P-JTf* CM MO o o o irr oOoOoP *- p N oo CM r* OOP OOO NAf-N CM60 oo 0 f* 0 0.0 0 0.0 NO-CUP CM-44 oo -3* >0 pop lAiAO o oo OOO 0.00 CO On O' oo 6o0 * oboooo bo r- f^-TO -,r- eo 6oo0.0o A0n<0 CM CM b o h* (A oooooo oo O ** * * CVI .a r- Cw! n> NO X 01 < X A < X X < UI > On C PO w 09n X < NO .!* r1o .O * ' OZK <-r- O <*G/>Voi>oo *o- fr UJ KOO -J W i* O *IA -.< XvO*- booooo P CM,60 ri*l o oo n .r- <a. . X Xo UI > OtCC OO O.On X < r*. N- ozrx !* O *f O 1 O Ui wcc~ C\xwooO<ooo/1>Aoootn.* < frr XocNoOco- U. sa ooo ooo VOpkP ooo _l CM < p :> o < S3 O UI > O'00 OvO w 0.0\S < 60 .OozVe o .r9- O UJ w p ..ar-P <\a6w0/>V.oo0i>%oo0tA^ <1-- 0Xv0o<*A- C- 37 DUP040009912 APPENDIX 0 SMSAs RANKED BY NUMBER OF YOUNG CHILDREN IN PRE-1950 HOUSING AS OF 1980 This table ranks all SMSAs by the Dumber of children in pre-1950 housing for 1980. The details shown include the child population distribution by "Inside Central City" (Inside C.C.), "Not In Central City" (Outside C.C.), residential unit age status, and the distribution into three categories of age of housing units. D-l DUP040009914 ^66ooofrOdna ro to fo to --t P -o o s ft CoL r* mU ft 3 CL 3t: o 3t--r 33 IO "d "O o ft <i. f+ c. eft ns yr n ft ft t * Vm m t ,w* trd fO fO w !S> ft Oft' -ftj 1 ? * .O f fOt'. n ft << T < IHS-*t 33 P f3tT fftt ft n' 3-<C ISS o a=o c ft fotp Ml X M iD O ft wW fftt "n *. O' "5 ft* P" >HC-- 35 M ft CD S' rr f*t S' fmtt. &s , ft M* * o X . 7C 1< fr-4 5t in 3 C/l > m <+ ft C ft APPENDIX TABLE 0. (continued) 1 0 6 ,9 0 0 2 4 ,2 0 0 8 2 ,7 0 0 2 0 ,2 0 0 1 ,4 0 0 1 8 ,8 0 0 (continued on follow ing page) C b-i r* p in in O' 1C M (H- 3 n in. Q. CL ao. ft ft ft' ft -H M H Cf OOP OOP ri * *: s m * . <+ ft Ci O 0) OOP C *~f ifnt' 3in ~J. -w. f--Mt a(D. OOO *. r+ o O ft Cvt+ 3in CL CL ft ft ooo *O. OV <01+ o c f*int*-.' sin' CL CL ft ft M OOO O *O. ft+t ` o c *-* fWtt*. 3f t(. a. c l ft ft M OOO * nO O ft O crint-- MSinCL 1 ft ft OOO * *'. rO O ft eet m w- 3 n u> Ml.- Ml. a n. a> ooo *o rt w to |~i ua m m w PO 4L CO NS CD to W MO' to W 10 ooo oo WooO oU> WNO)*WHW?4' * tGo3' 4CD*' o Mto M C4O sj to IO ooo MM w CO SI to too oto oiO ooo io to UD CT O') CD Ot 4* ooo ooo M4b ItSo* 4o* WWW PS |0 ooo ooo Nto> MiD 44$* to W oo ooo PUS)MHW MM in Mo oIoD (DIMM O OO ooo tooo ooo aec 4b 4* w to to MMN) b 1^ > In 06 to O O ooo ooo Oo OOo: U4ii- M>1 OOW Mo IP O SI ,<A) to io io l\J to l\5 o JD ft p US CTl s fO^ M (i) 4* H> eft r4ob Nini O 4Mb rpo <4rpo W iD' IP sj iD 4b fO M tMo` rCoD IP P4b rmo croh OWO' CocD Ooo too iPpOtooOton MM m rs f* Si o ih O' o o oo o MM wW- WM- w4. * MOM O0.O0 O o 4b 4* CO cS Vi tn oo Opo W M 4M W 4b O 0.0 op M fS ID WM w in Ip OOP OOP WSH ft ft H IP CO S O O'- o ooo in p m O M IP w w P; . oo ooo W M 4b. w 8 cn Is fs 4b OO o O' pv P .M ip at 4b 4tpft 4LiO W O PO p P'P ww w ro in fO M w O' O O poo VtoO c tOIDoi ft*' "5 3C"i -* CL I3D i& to oOSICIt 33o". fSin*T 4b SJ ch ftS4i * . ' 4n ip W rtootMowto OWN) sss p tn fs POHOl MoiMioMo CDCOQ LOSJ4> I*S > s O t 06 Ch 4b 4to* Mto Po M MM MS P 4b 4b rtno ^o wco P 4b M ro m IP W UT MOW wSl i4nb 4b Poisi ro in w S in 4b ib 4b w p Owi <w7Y www -fttt MitoOo IfD<t -* in iiOn icph *mT? nfPCt+ troo ui rroo to to to 4tn-Msj Oro 4oOf.OoroOoto Mw cn ip to w rWo rWo 4S*j tooooowooM ww to tcom ro w to ttoo iroo sipj sOo4 'oWpoPP stoiUW S4b ttoo ro m 4b 4b io to W to o Mo4b Mttoo tiwOD . tMtoo MMro srtoo MPOOtOo P4b rPPo OOro OP ttoo to croo w to ro . wVsDj pCO m8 ww Mrtoo 4oOb Otoo PPo MfOrti 9l*66000Wdn(3 j ; (continued on follow ing page) t-Q M MM M M M M M 4b to M c Si' rt. .O frf z ft W (A Cfl ar w b P 3 Z --h *mS c D* C. ft lya 3 z 3 3 ft ft rr o SD r**' <y in cr o y <B O *3 `y O c i* c5 z' <- cr C 3' ** Mb., o IB V *: wft z M cn m (A fz 3 ' -t o i jr ft M >' X f" 1 Z' *3 ft' < > w " z *--1 c M Z ft -3 7T ft 3 -ri mS ft 3: Ola Z CA > n Vi o f rt o ft ft rt X A ft * 3 O > e "if fy tfi 3IA a#* M ft. CL ft ft _ . . -4 nno . V ft o o ft ' aiwi o t-f ft 3 (n cn l mJ, CL fB ft o o. Mo *- y O< O. ft C b-t Pt 3 wW.: <A CL. CL ft ft rO*' . *4 ooo <y : V . rt &mT O O ft Jmi 3S. ts <y (A (A J w. do. ft ft M' o no ry Oft SH rt 3 (A CA <' CL d IB ft -4 nno .ry es Oft * o M <y 3 (A (A CL- CL ft ft H OO * ft O O ft * b* O tH rt 3 in cn -t. mdt CL Qi. ft ft -4 oo o * ' <y pp ft o t--i rt 3 < A< canla o. o. ft ft 4 oo . * <y O ft ** M to to 4* co 10 06 CD CD O to to'-4* VI M O05 OMO' Hsi Wat IT In M MM CO >4 CO O4*OO^ ttoo ^J o to Coi to to 4b CO to Oo Q M *si CO *4 H >4 O CO t<o4 t*SoI 4*4*. to o to IS> 4* CD o nooa- ios) M. to CD 4* " VI SJ M Mto O4* M -S4 fSD cn CO M 4b cn tnwOco to V Moo o Co 4b CO CO CoO o MOM to M O O o oww CD V 4b V*VJ to in 4 *sl to isa wtn^ to CD 4b . VJ H 4Q* O ^ 4* vi o o cb cn to 0 * * to cn Co to CO M vi 4b . CD 4& to C4D* M M <n to 4b M O to to w*44: M CO COM4 M ivs*l to t4ob vi 4co* 4b *4 4b to M "4 to to to to W 4b Si to to to o vi 4* co co to M *4V*VJ 4b' con to CO CO M CO to to M M 4b M 00 M V tMo: to 4b 4b M 4b CDVI M* VJ to M M 4* O vf -o m >. CD m c B cftr o zr -y -* CL f4t 3 m o 3 f+ C Qu o 3 ct ST <A t <fftt< y V) to m 4b^^M ^4 M CO J4 to to to CD p 00 IN4k W tone 4b p to pp to to to to 4b to CD CD M q : CD CD U) 4b to iff VI M VI to M 05 O ooo MM 00 WM O 2 3 1 ,5 0 0 6 2 ,7 0 0 1 6 8 ,8 0 0 1 5 0 ,5 0 0 2 4 ,6 0 0 1 2 5 ,9 0 0 2 0 3 ,6 0 0 3 9 ,2 0 0 1 6 4 ,4 0 0 1 6 5 ,7 0 0 6 1 ,1 0 0 1 0 4 ,6 0 0 122,100 6 2 ,5 0 0 5 9 ,6 0 0 1 9 2 ,5 0 0 2 3 4 ,4 0 0 4 0 ,8 0 0 1 9 3 ,6 0 0 zi>66000H)dna 9-Q 4UbS 4fOb 4Mk 4b P pCD u 03> S0O1O' 0. VS 3* rf(Aini 3r*e* ro3* 3foCv+t >s CInDD* >e* <30Mmw tr> > X0-rsK> w*CoTL o>w <r0o<jr: w3 OX O7feT*"' ' oX "30f > 3r3M*l* mo , CA 03> P <0 (oO 2 2 to 3raei"' 30)0 3 CO (A 0> <A * CT T otal in s id e C.C. O u ts id e C.C. APPENDIX TABLE D. (continued) T otal In s id e C.C. O u ts id e C.C. In s id e C.C. O u ts id e C.C. T otal In s id e C.C. O u ts id e C.C, T otal In s id e C.C. O u ts id e C.C. C H4 oe+Ii, 3twratit ftg- P *r> ft oo CcO+l':' 3M(A* IS' <P . an c? . rt ro+ <cf+l) I3(AM Cu q ! IS (S n . nv. oMrt 030 CM r(A** 3(A 0 CIDL noo* * ft np T otal OJMHNHO HIDd ;i OO" OO' OO' M NO fO M o6Ti MMOm MNo p M fs* NO M V0 MHIS> MHN aOQ sO soO MCO NNOO ~ Oo o o M NCOO P NO O M4k NCOO Sot NoO ooo ^ Msj 4NMO C3 4k 4b . "D -IDS M P 1 7 ,9 0 0 3 ,9 0 0 1 4 ,0 0 0 no P 4*N> no3 tao. 36' Mffl H MNl NO ^p : o o- mMMm: p ch op 3 1 .5 2 2 .3 3 5 .0 o: 5 | rUoJ epft u^4; <3Q ro (COaM 4* *0 M NO NO M No P *si M 4k 4*- P HlDH ro *sj ch P M NO M SJ 4k vtoo m *4 . p p oo NO Mp N4bo' M O tnro ^st MOM o po 'mSi ai CtsDs ytHOv xQ C.D KporMo M 4k P 4k sjfO M in H 4k 4b CD MCO P M*sJ CD <4 cf5 6 S o o N4S* cn NO n o u# cn oo MM M M N> O MM tn M *st CO' M o US M4' 4Mk 4k NNo Mch cNOo NO CD M*i.M00'WOS 3Clvi -'4s&i--Nr 0 r4ob (it'ttvi CfsO> -SaJ NISOO No cn co ro *O # 4< * m *sj a U> m in . COfSJ OJ CO O o tn M op P ch 4k oo H> , IS> cn o O B O 0 o MM M MCO NO oo-po fOoi J-> 0 n 4 w us 0p M rWo IS 8 q -t ro OS N> *p ro m o 4 5 ,7 0 0 3 9 ,3 0 0 6 ,4 0 0 M N> 4* Isa OoTooo in oo M4k. NNrOo N o *is| cn sg J.a.>.. l.--b> top m 07 to u> p M CD P cn ro M Nu%O cCnO M m p0O0 o o 3 5 ,8 0 0 2 8 ,9 0 0 4 NO P NO U) Ch -PO 4Oi O 6 4 ,7 0 0 2 5 ,7 0 0 1 3 ,2 0 0 1 2 ,5 0 0 M no ro M cb P 4b OP' OOO'O i M O1 zc &i --nsfr C'SL o M*sj 3 i O1 CO o ao 3c+ ST' (A M NO M M m cn O 4* 4* NM UNOiu>1i S4 -tj ii,, 31 i M : :o <rae< (A* 4k' 4k 4b pM UiOiOO to co co P NO 1:. M re | o1 nr3fe+ 4b Cd 4b p pro p No P P *sj NPO P i., M o1 oCO PP M4b cotncD ,rPo pP proo o ooo : --o1 01 ________________________________________________APPENDIX TABLE D. Rank 8i'66OOOPOdfl0 S"Q ccon C4O* co CISDO CMD CoD ho IS> CO to j\f l1ltif.i ZO , smff^ttr .<f-fCff<9t<ttt/.* 1 33fci<tnD 3<C : 1 <3wfEtli*' o3f<-ffC6t*ttBO''. . fC"tJL Oo ob wafmf*oO>5tmtfiafcncQf<f<mtnttin**"o. ' f'-0faCttj9L 3 8a*a-u' -affOtt wcn z--1 cfr<fttn+t - Zf*t mffff<f#0trtttt f3ffttt. a>t, 0> 3ffOttf <2 E o o c 3cr cft i SM SA/Status* (c o n tinued) P re -1 9 5 0 Number C h ild re n 6 m onths - 5 ye a rs 1950-69 1970-80 P re-1950 1950-69 1970-80 -offtt* cCfnocfOMnttLl*nrafCfOt-tLiKo ffHttI SfmfrttUXtt M3cmCfntLl. Oo oOfot+ oC cn a aft. aft. op op foftt to H4* HO 4N*i M I\ cn cn to si cb cn 4*^D Si OO O O OO si o-CoD oo 'WhOo O OfC0*rfmtt4tL-40f3ffO,ttt .*-. f0m-rtHmt*' ocfOrOrf'Wt>tt..i Oa*lCffo""tt-Li<.ofrHt4t-' fcMCcfttX**-'WffCa--ttL*I o p Oo rfott omrfdttm laf-tl cftl O*o *Ofeot'lom-rfHmttd rfOctt- 3ft-'* CftL OoV OCfo' tL.. rffo4tt ho is> si s4 Ul 4*' *sj O H-* M INi O 00 4* To cn IcSoO IcSoO os HM4*WM cri 4*; S. MW --q ho cn cn *H* *N4M* O cn O O w Si CD 'S O cn m #oo w Si Jh*kstoJH4* j* cn CO M 4* CO O CO bidU ho ro 4* 4* 4* CD cn bo co 4* h0 OS 'O f-*i4s-yJ c*4o 4* cn* o 53.0 14.1 (co n tin u e d on fo llo w in g page) cn SI *4 ^>4H4*9JS)J M CD Mo CO' M C> HsfHCDWO OS NS O' 4* 4* co ho cn CoTf* s W 4* M 00 ho H (ND> AWCO CD M- CO Hoo HcnW4* cn ^Iso b 3D* wffatt S CaDs estj>cn Ip *CsDj M HpIoS)pH CD SJ cri si --q o cn H WCD NS)I HM PWO 4* r4o* fS> 407* ICSDJ pro J--qr1 co as 4> CO CD Lml <J\tO as <4 4* IcSoS wN> Nas3 HCD 4U* CD 4co*. c4n* 4 --q bS" cn: to " 4^.ho bb' OJi Oi CpO 4p* J4-** 4M* CCOD .CO 4O* 4p* }4-J* 4ho*' 4* I4H*-' CWD CD CD S 4* CD 4* s| CD Co4* to cn cs 142,900 41,200 101,700 54,000 13.500 40.500 pCD c--qn;is* hsoi tn pM 4N* M4* C4fDc U> CD CO FO 4* H cn 4" 4S; Cn 4c&s- MHcn 4MtMn ' oOs'* oos 118,000 56,700 61,300 100,400 61,100 39,300 4&s fHo Oi CD sj- 37,3 7.8 47.2 cpn c' n 4co* CSDI tpD CD cSoi ho CD -s ,M . fD 103,600 54,400 49,200 112,300 31,900 80,400 o1s-. *oC.DMIIcoNNhSSi P e rc e n t Total 6l'66000t?0dn0 8-0 ' O W 10 sCDc *4 01 50 Ol fil 4k' u 3 7T tfion 0 ' 0: ocr X * 0 0 -ri r* ^ O ft *n f- ST' m*k wtft rtf 3 rA5<s6-. ' s0? 3 3 H =f weOf't SOI >5i0: > R tCoM 0 "O' 0 Tfft O HI * f s -s 2: fi -****3^ .fit < 30 fiA ft ft t <- 3l fit rft 8 SO 3 0 >0 1O X fit* x: A r* < ft (ft 3 A 3ft , afr 3. (Q 1 $ m* -X > r~ s ft i, (A w3ft* : (P+ fil rt 3 :' (wQ '; CVI * 3 3 3 1 X- : O C Hi <+ 3 (A (A mmim 0 C H3 (A IA =# 0 C HI Its (A (A 0* * O C Hf rt 3 V) ft nrfi ! 0 3C. kH rt ft ft ' 0 3C H' rt tn in i* arf* O. CM CD A 33 AO CL CL AA 3. O. AA CLO. AA CL 3. AA 0H H . ' .H H .H .H H ooo OOO OOO OOO OOO OOO 00 *+ *. V ft *. eft rt .. * rt- * * rt . r+ rsn-ft O. O' A 0 O fil fii --* w O O Ommi O OA ' Mrf 00^mui . CO O 4k H 4k 4k * ... ft* 08 4k . ft*' trr to ' w m. MH (n 01' INJ CD tft'H 4k <S4 4k IS> CD si VO Men es 0 00 0OOO OOO OOO O . O' O' OOO 000 0 0 0 O ' OOO O' O O O OOO 0 C I~t rt 3 tn tn a. c l AA H OOO * *. rt O- O A O 3C HI- rt ; in in n. 33 AA H OOO * * rt O OA ** ft*' sj ip WM O OO ft* sy.-fyt*i 0 0 OOO * 50 A 1. ft* CD O ">O X >CD 4>HUi tC CO CD Hi- O CO O O ' O 3 r* 3* 00C CO 4k A u ro 3- 0D sj Of* O : O O' O 3 OOO H O <W4 iro S; 3' ta Oa ft* r4 p * crs to "b fii tA(o9' S-'j- : j in ' .8 m ca u ai Co 4k f>0 CO HI si WH ffi4 O CO 08 >4 s4 4k O Of ID CD H* CO OOO O O O O O OO O O O' O O O O OOO HHW y CO rs> q OOO OOO GO CO m *sj CO 4k OOO O OO O 4k 4k 4k -M. H 0 C8 CS8 t58 0 OOO ft* ' ' Jkio. cn 4k ft* COq <4 ro u> 0 CD bO-ft cn cn to ftj 4k 00 4* 0 4k 0 0* 4k CO 4k to co Pq no to .. H- 4k CI A CO H Oco to -si tu O 0O0ls0l OOP 0M av h> M U5 O OOO O O O' WM 0 m -t- in 00-0' 0O O : 0M 4- 0 0erv m00c OOO o> m > JOffiSJ OOP sj BpiO HU td N h> I*'S' mA-M- CO S4. WWW 4fc'M rss m a> co 4k GO PSD Co 4* ro -A rs> no m IS> ft* ' H^ffi o -y -si CO VO CO k4 to miss HW0 4k CD CO fOMft H cn co *-* sj ca Itf-U ON M 4k N> CD s* tO * f\s CiD 4* Co ft HHW HH HHW Hn> HfSIW sj M VO 0 cn cfi co si H CO sj Ol 0 0 0 0 00 0OOO OO O O O O' OOO 0 0 0 0 0 0 0 0 0 0 0OOO OOO O O' fH H CD CO O O O M*;- if* 4k OO OO (4 4* 4k CO 4k OD ft* 0w * ft* OO' O0 O0 ft* ft* N> 4k O OOO OOO ft* Z- CD c- 0: a ^ : O O" A 3* "5 H . CD CL nA 3' ft* CD sj O' t CD 'A: O 3rt s tfl 4k *Nl CO IS -O -J A1g CD O 1 A A (A no 3 c a. IS8 0* Q ISO fs> rsj 4k 0rs> -sj "3 CD A < n lA 3rt fto U8 CO M 4k M H* - s* i W osiy CD sy 1 g WHU) ft- sj w W H sy G-8 PD OO H 4* CO 4k 4k. 0 0Co ^y OOO H O A oz660oorodna -0 a* IS3> o (0 4b CO 4b *4 4b 9) 4b 30 . . 3TP *o So*--<C I.1-Q3*>> <W tariT a. Sxi got* O--i :nHf "O *O< c tvr3oP> o c31 ` cn a3* f crbf>a' n a* ^a 3 t3o 3fi>- #M XH4 3 SM*'- X 0 -5 if>to-? * rT* 3o <> eM. > 3" CO <>1 . 0n31}* X o `o c v <a#a >* M*5<* z (/) 0 c+ ra7T-` n M< too a 3 -3 *(A9 3 O 4a -* X .\>- rO* :, r* 34 *3 n <cA :. * 2C Total Inside C.C. Outside C.C. Total Inside C.C. Outside C.C. Total Inside C.C. Outside C.C. Total Inside C.C. Outside C.C. Total Inside C.C. Outside C.C. Total Inside C.C. Outside C.C. Total Inside C.C. Outside C.C. Total Inside C.C. Outside C.C. APPENDIX TABLE 0. (continued) (continued on fo llo w in ' tn Mis*. **o 1O--i 4b to M tp M M CHD on o o CP oCO Pi M OM S;2 Mftd M|0 SJH ^JMOPN> 4b KoP Ooi M MMOro o Oo'o .i 1"O' 1li M* 30,500 25,200 5,300 oo 4* o wCMD *N><M4O* Ob. tMnisH> r0S35 >j oOP M rs> 4ObGO oo tp; 05 'O*' tor. - MISP HfO* 4* K> O' 13,300 800 12,500 25,800 3,500 22,300 wM*4 w1MOCSDS I&W S5 hO 4b 4Mb 0 atot?f V,> oo m no IaSO 00 40r- 36.1 51.9 27.8 40.1 57.0 31.7 K> oo rvs H tn fs> fss N> O IS3 I<S45 M4b-.UM> bp Na' i *tmn'uM> 4b t* 4U>b.JMb 40fcisi *y;rs> H ' M4* M P0O3 4b M 40b4 OO Co H OS 0 4b 4b uM> 4t*b> qb OP 4rs*s CO Mta 4b ooCD M ro ' 'W 'Osi'4b <mp p^.4rsb> U OJ vJ 4fSb> U00> 4M |SNN Pre-1950 14.7 51.4 6.4 0*44 4b Oo 0*0* aOO4r b 4OO* b*O*U' P MISP IS5 0M4 rs> ch ^ 11,000 5,500 5,500 Kp ISP OOM M00 ISP' a4b 4b I0S4p 0M4 ^ <4 1970-80 69-0S6T z- c 3-c5r a--cw.sr* *mQ5. 33<swa*ri << trf MO1 "O o3<+ 4b OJ aS 4fc rs> M MCD 00 Mm M W CP 1970-80 Total 34,700 23,400 11,300 140,500 25,700 114,800 80,100 22,300 56,800 25.3 4.4 36.2 44.900 14.900 30,000 36,500 19,200 17,300 4^b4^N S<! MO CO to4nb O%Mma 'oi - M *4 OV' ^66ooorodna Ot-fl *4 -s4j >4 >V4I VJ US NS NO4 3ft C VftS C 33n oft tft 5-. A --f(^*nt . *fODt fvt oft *So?O fo* mo '3 ft ftr 0ft0 3ft XCA oft f(ont fe(M0t* APPENDIX TABLE D. (continued) (continued on follow ing page) C *-* cfrt+fi 3fwt'. CftL fftt -H o4 *o c* on M( flltl 3<0 ft CL foOt. nf*o t.. eM<ft* fCft* f3(rfHt fat fftt OrvOr> t3rt* (PAf 3<A fftt fftt oo& r nf ST ocft+ <(n*(3n ffAtt Wfftti cso o *. * on ft f--Mt ft o*O. o*O\ offt* Oc (0 M(30 idt ff,tt. CftL -H OO O4OOrf+t fftt fftt rtrtD amn POQ OOO'OPO asin HCOIO gooooo woo tss MOoOotOOoO as cn re W *O4 OOO NS NOOS >4 CD NS 4o*Moo oCD *bj CD NS' OIOSS OOUSOOCD W4.WOObWOOnNSWIWOOM NS >P >oo us MsuNnS fotnolo u iss OooSooWopH wfWrSwOKiwOO- l NooS oCDo CD US P MOOOOOMOO O ouo> MO 40 M Vyiys oooooo *PPOOCwOOODOOwPA- * HHHH^WC 'OoLl'o005-o0 4b 4k p Iooq oocnooo wNoo>MVop. o4N0u0Ss NS M US ooO'*OoOo' US NS uv Vi 4b-p ooo o 4b CD NoJ oPoo NS CO *4 01 CoOO OUoS OMo NS CD UOOS OUSO MPMM US 4pOk oOCDoO4L A M >OOJ OONS OOP 4U>* 4b-mCD *ss 4* p AU}*, 4VbI nsusus v* i u* s v o H bl A pUS Vp* .CISDS" M Asi CD I^S4S NUSS NCDS P US P US ^CoOANS 4W* HM M N) M AO M CDDA US 4b ft A 4b P 4K4 iNsSitUt> NUSS NNSS N*SSJ WAV 4b- ISS 40 WWW HWH w 40 WP AUS MA 4W>- WUS' H4* WNS AP AO US w w O NS IOSIN5 |SS OP IfipH "si US Vt Vi HAD US <bj 4* H A^ OO CftT3O "5 b 1f3CtL 3<+ Vf-fftC1tt. "fDt 3ft (S) U 4k 4* M ISS P N4bS p. M*>4 p CD cri 4* on USM o as cn IPSSO. MNs Ns 4* p US U* US US US us M US NS ISS M MNS P US P PUS UOS M4b NS P US . NS MOM US m us er mm oCOOoNOS'o'9IU M H ISS OHIO aooo wfOQOtHwOOMOIOwfNsOt| M to pNS Ho dooiMoo .m4* wp: NS NMS 4Pb OOOPOOOCD NU*>MNSU> AOocOonOob UUM NS. OOOOOOO M MNS N^S OOOOViOCOD frti Rank Z266000t0dna pop 00 Oo c m ?c 3 c "O Oi rt* sir fter E/J ST 1 A fit ,C o-*a y b' <v if - =f+ *c *5 o cr Ic 2t -i fiQ JMC n r- 6-0 P O s Oi sr sc CtO M 3* p p n o s 3>C p 4* OU>k prs C > *: o n* ; 3 Oft* -05* CP n 3M*a vt Q. * rf r+ bs 3t a*. . (A (3 r* 3 P 5>- o pt < fli - r>> oii SMSA/Status* Total Inside C,C. Outside C.C. Pre-1950 Number Children 6 months - 5 years 1950-69 1970-80 Pre-1950 1950-69 1970-80 (continued oh follow ing page) Total inside C.C. Outside C.C, Total Inside C.C, Outside C.C. Total Inside C.C. Outside C.C. Total inside C.C, Outside C.C. Total Inside C.C. Outside C.C. CM rCaafA-. Waa3ka * --i O . *o +CVr>> 0(w+m* CM mCfWfm*tLlm' O wb3((ASSa O H O*. .V*O' CW* 4^*. C-D *IS-O* KiVoi o o 4* MNS ` M P *4 CD ooo M p*sf us UH Oo Oo O M US P US PPOM o op P ^ M- US in^i fs> ooo opo M P >1 US 'Vb4 POO opp M P '`4. US. PP P O O O O MM Us O US US 4L sj OOO OOO 85,900 34,400 51,500 31,900 17,700 14,200 N:M . M -4 4* 1 p O co Hn s 1 smjiufsi. *w Po OopP MM .0500 POP' OOO opo CD 4Ma OOO POO US fN> NS CD O OOP POO MM 4a P **# MO M OO o OOO ft CD IVWH O O' 4a 4* M HW O P P NS M Ns 6s in CO M P ooo . OOP OOP.. o p UP NJ uS P P fs> ooo opo MP us IpNS PPM O0O OPO PMP POP ooo OP o a{a M P CO M O ^4P NS oo ooo .M P 4a P Ul P OPO opo NS p NS M M ISS M p ' P $N.US . pa NS 4a 4 ` Ntf 4" P P <1 o M 4* K> ius ua. s ap Pop M^4 -aNs ^N4S NS M P -U P P H4H U* O Q - M- . P 4* CO USUi NUSS P-4 NUSS PPP u* p m P 4* *4 CO 4* NS US Oi 4*. NS 4*0 p Vp US 4 -N PsrfM MM P US afr- US O Ua ls'J ^ NS M us US US Oa Or P' PP NS NS NS O* *P N S O l>' CO 4a p P P US US *^1 P cx> NS 4a 4a PPM us p o P M US M NS M pHmJO 4s*i MO p US 4a ONSM- P M US PMP US CO P P NS. 4a MMH Po p W N> pje m HWN 4a NS US M -si P 4 <4 P US to P N0D P O P' ooo UJ US ^4 p *si P US US P O'O P OP O N> K> 4* fS> P M H* CD ooo ooo U1H4 NS P C0 ' POP 0 o M M NS OOO cri 0s w ooo ooo MO P uP> MP P 09 CD P OOP OOO 41.700 27.700 14,000 4a M. NS Jail P P MpM 25,000 32.900 65.900 Percent Total ez66000f0dna Zt-fl %o CD ID CD 05 sJ 05 tn 4fc' %o CO ha Hi fit 3 5a <q JU 5b w. n m < fit o fir sc o .3 , ' O Of tn *o. --i CD r~ o rm*-m- - o -5 3 S CwL 3" 3' 3' -5 mm* o*i 's& r *% fit CD ict fit (Q O< 3' CM o f* C S (3O O3 c+ 3m ID x. fit fit X iA mm*' i c 3 z o o rf n < > M ar HO *4 XI r+ > A w cr i 3k > :\ ar rf i6 3 -< w > -1 crht. z c fit rP c CA "t? SC i nr s z Cm. APPENDIX TABLE 0. (continued) (continued on follow ing page)v CM rP 3 CA A mW --HU c *- fIftf 3(A W* mdt o 3 PH r* 3 (A cn o C *r* --*p 3 tn tn --4. 4t o c rh 3 (A (A Mil* o. a. CL CM CL CL CL cl a m 8q 8 q <T> CD . *H .. H .H . -H O" o o r> o o O O' o o O' o rP V ft * . * r* * . t*' v rP v # rP fMikt3 c' *.rs OeH*)' *r> o Matl O O fit * * onft * *" * " mM' 05 ha do Mh' a 4* o o 4k 4k ID 4k Ul N3 -si 4> 03 -si 4h CO *sl ha cb o ha ha H H Ni o Ooo ooo o o o OO o oo o o O PH <- 3 (A V) M* fttt AA . . -H H H H o OO o O o V ct rP rP rP O O Mfitl P ^- fHiti. mfimt * -o N> > to CD t OfiCO 4k 4k H* 0-0 o * O o MM H* **4 "4 oo 4k M o o o O'' o o 4* u> a ai tn oo o oo M ho to 4k CO O CO O' o o oo ha ' -8 co ha co tn ha ha O oo si s| H o oo H* fO t-* isa w ha M to 05 ISS O SJ M 16 MtDH si *si tn WO ****.- to to 65 4* N> tn M ha cb 4k O O O o o O' O o o o HCJl W HH-H M M m to ra ha si VO 05 CD 4k sa ' * r w co 4L tn 05 c CO 16 to cn co tn OV 4k CO w w (*> 4kto to ha ho to OV4 oi cn thr 4k 4k 4k CO to 4k sf CD CD 4k ha 4* si SJ *- f-J CO 4* 4* tn * -vi ISJ M N> M 4* in*-* Co 4k CO. CO to to to 4k M ha. 4k -f* CO co SIH 00 05 - S J sj M 4k" fa q> H* H* ISO --q ai Go 4k ha tn M CO Hf W OV 05 SJ CD Ch o . 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CL ei. 0 0 0-rf pf HI H ^ . -H H ^4 . . *H -H O O OOO O' OOO o p Pi n* r+ . pt* Pi PP * <p f* tt tt tt tt O O tt tt tt O O tt tt tt "H O Htt HWW NS M 4k eoft O' VOj -Oa o CooO ooo oo LooD (OHO o o o NS Ns Co co co ' CO to rv> 4k NS o ' oto- o fSS o o ehoco ' c Vs o o s n s V> O ooo o % n s ps> SI' n s &w' co "W oi * o O NHH NS 4k N> NS . AM NS MHS 4* f*' fO M ?* O p J* OH M NS CO CD 4K Ui os ah eti *sl Ns CO to 01 Co 4k NS / uuiu 4k 4k NS NS N> 4k 4K- * HMOi * CD in si cft CD *sl. NS NS CO NS GO 4* tft 4* NS 4k - H* Ns NS NS p J-* 4k p p SJ NJ p CO NS 4k Co 4*' NS cn ov CO h- ift si NS o COOS 4k cr o ^ rr *5' 4. I3CD1L' Z Vi I C<D HO10f ns ' n(D 3c* ho M1-4 M M rs> co SCiU CO HI . -si O CD m ns O' SJ%J O r+o o C* O 4k O -N O V* ns o gg Vi tt 53.6 16,1 11,200 e66Qocmodna M tti < .3 'X >- O C* OP 10M M M M . NS M > X' O c* C er 3 3 c Ci tr 6D c* . ID ID (A *03 HI *o -5 *w 0 3 c X 3- CL 9 to w V XX X X . 5 < o cM c* 3 (A (A a. a. A r> o o VC* o0 -4- -4 o 0<* c* On -4 O c* 6t-q 00M M M 03 cn M00 M % M00 M CO tn to NS 11 O 3 c* (A 3 * c* sr < 3 70 I' o 3*:. fit e 0in i C H -4 o 0r* c* 0 ad W. oo 0--4 o a *: 3 0c* 3 l x CSj: 3V 03 ! H * H r- *H O 0* > *m4 0tA r- 3 2 * S0 01 o ri 0 -i O' O0 03> -S ft (0A 3 0 1X001 o C H 0<* 3 0 Ml* M* 0. CL AA .. ooo . . c* no o> r> A 0Q. 3 099' *o Ml* a in H o -4 O 0c* 109 c ! O3 oA 0X* gaW r* o3 3- a. X 5 < m4* m* >M *5 4 -i H* a. to A 0 - X' c- H H Oo 0 0r* c* ri 0M s* M 70 09 m SI Mo3 X X Cn A cn r* 0c 3 k 03 3 X H o fit a 1* c oA CL , X X M*l (A Ok X X 0X (t ft '3 in Sh -4 -4 -4 ooo 0 0 0c* f* <* aiW 4* M INS 4fe #' 4* Wl 4k 4' 4k *' 4a 4k <w 4k 4k M tn ^sin* fs> Ns INS to OS os M Ul 4k . 0: o . ' ooo ' O O O o O' O' O' O o OOO 4k * O O' 4k 4k W00 o: o 4k 4k V tn OS o O' O *XJ 14* A oi , H i 1p APPENDIX TABLE 0. (continued) (continued on following page) ^ MM .M M" 4 W 4k- N NS 4k NS t-1 O O N* s| ce to ^ sj bk) sj NS NS O OOQ o ooo : O o o o O O'O'O' M M O . MINS Or 4k O OHH rsi M MM O O' M* 4k to m o to - - o Oo NS NS 4k -- ' 8 OOO ooo tn M M CO or tn N 4k 4k K** N> f-* to N> O tn- SJ OS o tn 0* 9 M* 1* 0 4k NS si Ns Ul s| W kij . IS) 4k JLO to u to to to. 4* NS to NS SJ INS M CO M tn tn cn NS sd o sj 4 U> "M u> 00M 4k tn o M , tn tn OB " It 4 M 4k M tn cn 4k 4k M NS M NS 4 NS to oo 0 ha M tn M 0 O tn W OB fsJ 00 MNS 4* ^ si 0 M. H SI S4 M M MM NS M NS to O to m o oo o o o o OS 6 4k O tn oi m oo MX 4k- 4k' Ns tn N> eS . 1w w cr Ns M to to CO A Sr o O' O Q '< 3 H* o u> J 3 A 3 M - 4k to NS co 4 : SJ *'' as 14* -o 3 4k INS SJ o o O O 3 Q o O o O' o ft 3 in is U) to to -0 INS Ns 3 4k (TV A \ << 0a> 4k-- <n M M CD M A 3 o (A MU U) to to NS to M i A CO M 1NS *t o 3 OO tn o 4* A 3 C* M to INS NS to 4k to to to to o si 1to CO Li to S|. o MMM MMM 4k NS M O -kd SI o 4k M 4k NS 01 M 0 o o o O fr66O0W0dna fSj JfSo rroo M' rl\o} o O-<&j V3-(nP<d o3*. .<S: <3fneadf C0ofr+*tA oCy ! . oO <3e (3Q (0 *>o Mi(sD r0Mo0 rM osa PPMO 33fCi<ntC*' (0 >f-- *33(0f1ttj n r ommmJt** dXmS* T0mC*3*1m*i -5 33 (ft *fO3-t 3r*> 3: p I2-Q NMP ,Mr4ok IMCSO MIISS rMMo MIOS rpo 36no*E 3' O > O0u P' sin >Oi >r* -cood4 o o >' tmi l d33 -H CD 'mdtiml-Si*'. (S3fsQ t)' 3t r>&C(At- . **3 th o rfxi"i' a0nd D3ftf). Cnrfa` 3^ 3*fTt' z33<. 3' -rh- ro0o3 3330 TP Xo3I 3OT3P" P tC >'' 3<S3c>Prr(Astt>n**. M3Oft" MOrt* 3and r-otK* . 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SoJ :P MISS M Coo P M 4k CO 4k U 1 0 N CO M P CO p m Mro PPPOQMPO .M *H ro Poo Pop;Moo ^. rfSo> rHo 4 ro 4U14 o ai m M 4^' P rMro PPO' p CO oo M4k V1 p p CD *C O Ooo' p rOoo' I0SD M IS P co wp' CoO o IS IS ro p 4Pk P M P P 40 PO CCOD M M10 O nMCO P M40 s ,P MM P 4k P CO nPr' p p p oSI Mapi o 4k JO CO nOJ n4k SJ. ; :!| O4k fs OP MPP pi ZC3c3r- 3o- s|; 3rot* O p PM P i MPsj Q-3i. 3 ;; : 1;! 3c^: . w3CM P O O f ! 3o i:' r* 3(A 3 Mis IPS MP P CD M *3*1 . MPPO i P: < 33*3r j! CO P 4k p mdaro 4k ro sj l MPcoppnr U3o5 f33t* P !' *4 M 4<o*::- 4CoM- 4k ro co ppp 4k 'Sj N fO P P 4k Co P CD CO p CO pP Mro cIDo P 4k P rCoD p 4Pk P N> 4k O' ro PP 4k P s 4k IS SJ Pro rroo to m o ro ;; Mpsj , CtD !: mro !P ; o MO oOir S rPo- HPHOISP) Poo Ooo oPo I4Sk- m&o P M p MoO- IooS CMO MM IPN OSf OSOI OO rroo oo MM 4k O M o CD 4k O CO ooo -*<oISI*SSJ P Msj P IS : -' : 0ft f3 S66000f0dna APPENDIX TABLE D. ( c o n tin u e d ) (continued on following page) ov O O o o o oaoo m 00 r* CM MT" m> 10 o H K O <n o f-- pH H rH H O o O ooo O O O O O O o a a ooo o o O O O 00 ai OrtOl 10 00 00 M CO #A o o K O ^ 10 *r pH CO CO 00 r4 r-4 H rM CM ' 8. pH rH. pH pH o 00 f mO O 10 f>L ,<. ^ H ps O ov in m pH 10 4J Oft C (fi: 4) I .^ ao 00 CO 10 uo r u 10 10 o o 05 M H 03 0V:'i ; ro CM CO CO if CO fiu rt . HI O U 10 to an m ' - ai fS 10 CM co <n > ;{| ' ir 10 00 rs r< j 10 fc. " rH CM pH H pH H a. (A - JS !. +* o a O O O c 03' a Q O o o I m CM CM co -- 00 s O' * PS 10 ** 10 V0 *r . 10 av H c . t- vTO an O O O o o d f _ 10 o O o o o z I CO 10 pH . CM r Q uO ' e 10 ** r c0 10 CO - 3 ai Z pH 00 O COr* CO CO O M> pH. pH 10 - o 10 H fN. 40 CO CM pH M3 CO fS <0 mt - CO i0 Mr i0 10 mt 10 m m 10 8 q CM i0 i0 an CM ai is <t 10 10 a . CO r*^ aft 00 CM O 10 a o in H 10 CO 10 CO 10 CO CM 10 4* CO CO CM fS- 10 op <o ^r oo O CM IS 10 CO Oft 10 10 aft t S r4 pH Oft CM iH H 10 pH pH pH jH; H o O' o ooo O d d O O O o o O' O O O'- O o o O OO rM ai m ^r HI rH A* * in * Oft 10 N * *- 10 10 CM 10 10 01 PS in ID rs ^r CM rM o o o odO O O o O 0 0 o o o OO O o o d O 0 0 rv H CO" o 00 <0 00 10 CM CM m mi m o inNoj cO 00 *t CM H' H 10 CD tH . tf" 0) Cw o o -- oo oo an CO HH O err mi' H o o 00 mi i-*: o o r* H o O o odo a Q o O d O o o o ooo o O 0 O rsi fSr rsrcsi 10 10 10 m 10 m m m> m rH f-4 rt PHI H H H pH lH pH iH 1: .* p" p"m J 0 4* 43 4* 4^ o 0 O o0O H*. H H- H* K ' <0 p* 8 IS *c3 <eoo jmm p' ** 10 10 10 to +* +* 4- 4i * H 44 4^ 4-> 0 Q O ogu a O 0 O O H* K H H'- h- H 41 4 *a -a P- r- 10 10 C43 i- 3 O < 1A 9 +* to V) < CO X V) < A o u c4 w o H*!. Ur a CO r A" z u o Q0 u z . jn fc* o Jit u z k o fc. e o X < O -mi' O u "H zo U. o 0c > 1o0 s0CK ft M a p c o c-. 0> u 1 " aif^* *03 41 31 <0 01 V flu. 55 41 a. 5 m 14 C 41 JS 43 < < > e o 4^ A. X 3 06 ft V) i S z 43 u o Fa s z > z . ui D 43 > Hi (4 U. M 10 0 u o 0 1 4> p' #" > Hi iu 3 41 4) to iO 10 JZ: 10 f--f v- H1 01 Cf s.- 30 Xi (0 0 H* z * >s1 <0 jQ < 6 : < <0 '8 0 O 0 u Hi 3 H* > z 0 c 4> 04 U. m>to to u 0 10C 10 0* 0 0ft o rM 10<8 10 to 10 in (0 10 PO CM CM CM csl CM CM CM 10CM 0 10 CM CM 0-24 10 CM !0 10 K CD OR 0 10 CM 10 CM M3 CM 10 CM 10 CM CM 9S66000f0dna ^,r- O to to O O 0 00 a o o O o CO O o 0; O o o O r< O A 000 000 )A <* A'Wf s . O O O O O A' O H" c--d ds fH rH CM tH to CO fH. CM to rH Ok rH CM rH in rH m to a* tn cvj CM rH. rH to rH a* ' fH O 00 1 r> 0 O cr> (O lO o rH <n<o CM JV o ^1*. .: 0 a> to d 0 to o in 0 K CO d 0* id to d 0*" CO 0" CM CM tn: 0* o c4*J 0- n u3 id to 0 0 0 CM rH 4-J c ID a) 1 tn 00 oO . j: 0 to H 0 a f co a. rH CM (ft t <0 a >t ' t o to cri " rH 1 f ': 0 50. in JZ- *4 ' o c CO o 1! :g o r-* to cn rH T03) e a; 3: i' &. Ci| TJ 44 r^ OY r &> to c J= Of 1 a y a a u E tO' 3 cn Z rH. to d rH o o cn CM rH O CM oo" lO ' in ' rHCM CM O oo to O *00 oo 0 to CM 0 Cft m to rH in to O' o to rHco: 0" to CO to CO rs. in o 0"" op o id CO Mf" 0^ d CM rH rH CM CM O oOo o Q o 0. co mk rH k. to tO in H Ot CO rH o rH to O CO o- o oOoo O CM 0 rH A Mf 0^ oAto CM co CO CO rH f- tn r-l 00 0 O 0 O in tn O co 0* n- m n- 0 0 ro csi H in 0 K fO d iH rH -4' rH rH O O O' O O O OOO *- CM rH rH A A' A tn A CM CM in 0 K rH rH O O <0 O OO CM 0 CM rH rH O O CM m CM CO CM CM co co i-* CM d rH CM - O O 0 OO OO 0, rH ro CM 0o0> CL o* Ic-- rH O c o rH x> cd 03 c r" 4c4 ou O is. A' o UJ o'- ' o o- o O o O O ' ; O O CO Oft- ' rH I s o to CM o: o 0' 0 0 CM CM CM oOo 0*_ 0V m <sT CM CM o CM -- ; O CMA CM CM CM CM CM O cy CO A A' CM tH O rH CM iH CM ' rH CM 0 A 20 CM CM CL r SUKJjj (! CL. <! : rim to 44 0 44 " 0 A* r 0 44 r-- 0 *0 4- r-" 2 !' 0. 44 44 0 44 jm- * 0 0 O 44 44 *; *0 44 r- 0 44 r*' r** 00 44 44 0 44 O 0 O' o O H* H*. H h" H* O O Hr O h- 0 h- 0 H* O H- 0 O H* . . O H . f-- 0 1-- OO H- 00 T3 T5 r *r <ft (ft C 44 fH 3. O l - U. 3C 0[ h-4 A C A A' e: 0 0 44 0 4^ 0 0 44 os 0X 0 .X H- > 0 X (ft X. - 0 ' 0 0 0 3 -- X 0 -4 ea +> 10 ^ 44 0 0 H* jr " o 0 3C 0- -4 U. is 44 a M 0 tO '`V <co a. E', 0 3= XO (ft HC (A H* 4 scA S P0B' r 0 *- 3: <- as 0 > * c 0 0 0 0 0 s: V) f. C SE A 0 0 0 0 LIt, 0 - T*' s 0 H 4- 0 s* 44 , b 44 3: 0 44 m 0 e; <0 00 |B f 0 0 JOt 0 c- OM 0 (< * . CM |" X- 3 x: ut 0 . SE &. 0 X .0 I- > J0= (ft. < > +> Cft 0 c >i o L0U >| 0 0 mi S* *m mi J=u c 3- H V r* 0 44 > 0 44 (ft 0 3B < OS 3C < A* A- O 0O (ft 00 *0 0.- OV 1 CX *f" O fc. *r* 0. X 1 0 c 5 < 0C OC i"' 0 O r- X A cm A' > 0 a 44 >% 44 03: 0 e 05 u 44 0 C O H0- 44 0 *r 0 T5 (? *r* *. 3 JS >3- M- er to CCOO Q CM CT* o CO -0* CM CM rH 0 CM CM CM ro 0* 0* 0"' CM. CM to 0* CM 0 0 CM 0* CM co 0CM 0 CM D-23 0 rH CM to 0 CM CM. CM CM CM 8 i66000f0dna APPENDIX TABLE D. ( c o n tin u e d ) r*i 2: O O00Y<M CHM Hf-4 O g4 00 OV Hrt or->t 0 g k CHO OCOO* 0 .ui 0r-j f-i CM irnM O O * pH s A m rM 00r-At ' 00 OSA rHs in H Cr-Ot 00 0 r-t 000A O 0 s ir Sr 040*s CM mt CCMM 0 g CM i CO icno 0' (SI CO 0 tn co P-* O in <S CM: CM os 0 to 10 44 e0 O to.: 20 41 0 to in CM <0 <0 CM 0 ui <* CM COO CO CO CM r4 CM MT' as 00f% <n OCMS m* as co COo rt in sf tH* OinS C*Or csi 0 cO 0co N* to CO CM 0 0 <S*I cO <cntr in <M to cn (SI 00 iCnM m. CM CO CM CM CO o CM 0 OS OO o-- co oo 0 .4 CM --(S+I ' oo* oo o oo r* Of oos O O oo (SAI CO oo CO o toA o CM m CO o o OO An Ct o0s & in 0 0 O. O 0 O O' 0A' 8 0A' O r-tA' 0 0A > O' 0A o o co* to o co * oAr o0' * CO *r os *r o 0CTkA' O. o OS o 9. Oo COA 0 A HA A- to in to in O' o OS 0 r*. O O r* in oo o Of 0 Oo' ooo rt CO CM CM CM csT o fmm +m0* H- 4<40 a r40r--4a r-- H- <0a-> H41040 i*. 4<40 O H- A" 4(40 O' r4W4--. HO- 4O4 O 1-- 4(40 O J- r~ (8 *J O 1^- +140 a i-- r 4140 O r-- 4140 O 4140 '' <u0 |iO>w 44 ic oai- -a0> tu U1 4* fc. O u. b tt 44 jtj # c 2 s *cs 0g*0. J f-- LJS ?5I 13. X?4* 44 a. 2 * M a 2 S3 V) (A b A* CD 0 1 > u 1 3 U0i- u * * c * 2 -- <n t. 3 V01) uC 3: 0 o ocr A UI ouas Mo w "IQ s<*r in Ou 0o UI cUI 1 eP<"~0r' Id. 44 0 O fc. <3 O 44 I A fc. 3 a 41 a. UI <0 u *-- 0 Kto a0c>1 * u> <c C 4b1 0 5 V) o 0 O c. 10 0 4) a0. X h- CX 4m? c* C4/4> Mol 0 ?r- :c Qd> ^& dq O6 CO 10 Z Sus b* 0 to f0CSM- 0 as CM 0OS CM 0OO 4U4I 3 O 0 u u. 10 41 c>* S" A". (0 <9 # 2 44 e110 u a. 0 u. rt O co *34 <0 *tMrfctf' 0-26 4 5 .9 3 4 .4 37,500 17,200 12,900 19.7 866000^0dna * r- P 4> O H- o co O' i--4 O' O' o O O' O' rH' to fv o rH CM rH rH Oo rv <o fH o oo CO rH p" CM rH. rH o oo CO CO oA-- rH rH rH oo O tnt rH to P rH Oo cn 00 oo tn o 0*1A CM rH oo 00 to to 03 1 CM rH CO rHi P m 0 IV i--t in CM; oO r-- PT o> to in CM to: pto rH iO CO to rH CO OV P Pp tn in to m tn tn tn rH' to O' P +> Cft f o o J c to at f. u CD s. to CM CM CO CM CM to CO Hf CM CO IV GO- 0Y iv CO O to to CO to rs CM CM 00 in rv in to <u OV ji CM P* tn CM CM CO in p p" co CO w P* m P q. rH tn <5 ; 1-.. to *0 a> cm H : p 1--4 tn rH Ch fv tn CO |V rv tn rH P t a> 1 CO CM rH a ai C* * tn to to tn in to r- ! rH rH rH rH rH a. I CO o f : rv a rH O' Oo m in o in rv o P 00 O' A CO IS co o O' rH in oo tn U oo to tn oooA o o Cf) A ad rv P oo IV rH c uat -a as ; o Q o O' o o r-- W O C Of t i P on . to rv A rH CM in CO M* CM CM co CM m tv CM; in CO ' C 3 as 3 rH o p CM rH rv CM A P P E N D IX TA B LE p . ( c o n tin u e d ) 197 O O O' O " a o O O' o o tH I P P tn CO PO CO CMA ' o 0V to Hf Hf 01 rH rH rH rH rH rH rH rH rH u Cu (C . . r*9 P td (0 (0 r-- m r-- to r*" O (0 r-- <0 r (0 r-- 40 r10 +> 4* 4-> +> 4-> + 4J 4^ 4-: 4^ 4-> 4^ 4^ o H* 1-O o H- n H o H o H* o 4-- O H* hO-- O H o H- o h OO r-- O co ' rH i-- P 4^ o >-- 7,40Q T otal 286 G re e n s b o ro -V f ns t o n - S a l emi H ig h P o in t & B u r lin g t o n , NC 5-C z1-- S * .J <n * a lir X tn r-- A A P u r - r--' 3 > to c S. . (^A tn < s- *r- c > o O ; * O *- Q-' tft P m CL 4J in sc U^ A O dr z0 A- ffmm' & o M tn 01 ^ J. 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[BAoiuay (y rsas sssqj. `SBaaB ueqan [Biquaptsaa ut [ios paqEiu -uiequoo pB3[ aoq s3AtqBuu3q[B [Bipamaa pasodoad aAtq saqen[BAa qaodaa stqx Butqqas Xq.taoj.ad qons aoq aouEptnB saptAoad [3Aa[ uotqoe uidd 000*1 aMI Xq.tAiqoB [Bipaiuau aoq saiquotad qas oq XUBSsaoau si. qt yuxqq aw *uidd cog qo- [3Aa[ uotqoB q qqjw paAatqoB aq p[rioM Aqaj.Es qo 8B[ 8 aaqsaaS q qsqq 3A3t[aq aw a[^MM "BqosauuiH ut paEpuBqs Xataodiuaq aqq pus `Xoi[od s ,o q 3 aqq `[apoui otqaupjotq Vd3 q `saqqs punqaadng [eaaAas qa si3A3[ uotqoB qo XaAans q uo pasBq M stqi -uidd 000*1 X |.SA3| uoiqos XqLao usd s asodoad a `qaodaa siqq ui *[tos aoq paspusqs psa[ q qas qou s6q vd3 `suitq siqq qy 'saaas ueqanut uounuooun aaa esaqq *aaA3M0q `uoiqsuLuiBquoo [tos qo aoanos 4osur s aq os[B u s o saaqtajas pBaq *qsnBqxa oqPB uioaj: si p6a[ qo aoanos qusqaodtui ssa[ aaqqouy *s6utp[tnq qo sapjs aqq uioaj. paaaqqsaM pua qqo paddtqo SBq ao qqo padsaos uaaq aaqqija ssq qotqM quiBd pasBq-pBat si [.tos paqBULBjsquoo ut pB3[ qo aoanos 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W AA fM OOO-*Q0i-m.O<0n OO<n Sl oo<n CM Urtrt CM CM om -- T44S`<J <J 009 *<aD 01 9 4<49 Q J-* .p- 4<49 O H* 449 O H- 44 P 14" ra +o H- PP 4o I* .#-- * p- 4<49 44 4*49 0. * 04 4e4 g'. g> 4*49 O ,o H- f- O OO OO o o. r 0 3a H- . aa ,5oo. hoA P-* 4*49 O 4149 O H- 4*49 O iCn +mj >- o-a we*i 9g3in in in MC O434 APPENDIX TABLE D. (continued) 73 O 2 4C fmm tn o 3X 44 1 *9 a> 44 iH t/> *9 Sj 73 U vs 01 X V) 3 *9 --X 44 u o IX. c co co CM a: CM A *-P 3 4O4 CO <9 u as iii A V) co O " -Q <9 s vs a X X PA X u A V) H tX sc So V Gu O fc" e A< .A .A i c to A Ao e A vs m o l-M < < X k *H v> A >, X e (A. 4? o <9 p* >% u 44 U VI o (A e 44 Q> *f4 ID v 4 .C 10 *9 A c A 44 ft. u. o 3o JO JO c X3 C9 3 0S^1 0t-1 O) *o (9 c inB T> RJ o 4* pH pa 19 im 91- ft. O JS *s O X < O m 93 o O o u VI D Hv f0t1. P 0B1 X '3 o > ft. . 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Minnesota Pollution Control Agency, 1986, Draft Legislative Report to the Committee on Health and Human Services. St. Paul, Minnesota. 2. City of Boston, Department of Health and Hospitals, Office of Environmen tal Affairs. 1985. Boston Child Lead Poisoning: Request for Immediate Clean Up of Lead-Contaminated Soil in Emergency Areas. Boston* Massachusetts. 3. Duggan, M. and M. Inskip, 1985. Childhood Exposure to Lead in Surface Oust and Soil: A Community Health Problem. Public Health Review 13:1-59 4. MASSPORT. 1985. Plan and Instructions for Safety Removal of Lead Contam inated Soil in Tobin Bridge Community Project. Unpublished, Boston, Massachusetts. 5. Minnesota Pollution Control Agency. 1986. Draft Legislative Report to the Committees on Health and Human Services. St. Paul, Minnesota. 6. Nicholas, Steve. 1986, Dealing with Lead-Contaminated Soil in Boston. A Pplicy Analysis Exercise for the John F, Kennedy School of Government. Unpublished. Cambridge, Massachusetts, 7. Special Legislative Commission on Lead Poisoning Prevention, 1987, The Continuing Toll, Lead Poisoning Prevention in the Commonwealth: Current Efforts and Future Strategies. Boston, Massachusetts, 8. U.S, EPA, 1985, Administrative Order on Consent, Docket No, CERCLA Ulr5r83. 9. U.S. ERA. September, 1985. Superfund Record of Decision: Cel tor Chemical, California, iL U.S, ERA. March, 1986. Superfund Enforcement Decision Document: Pepper's Steel, Florida. U. U.S. EPA. September, 1986. Superfund Record of Decision: Caldwell Truck ing, New Jersey. 12. U.S. EPA. September, 1986. Superfund Record of Decision: Arcanum Iron and Metal, Ohio. 13, U.S. EPA. September, 1986. Superfund Record of Decision: Industri-plex, Woburn, Massachusetts. E-24 DUP040009955 TABLE E-3. COST COMPARISON FOR REMEDIAL ALTERNATIVES X** *0 ro X* m * ' X o x X i-- V) i-- O . 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Ml --?4 .3 ro in 0 tr * ro ro w *-- ro 0 c * ro b (X b la ,.4 ~*i ro --* -ru P -* CM -~4 nl 4 ro n ro La in rr r* w ro .V : Q. ro 0 3 3 23 -4. 2 n 23 ro w tn Sw4 -H rh 3 O r+ ro ro 3 ro ro 0 3 Zro a t--2; t ut rZo s . rZo 2HHH COO 2 : c x oo*:^ sc ro in o ro w a ^ -- r* 3 3 3 rt ro ro "!-* a. 6 i/i rn --* z o ro 13. *H 3 in ro v> . ri* ,r+ ~o C- r ro ro -3 ro ro 2ro3 CL 2 25 r+ 3 r2o3 Z 32 O' 0. rTo1 2 roro ^* 2 2 2 --* ,?r O --* o 03 n Z o 2 c+ > in 'sr O C C3 O '3" ro 25 3 ro o z :ST sr ro ro .ro ro ro -4 * ro ro ro ro o 5.3 a. r(ohomroor)o ro -s C/1 *"h 2i --h < + c** ro ro v> < 6 M# o ro o X Cl '3 . 33 n ro ro ^,lu^ n .3 -s *-*;*: 3 . 7r o* <ro rroo "2 . r*vO <2 < .--* o 2 3 2 * - in SC rr< ro 2 SC ,c2 -** Q- -' , ro 3 -- a. rH 2 33 X CL > ro ro ro 3*,0 . ro sr in ro -H >S "5 "'S 3 - ri* t: 3" o c ro --< 3 ^ ro --(ro ri OC n rro** o p .o o o o 3 '3 --* 3 o : 3 ro 3 o c> cr ro in c c: c a 3 in O -5 V) S t --ro n I ' 3 in in tr XT D 33 r* ,c+ o O . -jy`*n pro in 3-.^ 2 Sr k; *< 23 sr 25 O Sr 23 2f --4* 3 tQ 8 -n 11 2 2 2 2 22 2 2 2 2 2 2 2 2 2 2 2 2 2 2 2 ti *n "n 8 -n -n -n -n -n -n 23 -4* < --4 lt --la 4i .-Ji .H4>'<-l< -4> --4- aaji .-4i _^4( -ji --l W< -4 q 48 W r+ ro <0 = 3333333333 3 3 3 3 3 3 3 3 .3 3 3 3 3 '= 3 3 3 3 ss 3= ^3 3=> 3 . (U eL fi,,1; 2L 5L L 2L L 2L 0,111 > tu ,cu CU 0> m (U tu 3 m u a> 6 -- m m m 6 w rfo2 in to w Ji- cn tij w OJ ji tn tn ^ tn -j ts> cn 6 cn tn ui c*> to N> cri O O 01 IJ3 U M [C a -t>4 P ( M M SI OtDOU 03..M W W 03 W O CO U3 W CO CO ID tS -t ->J 0^ ID M CX> 00 03 J\3>4 00 CT! ID 03 t*> M 03 03 4! -vl S Ol 06 CO >sj 03 (-1 IS> 09 ** + fs> O -J O N ji U) Cl vlU O CO W auo IC W U) W N o w cn O li) -M U o (J1 ^ Ul W N intn no swc oro ro n 2 r+ Tr ro ro ro 3 -^* 0 20. DUP040009957 APPENDIX F FINM. ANDPAOPOSED JKT10NAL PRIORITIES LIST WASTE SITES KITH LEAD AS AN IDENTIFIED CONTAMINANT F-l DUP040009958 FINAL AND PROPOSED NATIONAL PRIORITY LIST (NPL) WASTE SITES WITH LEAD AS AN IDENTIFIED CONTAMINANT irj OO O O O O O O O O O GO . O 0 .0 0 o oe o O o o o o o o tn in VI Cn PI yi cn ^ 4* 4-P> 4 -t 4 4* 4 4*.4* 4* .4* 4* 4 4* 50 Ttl CQ -3 .rO* 3> 3 rK ' r--<r8-ro -i8rt-rf--"i 8r-28 -42-'nvn) t/o> *oAv.oasoas!arst-.^s'<ps'p<sp<e6'><'H>n -,rrir-mrri.-Pn-tri f-?n'r-n*-fn*PrrP"rn^p ccn+: i32p,nssris r" 8 q Sc i x* a *-i fi -s 1 o -* n --*, -- tu ** a I vP> Q3 .3: 3 3. rcnr rID* 8 q-c o w>c it > 3 in O B> 3 -* 0 t*.m --> 3 o v> -j > Co * 8q < *< 3 _w O ID : 3 8 q --> > c,n o w in to a Svj ft*.--NI*5<sCo' O iB-. I o'(>iUnu PaOs-u<+- e> n . -- < 0 H p a % So PIDOVi * or Vo> Wcn O-S'SC 3--toX 3 O),+ X --* 3-0 O .3 P P . <+0 X3 O--i --3 I tft *0I P23* 'f f' l coin r+ rf"P frrsr o 3J* Q) 3 5* 33--`OP (D CO fIipt Op l1rt* 3P j*5" i>!* 2**# p - snr 5 o <* <t/>* *o * 3 1DH (CA -*- *f*t --r oxve -- 8 q . --' <r* cn -r-O-* u a. > 0w<igJ <-**/> ^-I5P .ao c+ CL 3 c-st* r3* 3 o-h. * - * I u% 3 -J ."w? < -r-* mi* 3 fita Oc. .lC*r> tf o TOO r- o. -a -h as r*1 y&i o "O IS .CL "H1 S' a cn .mdo r+ 3 on Cm Cm 00 3 r** .3 * r* C<s a o p "h O "'.po r >[ 3w. ac % n- no< 3 f* r* O : . ar i *wo* o('u* rMQ I-VC o w--..i r S' O sr G to Oo ^ 3cr "H* C03 03 03 .CO Ccn -n :-"32C*a3co0> -D-PX -rOsf-rhC-fcGO1Sf3iat OOcoP^"C'PO ^-0hjOp^et5A0o3T*t -- -4* *?53 O P 3 O p ^ V> <+ O W n r+ O O. rt" W 7T r+ c* r+* o O 3 " " "O ^5 *H *O?3 --I 3 3w t3o CM O :mc3r* ---of O<n*+ f+ 3 C+ ST- r+O3 ooa G -* !trt ,srf:- w CS-2 ^- P n . -3 >r ms et ui 3* o 3< Cr :x-* W -a* -Ba* B T5 on c -s 7T 3 oO o 3 3 (O 40x> -o **n -o "n-n^o -n *r\ -n 8 - 6 n "n -n -n -n 8- 8 *n*rni -n -p n -p -n -ti -n *n -n -n -n -n 5 l~l* --* ^ ,|W* --a* --a ^a* --* --a.--J a .<at --a* *{ >a "j a -a. w. .a* a< CU ca T03 3 -"O03 3 "PD 3:P 3 3 -3 ..3 3 3.3 33 .3 3 3 33 "O03 pO333 :3 3 3 3 3 3 to P --* O in L Q. V> CL U% V CL CL W W ^ W LO OJ ^ CO rs0 -P Ol Ol ^ U> Ut CO CO M 4^ N5 01 CO -P* CT Ol ^fc js. u> ui cn .C* n.N* 5y3 05C* DC.* J^:O' J*CO.* C*AL O* >*4>.**4>*Jfs>O.*COfS5 >4**,>4U plO UDi * COfS`5i*i?rs > *CD'^'s.J*Ns V D N> OJ 4` 0 (oSjc)go^'LD*MWrMo0O4-wi Ay4iy>i^soivo0oPoOcMn f^v4iP0 Oto0rv^iccnoau>iwH^i>aiHo6uo^ctnoHcn>oJ-i0^ ^w--6 u--t \8^fs> cnn vccn so x 01 (if+t 73T0NJ (D w. -5 .3 .3 CL (Q DUP040009959 I FINAL AND PROPOSED NATIONAL PRIORITY LIST (NPL) WASTE SITES WITH LEAD AS AN IDENTIFIED CONTAMINANT (c o n tin u e d on fo llo w in g p a g e ) -i OOOOOOOOOOOOOOOOOQOOOOC6 OQOOO 4* Ja 4> Ul U W U to t*J U> U) CU W U> U> Chi W'g UUWUWW o ooo o (*} b) u w w ft m IQ 23 o 3 i 8 -n2> :>> :><<< <,<<23rot o t o t o *o * r" r" r~ r- r"'ir-.3* 2* 3 3> 3 3> ;>3>.,:> =3> 3* 3> 3> J3> > 3> :> :3> .3* ,,C3 '2.SOOO p ,p m rn m CT fftt fftt &o Sa*3 .> 3 V) ZOW l?-.CO 30 35 3 0 :2 -m rt * c e o p 4 3 . --* < xs (t ft ft < </> B=C 33-g .3* 0 ft ex -` sr ft IT C 3 ft V* 3 .S ft ftr> ^ ft Pi . P S3 Q. - o P ct ' 3 ft V> 3 P O 3 ft ft W <H. ft 0 ft -3 3 0 ft ftw 3 P S3 0tft 27S9 .O'JC pft > o* </> o m * 5^ ex pft O'---'.3 :C 0 3ft C n 3 --* P O -- p- |Q CL Q. P rt CL o 3 3 3 p 3 . -ft Op --*** P . 3" . ft ft ft -M -p mo ft c rt o r- o rt ft ft . ft ft- P P 3P . 3 3 IA C ft ft 3* ft OO fctt fftt<n 3 .m ft rt :> I-3 * ft W Oft CL P .03 ft ft P ft tt ft. 3 .03 P cr> 3 -3 *< ft or CC ft ft P O <D <p c+. p p ,e ft -rf*5 03 p ft OW ft O P- ft :3 ft < 3 -0 < 3*q rr O mm* fll p X3 ft 79 -* O ,3 ;3 ft o -t ft - -rfo -* n fftt _rs>Li. ---4 .ft r-^1 ST . SC c m <rs P "O it -rf* .ft 3 ft 4 g ft ft et r+ etc: 3 2 .3 n .0*0 ml. 21 o r- 3 ' .! ft 3 ft ct IA ,f1t :p * ft rt <o ,p p a TO *C` ft o r*3 o oc oP IQ ft 0<< 3 nSL O * IQ 03 0.0 0 0 V -- O P* C (A --M a **,-* & ft #--(Q ft P C c* ft 3 3 ft .S'.-- 9 .ft ft ft 3 ^-D CL O OV< tmU ^ >.3 in p- Oft ft 3 P P P , a. 3 0^< p ft e <~*.2C 6-*p 3 ft ft 0-3 : ft -3 o 3 3C o TO O to M O (/ 3 * ft o * o 3 r- Pft --v3 '3 " TO .ft O3 -3C P -3 CL *< SP ft 0 ft ft ft ft CL O P ff ft -p3 ' *-c o < * 8.2 ft 3 CL ft -* 30 ft a. t o r~:a n 2? ft n < ft R ft -- t---(ft 0 2? --1 3 tn in p 3 ft ft < ft rt .ft 3: W ^*-ft 13 rt ft ft 3 ' w ft r CL ft 3 .3 IQ ,CL fftt ft f3t s o o r- ,o :a> 3 Pi t*. ft ft ft QT .X ft ft ft < fl} --< mmtm *-* p t. fl> o .CinL --a. ft 3P ft -6 . 0 03 "0 *T| 3 era </> < r-sc .ZT 0 C ft 3 ft .79 ft O ft ft nO *3ttP* row rr o ft rn ft ft 3 rt 3 ft o fpt TO ft ft p "O *< P o 6 o ft ft .. 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"O Prj T3 T| Tt P W. -j -4, mmtu 0 30 33 23 ft 23 ft jft o --- o -- --< in in ft ft CL CL <A fftt ft :C in t>n4t^ji4j>U4si .ure)Up)OrsJ5 CJ34JLO^Opnl^jnup>^-fftcU*O> lL-SUCjaC04*i>O4 JCT4i ^U0J Jf^S>J^cncao<* iVOJ Ai^fS5yu^nj4jiScko CO CO fV> OD DO .04 >4 O ^cn ->4 VO ua tn OJ ^ IQ ^ W U3 P O* U> ^ W ka om^rawAH^jaNj.HCpf'OMra * 8* 6 o ^ ip o ' w W ft UUd Nj H HOW ft TO (D ra ra Ln i-rf t--4 j--4 >j tnA *V<> Sft3 3ft: Ow3N P ,rt x* ft ft ft --< p 3 3 0. IQ DUP040G09960 ' 9-d FINAL AND PROPOSED NATIONAL PRIORITY LIST (NPL) WASTE SITES WITH LEAD AS AN IDENTIFIED CONTAMINANT X -H ar J so o < 3 s O .*1 : O ^oomoWo' po'o' omwaOixOi'adMoOO Oo oo CC:CX0O M.o o o->.cr e= cr 3* 5 :3> > s ?o so ca 3 > > F5 --c -' -i 90 re m ID .numi*' "3t>? a CO rf CD <P CJ VI r** a CD 3 & VC (Q fiu 3 m X iaJiV' 1 < CD T4 O "O CD 3 e+ 8 mi* </> .et mi* : 3 to o "* 01 tft <* fD mi* zssH2cao!ari6o%sn ' (u n p . 011130 c o 2 p - p >p p o 3 < no. Hii p .-- 3 n 0.0 3 re 3 re 6 O ( ! 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OJ * .C*^ > o>N(N>issoioiP-^i-iir>curs>'jji,4 0 -p si n > 0 >1 f\> re 01 rersjs woo cn --^ 90 re n*< 0 tn q 3 ,1st 1T ft^OJ m--q 3:sa IQ DUP040009961 FINAL AND PROPOSED NATIONAL PRIORITY LIST (NPL) w ^ s t [ s 8 t [ s w 8 ' LEAD AS AN IDENTIFIED CONTAMINANT S-J ooooooooooooooooooo 0-0 O O O O O O p o p p o CD CO CC J Nj Nj sj Ni sJ s Oi CfJ Ol Qfj 0> >>J Cl O <7* O O O Q1 * 1 5 t Ot ? CJi m CO t> - > o 3 (A ** p V? sz p 3 >3 M M HM 3 cr O p rt * O *3 3 CA CL . P M V> s.^ X" r" M TMb < 3 tA p 3 * Pmi w o 3 M3 ;q 4 . X 3 cn M3 p 3 ,c+ o o 3 TJ mmi X *s HXOwqOXHXO^ODXXWSXOO s *? -81 f+ t # ft 1 O (0 C Itt fl) .X 40 P 3 ft B) 3 X:Q fit 3.(+.(P W 3 p Q. 3.M M s P 3*3 Q. P 3 *D P =T 3 ,, P ft*1 ^nVCSC --* -5 W a C ffl 'JiJ 1 r^ a C 3 c r* p 7C P V> P r+ X* P Sn P HON 30 n 3 3 M3*0 . P 3 M3* OO O Q- X" p C " a. -* m o o p s a. m m o p .a. .o r*- MOO x* CZo p v> m*o CL P (A P *. >T 3 --1(Q3OJ 3^<,e ,ct* c+ *< .- 3 C (A .T--!IQ<A *3f<t HOMMJ3* w. 7T<< .3 w 3 3 *< tn 3P O a. (Q 3 JO Mi 8 -n -n8 8 m 8 m 8 6 8 8 8 ^ *p 'H -ri -T1 -TI -T1 T3 -n Ti *tl -n -Ti -T! T1 T1 -T1 -tl -Tl in *J ^ -*<--** "* "J ~J* mi, -J _! w W* *j `mi* .tail ml* .wila il arfi 4 ,a4 <wJ' mim ,ll r*m 33 PP --^ =-* 3 S 3 .3 O 3 3 O 3W 3 -iws 3 WO 3 W m* W t .rf W W3 ..a3rf -3 3 -3 3 3 3 "3 3 3 3 3 P P CLl P M3 * --|J --I P ,m| tpmmd M3 O pP' Pp" Pp p M3 P p p p P P *3 pp pp ppppppppp.pp M Cft W Vi P c+ c <A <SB3. QfB. IOB. & ^^^S^^^^UWUIUhlUUWWNUIUUWWWMOlUUSlWOmiWW^ .*H'*W*W 9*9.W S*mo.pWIONOO ;lH*Ol-1' ,>l,in* O.M O*HJ.W''.W.OB 'tO lDO >iBlOOOOS 52 H P c& cs si q o 6 ui m q>.cn cosiottH^qroNiocoHo^ujvn^cuH^ tftqroH Oi^.wois>q o tn 4* tn >4 cn 4.^ oi i i s vi si 6 cnyi m N6 v o 4*u > o o o -p* (A (A3 X n << p p .10 <t+A T3-T*QNM) CQ3 :3 Q. DUP040009962 # .Poststratification by age, sex, and race. The estimates were ratio adjusted within each of 76 age-sex-race cells to independent estimates, provided by the U.S. Bureau of the Census, of the population as of March 1, 1978, the approxi mate midpoint of the survey. The ratio adjustment used a multiplication factor in which the numerator was the U.S. population and the denominator was the sum of the weights adjusted for nonresponse for examined persons. This ratio estimation process brings the population estimates into agree ment with the U.S. Bureau of the Census estimates of the civilian noninstitutionalized U.S. population, and, in general, reduces sampling errors of NHANE5 II estimates" (Annest and Mahaffey, 1984, p. 41). Table 6-1 presents the arithmetic and geometric means and standard devia tions for Pb-B levels of the indicated population segments for the midpoint of the survey* March, 1978, TABLE 6-1. BLOOD-LEAD LEVELS (ug/dl) OF PERSONS 6 M0NTHS-74 YEARS, WITH MEANS AND STANDARD DEVIATIONS OF THE MEANS BY SELECTED CHARACTERISTICS: UNITED STATES, 1976-80 Characteristic Estimated Population 10 a Thousands Number . Examined0 Arithmetic Geometric Standard Standard Mean Deviation Mean Deviation A11 persons, 6 months-74 yearsc 203,554 9,936 13.9 6.05 12.8 1.51 All children, ' 6 months-5 years White Black 16,862 13,641 2,584 2,376 1,876 420 16.0 14.9 20.9 6.56 5.60 8.18 14,9 14,0 19-6 1.48 1.44 1,44 All persons, 6-17 yearsc Men, 18-74 yearsc Women, 18-74 yearsc 44,964 67,555 74,173 1,720 2,798 3,045 12.5 16.9 11.8 4.68 6.76 4.64 11.7 15.8 11.0 1,45 1.45 1,46 aAt the midpoint of the survey, March 1, 1978, Wi th lead determinations from blood specimens drawn by venipuncture. Includes data for races other than white and black. Source: Adapted from Annest and Mahaffey (1984), Table X. APPENDIX G METHODOLOGICAL DETAILS OF BLOOD-LEAD PREVALENCE PROJECTIONS FROM NHANES II DATA This Appendix discusses the statistical approaches used for projecting prevalences of blood-lead levels in strata of children and pregnant women In Chapters V and VII, Highlights of the second National Health and Nutrition Examination Survey (NHANES II) methodology and the regression analyses carried out with the NHANES II dataset by J, Schwartz and H. Pitcher of EPA's Office of Policy Analysis are included. A. THE NHANES II SURVEY ''Because the design of NHANES II is a complex, multistage probability sample, national estimates are derived through a multistage estimation proce dure, The procedure has three basic components; (1) inflation by the reci procal of the probability of selection, (2) adjustment for nonresponse, and (3) poststratification by age, sex, and race. A brief description of each component follows: Inflation by the reciprocal of the probability of selection. The probability of selection is the product of the probabilities of selection from each stage of selection in the design -- population sampling unit, segment, household, and sample person, # Adjustment for nonresponse. The estimates are inflated by a multiplication factor that brings estimates based on examined persons up to a level that would have been achieved if all sample persons had been examined. The nonresponse adjustment factor was calculated by dividing the sum of the reciprocals of the probability of selection for all selected sample persons within each of five income groups (<$6,000, $6,000 to $9,999, $10,000 to $14,999, $15,000 to $24,999 and $25,000), three age groups (6 months to 5 years, 6 to 59 years, and 60 to 74 years), four geographic regions, and within or outside SMSAs by the sum pf the reciprocals of the probability of selection for examined sample persons in the same income, age, region, and SMSA groups. G-l DUP040009964 -- Further, if eg and vg are the same percentiles of the log-normal and its corresponding normal distribution, respectively, we have exp (u + v s) Solving these equations for u and s yielded: (4) u = ln(a) - 0.5s* and (5) which had the solution 0 *= [ln(e ) - ln(a>] - vQ$ + 0.5s2 yy <6) s ~ vg (vg2 - 2[ln(eg) - ln{>3)***" Only the smaller root yielded sensible values for u and $. We used the logistic regressions to estimate eg in equation (3) and the SURREGR regressions to estimate a in equation (1). Using the estimated values for u and $, we determined percentages of the distribution above 10, 15, 20, and 30 pg/dl by looking up the results of [In(10) * u]/s, etc., in the normal table. We used a logistic regression equation to estimate the percentage of children over 30 pg/dl to control for problems of multiple sources of exposure. If we had simply used the regressions explaining the mean and assumed a con stant standard deviation, we would have predicted that removing lead from gasoline would have resulted in there being no children above 30 pg/dl. This seemed unreasonable because paint and food are known alternate sources of lead, and also are associated with high blood-lead levels. The logistic regressions confirmed that the geometric standard deviation changes as the mean falls. In previous analyses (U.S. EPA, 1985), this approach was implemented to provide nationwide estimates. Since Congress wanted estimates broken down by more demographic detail In this report, we have run the above procedure sepa rately for each combination of urbanization by race and by income. Obviously, the uncertainty of the estimates for each of these subgroups is much greater than the national estimates. G-4 DUP040009965 8. PROCEDURES USED IN PROJECTING PREVALENCES (ADAPTED FROM U.S. EPA, 1985) The use of NHANES II data in the models to project the numbers of children and women above various blood-lead levels was a decision by the authors of the report. To estimate the numbers of children above different blood"lead levels in 1984, we relied on both linear and logistic regressions estimated from the NHANES II data. Both regressions were estimated for children aged 6 and under, .using only children residing in SMSAs. Independent variables included lead in gasoline and the categorical variables (for race, income, and urbanization) for which separate estimates were given in the tables. These regressions were used to forecast the continued decline in blood-lead levels from 1980, the last year of NHANES II, to 1984. The linear regressions predicted declines in the mean blood-lead level while the logistic regressions modeled changes in the percent age of children above 30 pg/dl. The methodology outlined refers to the origi nal application to gasoline lead-based changes afid with the criteria Pb-B levels indicated. Changes in lead content of other sources were not factored in the projections. The criteria Pb-B values of 15, 20, and 25 for projections in this report were handled the same way. To predict how the number of children above each level would change as the amount of lead in gasoline was reduced, a mechanism was needed to forecast the distribution of blood-lead levels as a function of lead in gasoline. In this analysis, we assumed that the distribution of blood-lead would remain log-normal as gasoline lead levels declined. Then, estimates of the mean and variance of the associated (transformed) normal distribution could be used to determine the percentage of the population above any specific bipod-lead level. The estimates of the mean and standard deviation of the underlying normal distribution were derived from logistic regression estimates of the percentage of children with blood-lead levels above 30 pg/dl and linear regression esti mates of the mean of the log-normal distribution using the Statistical Analysis System (SAS) procedure, SURREGR. 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