"-"'—""— -—--_-- \u-o-I‘ _ -__-_-————._.———-.——-—--. ' , . - q ' ' ' " ‘ I ' u . . , 9‘ ‘ u o . . ‘ . . .. ‘ I, . . t . n . I . ‘ . ¢ . 9 ~ 0 - ..‘ . - . . J ‘ I. |§y ‘ ' ' L. t‘ , ,‘ . . .._ . I 0- -| ~ ' ‘ ' ‘l .I I l‘ I 4'. “ .fl.‘ . ‘|.,". ‘. . .. . g N‘. .1". 'no q. !....‘\'.. .'. II ‘I ~ H U“ ‘ ‘3 V l‘ .' o 1 c < ‘ n - , ., . ' ‘ .‘ I . I I . ‘c . . . .. . .H . . ‘ I -o. .‘ ... I ' .. o u 0‘ c . o . a . . . . I ' I I ' ' l GEOGRAPHY or LEAD museums: _f DEVELOPMENTOF A MODEL -' Thesis for the Degree of M. A. MICHIGAN STATE UNIVERSITY JUAN [TA GASTON 197.2 ' L W E.- ‘J LIBRARY . WWW“ ‘L— J ‘3 Bmomc 3v“? "MG 8: SUNS‘ if BUUK BINDERY INC. : mmnv BINDERS ‘ “mum: APR 2 5 2003 ~ {EH19 6‘"? ABSTRACT GEOGRAPHY OF LEAD POISONING: DEVELOPMENT OF A MODEL BY Juanita Gaston Lead poisoning in children has become a major health problem in urban areas. It has been observed that among residents of pre-World War II dilapidated urban dwellings 10 to 25 per cent or more of the children twelve to thirty-six months of age demonstrate increased lead absorption, as evidenced by increases in blood lead levels.1 In this study, a spatial model for predicting lead poisoningis deve10ped,_and subsequently tested in Lansing, Michigan. The model uses the_conceptsto£~age of. residential_st£uctures, and condition of structure cor- W-r‘ related with family income to derive the sample study 1Jane S. Lin-Pu, "Childhood Lead Poisoning--An Eradicable Disease," Children, XVII (January-February, 1970), 3. Juanita Gaston area. On this basis nine census tracts (2, 6, 7, 8, 13, 15, 18, 19, and 20) were delineated as the study area. Certain variables were added to increase the predictive value of the model. The predictors selected were: (1) a history of pica; (2) existence of anemia; (3) number of siblings living at home; (4) sources of income; (5) marital status; (6) supervision of child; and (7) amount of time child is left in care of others. Children between the ages of one and six years, living in pre-World War II poorly maintained houses, are usually screened for lead poisoning. However, for the purposes of this study, the ages one through four (highest risk) were selected for the study. The data used were obtained from the City Planning Office of Lansing, the Assessor‘s Office, housing charac- teristics of 1960 and 1970 census, and questionnaires. The statistical tools of multiple regression and factor analysis were used in the analyses of the data, in con- junction with maps, tables, and graphs.2 While the purpose of this study was to develop and test a predictive spatial model for lead poisoning, at this time, the fulfillment of this endeavor has not been 2Circumstances beyond the writer's control, such a as the unavailability of deleaded capillary tubes, with adequate anticoagulant, led to delays in collection of blood samples. Hence, only a partial analysis of the data is given. Multiple regression and factor analysis were not utilized. Juanita Gaston accomplished. Although the model has been developed, the testing of the model is still in process. Therefore, the study does not verify the validity of the hypotheses: Hypothesis I The highest blood lead levels will be found in areas of dilapidated pre-World War II houses whose occupants have low incomes. Hypothesis II Children with exaggerated oral tendencies living in dilapidated pre~Wor1d War II houses have higher blood lead levels than children from higher incomes living in pre-World War II houses or children from low incomes living in relatively new housing (built after 1940). Hypothesis III Childhood lead poisoning is more common in families with problems that impair the ability of mothers to perform some of their child-rearing tasks. Nevertheless, the model proposed here, is simple, practical, and relatively inexpensive. Thus, the model may provide a framework from which cities and communities can develop and conduct intensive local programs to detect the incidence of lead poisoning. Such studies may even- tually lead to determination of the quantitative extent and geographic distribution of the lead poisoning problem in the United States. GEOGRAPHY OF LEAD POISONING: DEVELOPMENT OF A MODEL BY Juanita Gaston A THESIS Submitted to Michigan State University in partial fulfillment of the requirements for the degree of MASTER OF ARTS Department of Geography 1972 ACKNOWLEDGMENTS I wish to express my warmest gratitude to Dr. Gerald Rice, Bureau Chief, and to Dr. Thomas Kirk, Pediatric Consultant, Maternal and Child Health Division, Michigan Department of Public Health; to Dr. George J. Dellaportis, Director, Ingham County Health Department; to Mr. Al Vander Kolk, Chief of Standards and Analyses Section, and to Mr. Robert Nordlund, chemist, Division of Technical Services, Industrial Health and Air Pollution Control, Michigan Department of Public Health; to Mr. Jim Spackman, Coordinator for Community Renewal, and to Mr. George Mayer, Planner, Lansing Planning Office; to the Chemistry Department, and to the Glassblower Shop, Michigan State University; to Computer Institute for Social Science Research, Michigan State University; and to the College of Human Development, Michigan State University, for their c00peration and support. I wish to particularly thank Mrs. Vera Thompson, the licensed nurse who assisted in the study, for her untiring patience and encouragement. To the mothers who ii participated in the study, a special word of thanks is extended, for without them the study would have been impossible. I wish to express my sincere gratitude to my chairman, Dr. John M. Hunter. I am indebted to him for his patience, concern, and guidance in helping me prepare this thesis. A special word of thanks is also extended to the members of my committee, Dr. Stanley Brunn, and Dr. Daniel Jacobson, for consenting to serve and for their helpfulness. Additionally, I gratefully acknowledge funds from Biomedical Sciences Support Grant (71-0848). All the suggestions and the aid received from the various sources here mentioned have been valuable. It is my hope that the best of which I am capable may be of service to the readers of this thesis. iii TABLE OF CONTENTS Page LIST OF TABLES O O O O O O O O O O O 0 Vi LIST OF FIGURES . . . . . . . . . . . . vii Chapter I. INTRODUCTION . . . . . . . . . . 1 Statement of Problem . . . . . . . 1 Purpose . . . . . . . . 4 Nature and Scepe of the Study . . . . 4 Objectives . . . . . . . . . . 6 Limitations . . . . . . . . . . 6 Definitions . . . . . . . . . . 7 II. THE CLINICAL ASPECTS OF LEAD POISONING . . 8 Definition . . . . . . . . . 8 Ways Lead Enters the Body . . . . . 8 Signs and Symptoms . . . . . . . 9 Diagnosis . . . . . . . . . . ll Prognosis . . . . . . . . . . 14 Treatment . . . . . . . . l4 Long-Term Therapy . . . . . . . . 16 III. REVIEW OF THE LITERATURE . . . . . . 18 Incidence . . . . . . . . . . 23 Etiologic Factors . . . . . . . . 33 Environment . . . . . . . . . . 38 Sources of Lead Poisoning . . . . . 41 Seasonality . . . . . . . . . . 43 Diagnoses . . . . . . . . . . 45 Sequelae . . . . . . . . . . . 47 Hypotheses . . . . . . . . . . 51 iv Chapter Page IV. GEOGRAPHIC PREDICTIVE MODEL OF LEAD POISONING O O O O O O O O O O O 53 Construction of the Predictive Instrument . . . . . . . . . 55 Selection of Predictors . . . . . . 61 Study Design . . . . . . . . . . 61 V. PARTIAL ANALYSIS OF FIELD SURVEY . . . . 65 Analyses of the Interviews . . . . . 68 VI. CONCLUSION AND RECOMMENDATIONS FOR PREVENTION . . . . . . . . . . 89 Recommendations for Prevention . . . . 92 Policy Recommendations . . . . . . 96 BIBLIOGRAPHY . . . . . . . . . . . . . 98 APPENDICES Appendix A. Questionnaire . . . . . . . . . . 107 B. Process of Deleading Capillary Tubes . . . lll 10. 11. LIST OF TABLES Clinical Classification of Severity of Lead Poisoning . . . . . . . Analysis of Returns for the Interviews Comparison of the Number of Children Tested by Age . . . . . . . Prevalence of Pica Among Total Population . . . . . . . . History of Pica in 314 Children . . Distribution of Children with Pica According to thevape of Object Ingested . . . . . . . . . Characteristics of 214 Families by Census Tracts . . . . . . . Summary Characteristics of Total Sample Population . . . . . . . . Distribution of 214 Homes by Age Group and Condition of Home . . . . Income Distribution of 314 Children and 214 Families by Census Tracts . . Distribution of Income and Family Size . vi Page 12 66 73 74 76 77 80 82 83 85 87 Figure 1. Location of Study Area: Lansing, MiChigan O O O O O O O O O 2. City of New York--Reported Cases of Lead Poisoning . . . . . . . . 3. Spot Map of 219 Cases of Lead Poisoning by Philadelphia Residences of 4. Community Areas of Chicago . . . . 5. Age of Housing by Census Tracts . . 6. Median Income by Census Tracts . . . 7. Scatter Diagram of Median Income by Census Tracts and Per cent of Pre-1940 Residential Structures . . . . 8. Census Tracts Ranked According to Risk 9. Dot Map of Distribution of Sample POpulation . . . . . . . . 10. Distribution of Sample Population by Ethnic Group and Sex . . . . . 11. Age Distribution of Entire Sample P0pu1ation . . . . . . . . 12. The Prevalence of Finger Sucking, Thumb LIST OF FIGURES Sucking or Using a Pacifier and Pica for 314 Children, 1 to 5 Years Of Age 0 O O O O O O O 0 vii Page 25 28 29 56 S7 59 60 67 69 72 78 . . . Cities have shown a unique and enduring propensity to create health problems and then elect to treat the symptoms rather than deal with the causes. --Alonzo Yerby, Address, 1964 American Public Health Association viii CHAPTER I INTRODUCTION Statement of Problem Lead poisoning in children has become a major health problem in urban areas. It has been observed that among residents of pre-World War II dilapidated urban dwellings, 10 to 25 per cent or more of the children twelve to thirty-six months of age demonstrate increased lead absorption, as evidenced by increases in blood lead levels. Two to 5 per cent show evidence of lead intoxi- cation.l More specifically, a recent HEW report estimated that lead poisoning affects 200,000 to 400,000 children annually in the metrOpolitan areas of the United States. Of these 2,000 to 4,000 children are left with some degree of neurologic damage; about 800 children suffer mental retardation of such severity that they require institu- tional care for the remainder of their lives; and about 200 1Jane S. Lin-Fu, "Childhood Lead Poisoning--An Eradicable Disease," Children, XVII (January-February, 1970), 3. children die from lead poisoning annually.2 It is believed that lead poisoning kills and cripples more children than did polio before the advent of the Salk vaccine. Lead poisoning, however, is quite different from diseases such as polio, diphtheria, measles or some other childhood disease. Jane Lin-Fu states that "in the history of modern medicine, few childhood diseases occupy a position as unique as lead poisoning. It is a preventable disease."3 HThe question arises as to why countless'thousands of children suffer from lead poisoning when it is a pre- ventable disease. The answer lies partly in the nature of the disease itself. The diagnosis of classical lead poisoning includes a high blood content of lead, convul— sions, vomiting, anemia, abdominal pain--external symptoms which can be readily confused with less dangerous ill- nesses. Furthermore, routine physical and laboratory examinations rarely contribute to an early diagnosis which is required if serious sequelae are to be avoided. Secondly, the answer lies partly in the amount of funds available for screening children in high risk areas. Novick reported that approximately 2 million children in 2Robert E. Novick, "The Control of Childhood Lead Poisoning," U.S. Department of Health,_Education, and Welfare (WashIngton, D.C.: Office of Secretary's Committee on Mental Retardation, 1971), l. 3Lin-Fu, "Childhood Lead Poisoning," p. 2. metrOpolitan areas throughout the United States are at \ risk to lead poisoning.4l For these high risk children,Lit _ is estimated that at least $50 million are needed yearly f, N ._.l . fof}prevention proqrams, whereas only $7.5 million are allotted.S Clearly, to use the available funds more ef- ficiently, the need of a rapid, simple, and inexpensive model for predicting the incidence of lead poisoning in urban areas exists. If developed satisfactorily, the model could be applied in a variety of urban settings to assist in the health care planning by city and state health departments. The findings would be helpful to departments and agencies concerned with urban planning, urban renewal, and regional planning. The model, when properly developed, could be used in rapid surveys to ascertain: (1) whether there is or is not a pica induced lead problem and, (2) the extent and degree of the problem, if one exists. Spatially pin- pointing residences at maximum risk will also help in the development of appropriate preventive measures by health authorities. 4Novick, "The Control of Childhood Lead Poisoning," p. 2. 5Robert J. Bazell, "Health Programs: Slum Children Suffer Because of Low Funding," Science, CLXXII (May, P11132086 The basic purpose of this study is to develop a spatial model for predicting lead poisoning, and subse- quently to test the model in Lansing, Michigan. Hopefully, the model proposed, which is based on income, age of hous- ing, and condition of housing, will provide a framework from which cities can develop and conduct intensive local programs to detect the incidence of lead poisoning. Such studies may eventually lead to the determination of the quantitative extent and geographic distribution of lead poisoning in the United States. Nature and Sc0pe of the Study In this study, a Spatial model for predicting lead poisoning is deve10ped, and subsequently tested in Lansing, Michigan. The data used were obtained from the City Planning Office of Lansing, the Assessor's Office, the housing characteristics of the 1960 and 1970 Census, and questionnaires. The model uses the concepts of age of residential structure and condition of the structure correlated with family income to derive the sample study area. On this basis nine Census Tracts (2, 6, 7, 8, 13, 15, 18, 19, and 20) were delineated as the study area (Figure 1). Children between the ages of one and six years, living in pre-World War II, poorly maintained houses are usually screened for lead poisoning. However, for the purposes of this study, the ages one through four LOCATION OF STUDY AREA: LANSING, MICHIGAN - u o- no. u- ..... nnnnn nnnnnn ...... ooooooo n uuuuuuu ---------- I ......... uuuuuuuuuu a uuuuuuuuuuu uuuuuuuuuuuu oooooooooooooo ------------ . ----------- ---------- nnnnnnnnn uuuuuuuuuu uuuuuuuuu ........ ......... .......... uuuuuuuuuuu nnnnnnnnnnn uuuuuuuuuuuuuuuuuu ooooooooooooooooooo oooooooooooooooooooooooo uuuuuuuuuuuuuuuuuuuuuu oooooooooooooooooooooooo ooooooooooooooooooooo oooooooooooooooooooooooo uuuuuuuuuuuuuuuuuuuuuuu nnnnnnnnnnnnnnnnnnn ooooooooooooooooooooo cccccccccccccccccccc oooooooooooooooooooo ........ 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'vv ooooooooooooooooooooooooooo ooooooooooooooooooooooooooooo ........................... ooooooooooooooooooooooooooooo oooooooooooooooooooooooooooo ooooooooooooo oooooooooooooooo 00000000000000000000000000000 oooooooooooooooooooooooooooo sssssssssssss deco-oscuoo. no... ooooooooooooooooooooooooooooo ooooooooooooooooooooooooooooo oooooooooooooooooooooooooooooooo oooooooooooooooooooooooooooooo ooooooooooooooooooooooooooooooo 00000000000000000000000000 OOOOOOOOOOOOOOOOOO D I 00001.. oooooooooooooooooo a a .00.... oooooooooooooooooooooooooo .......................... oooooooooooooooooooo ~ 0000.000 00' ooooooooooooooooooooooooooooo 0000000000000000000 t ecoooaau oooooooooooooooooooooooooooooo ........................... . oooooooooooooooooooooooooo oooooooooooooooooooooooo D ........................... ooooooooooooooooooooooooooooo ooooooooooooooooooooooooooooo ooooooooooooooooooooooooooooo ooooooooooooooooooooooo oooooooooooooooooooooo 00000000000000000000 oooooooooooooooo ooooooooooooooooo oooooooooooooooooo ooooooooooooooooooo ooooooooooooooooooo 00000000000000000000 oooooooooooooooooooo oooooooooooooooooooo oooooooooooooooooooo 00000000000000000000 oooooooooooooooooooo oooooooooooooooooooo oooooooooooooooooooo oooooooooooooooooooo oooooooooooooooooooo oooooooooooooooooooo oooooooooooooooooooo I IIIIIIIIIIIIIIIIIII V 7 2‘ v - A: ogxmemmfl I970 CENSUS VIM" Figure l.--Location of Study Area: Michigan. fi—A Lansing, (children at highest risk) were selected for the study. The control group consisted of fifty children from low income families living in houses built after 1940, and high income families living in houses built before 1940.6 The statistical tools of multiple regression and factor analysis were used in the analyses of the data, in conjunction with maps, charts, and graphs. Objectives 1. To develop and test a predictive spatial model of lead poisoning. 2. To ascertain the extent and degree of the pica induced lead poisoning problem, if one exists. 3. To summarize_the significant features of the spatial distribution of lead poisoning, as an aid to general understanding and help in planning and implementing prevention programs. Limitations In executing this project, the writer was handi- capped, in some instances, by the inaccessibility of multiple dwelling units. Therefore, most of the children in the study were from single family dwelling units, with 6Manufacturers began to phase lead out of their interior paints during the 19403 and after some resistance reached a voluntary 1 per cent standard by 1955. a few children from two and three family dwelling units. No apartment buildings were included in the study. Another handicap the writer was faced with was that the number of children listed in the Census data and the actual number of children in a census tract was quite different. Approximately 2,900 children were expected to be found, whereas, only about 600 were found. Conse- quently, the sample was much smaller than expected. Definitions Pica.--The habitual, purposeful and compulsive search for and ingestion of such non-food substances as cigarette butts, paper, matches, dirt, paint chips, and SC on. Exaggerated oral tendencies.--Finger sucking, thumb sucking, and/or pica after one year of age. CHAPTER II THE CLINICAL ASPECTS OF LEAD POISONING Definition Lead poisoning is a systematic intoxication which may occur when the concentration of lead within the tissues reaches or exceeds a critical range.7 Lead poison- ing can be separated into two categories: (1) acute lead poisoning, which is rare, occurs after the ingestion of lead salts or the inhalation of lead fumes, and (2) chronic lead poisoning, which is common, especially in children, occurs after the repeated ingestion of lead contaminated materials over a period of weeks or months. Here, the writer will be concerned only with chronic lead poisoning. Ways Lead Enters the Body Lead enters the body through the gastrointestinal tract and in the instance of acute lead poisoning, through the respiratory tract or skin. Except for acute poison- ing, it is a slow acting, cumulative poison, and symptoms 7Robert A. Kehoe, "Lead Poisoning," in A_Textbook of Medicine, ed. by Russell L. Cecil and Robert F. Loeb IPE11adelphia, Pa.: W. B. Saunders, 1959), p. 498. may develop insidiously and at times, be intermittent. A single ingestion may produce no symptoms, but the same quantity continuously ingested three months or over may be toxic. The slow absorption and gradual accumulation of lead within the blood and soft tissues produce the clinical features of lead poisoning. Following absorption, a large portion of the lead enters the portal circulation and is excreted by the liver. The remainder is distributed to the soft tissues (liver, kidney, brain, and pancreas). Lead slowly leaves the soft tissues for deposition in the bone where it is stored as tertiary lead phosphate along with calcium.8 Signs and Symptoms The occurrence of symptoms depends upon the amount of lead in the soft tissues and blood. The amount of lead in the urine roughly parallels the amount in the blood, and is thus an indication of the rate of transport to and from the tissues. The early manifestations of lead poisoning are usually anemia, hyperirritability, incoordination, lethargy, vomiting, constipation, weakness, loss of weight, pallor out of proportion to anemia, headache, abdominal pain and colic, loss of appetite (particularly for 8L. Emmet Holt, Jr. et 21., Pediatrics (New York: Appleton-Century, Inc., 1962TT p. 745. 10 breakfast), insomnia, and subtle loss of recently acquired skills. These symptoms often suggest a behavior disorder. Furthermore, the physician may erroneously attribute these symptoms to iron deficiency anemia which is commonly seen in children with lead poisoning. The persistence of pica resulting in the ingestion of lead-pigmented paint chips for a period of three months or longer leads to the subtle onset of clinical symptoms.9 If ingestion continues these symptoms intensify with clinical manifestations developing over a period of three to six weeks.10 Gross ataxia and the onset of acute encephalopathy indicated by the appear- ance of signs of increased intracranial pressure (forceful and intractable vomiting, lethargy, stupor, coma, and convulsions) may occur. Muscular incoordination, peri— pheral motor paralysis of the most commonly used muscles (dorsiflexors of the feet or wrists), joint pains, hyper- tension, bradycardia or labile pulse rate and edema of the optic nerve may be seen. If not interrupted, the process culminates in prolonged convulsions and profound coma within a period of one week or less. Rapidly increasing papilledma may be noted and death at this stage is usually attributed to increased intercranial pressure. In those 9American Academy of Pediatrics, "Prevention, Diagnosis and Treatment of Lead Poisoning in Childhood," Pediatrics, XLIV (August, 1969), 295. loIbid. 11 patients who recover from this stage, severe residual injury to the central nervous system, including recurrent convulsions, hemiplegia, blindness, deafness and severe mental retardation, is commonly seen. Severe behavior disorders, interference with attention span, and learning difficulties are commonly seen in patients who recover from mild encephalOpathy.ll Diagnosis Partly because there are no pathognomonic abnor- malities on physical examinations, early recognition of lead poisoning requires a high index of suspicion. Specific laboratory tests of value in the diagnosis of lead poison- ing includes determinations of blood lead concentration, urine lead excretion, and urine c0poporphyrin excretion. BlOod lead levels greater than 0.06 mg. per 100 gm. of whole blood are indicative of exposure to lead (Table 1). Lead intoxication is usually associated with concentra- tions greater than 0.1 mg. per 100 gm. of whole blood. Urinary lead is almost invariably above 15 mg. per liter when lead poisoning exists.12 Other diagnostic measures include changes in osmotic resistance of circulating blood cells, in vitro 11Waldo Nelson, Textbook of‘Pediatrics (7th ed.; Philadelphia, Pa.: W. B. Saunders Company, 1959), p. 1376. lzIbid. 12 ucmo Mom .mofi ooA ucmo mom .005 oonam Damn you .mofi Hmno UOOHQ maosz .mEb ooa ewe .ne .mnoox vocab oa0£3 manna 00H\.ne .0100I00 pooHn maosz .50 00H\.ne.0aovv woodn maon3 mo .HE 00H mom .mE om pooan maons mo .Hs 00H nod .02 meaov noose adore mo .Hs 00H Hum .05 00 on ma eooan «Hons mo madam 00H\.ne .mnoma ocean maon3 mo .20 00H\.ne .mnomuom noose asap; 00 .20 00H\.ne .0100Ima meoumshm ensue msoumsxm 0H“: Husuoz 000a Heme 000a .ucoseueum season 000a .moauumanom .GMSHQOM .EHOmflgu m.HflHw£00 GOOOHDm m0 Emflmod GdOfiHOc—fl cease .HE ooa oaoas mo .Em Hum .05 00.0 00H\.ne .mnoma usoumssm mused woods noose means woods 00 .Ha oHog3 mo .HE mo .HE ooa 00H new .05 neon Hem .mE 00H\.0100.0A \.05 00.0 00.0 o» 00.0 00.0 o» 00.0 maoueasm use: 000a .Ha 00H\.0s noose «0 .He ocean no name “mm 00.0 on 00.0 00H see .0100 .Hs 00H\0:00 .Hs 00H\0100 .05 00.0-mo.0 Husuoz mmma 0m0H 000a .mcouca 000a .nmm.mm emma .comauuem «was .emm.mm museum .macua .muohm can c0300 .hoavmum w Edamwno coumcwucdm oeumocmuwo .Amau>oa 060A voon Gav mcacomaom pawn mo >uaum>mm mo c0wumowmammmao Hmoacwaonu.a wands 13 assay delta-aminolevulinic acid dehydratse activity in circulating blood cells, delta-aminolevulinic acid in serum, baSOphilic stippling, a lead line in the gums, con- centrations of lead in hair, and roentgeongraphic evidence of increased densities at the end of long bones. Of these, blood lead level is considered the best diagnostic measure for lead poisoning. Unfortunately these tests alone can- not be depended upon for identifying a child who requires chelation therapy to prevent encephalopathy. ~Whenever a child residing within a high risk neighborhood, i.e., pre- World War II dilapidated housing, manifests any of the suggestive symptoms, appropriate diagnostic tests are indicated. These determinations should also be included in the study of children with pica, convulsive disorders and behavior problems. Chronic lead poisoning may simulate poliomyelitis, postdiphtheritic paralysis, localized neuritis or poly- neuritis, rheumatic fever, brain tumor, brain abscess, tuberculosis, meningitis, asceptic meningitis, diabetic 13 coma, severe hepatitis, and "cyclic vomiting." This factor adds to the complexity of diagnosis. 13Lawrence B. Slobody and Edward Wasserman, Survey of Clinical Pediatrics (New York: McGraw Hill Book Eampany, 1968), p. 1346. 14 Prognosis The prognosis of chronic lead poisoning depends on more severity and duration of the illness rather than on the type of therapy.14 The usual mortality figures range from 10 to 25 per cent with almost all fatal cases being those with severe encephalopathy.15 As equally dis- tressing as the mortality is the residual neurologic damage from lead poisoning. Significant sequelae has been reported in from 25 to 75 per cent of the cases and in- cludes paralysis, blindness, and organic brain damage, especially in areas of visual motor function and language skills.16 Treatment Once a lead poisoning case is detected, the child is usually hOSpitalized for several days and treated with chelating agents that bind the lead ion and remove it from the body via urine excretion“) Prior to the late 19403 the “N treatment of lead intoxication was directed at shifting lead from the blood and soft tissues to the bones, where it could be excreted more slowly and under Controlled 17 conditions. Such therapy included diets high in calcium, 14George J. Cohen and Walter E. Ahrens, "Chronic Lead Poisoning," Journal of Pediatrics, LIV (March, 1950), 272. 15 16 Ibid., p. 273. Ibid., p. 276. 17Ibid., p. 275. 15 phosphorous, and vitamin D followed by citric and other organic acids.18 In 1950, dimercaprol (BAL) was found to be as effective as the diet therapy in treating lead poi- soning. In 1952, another chelating agent, calcium disodium ethylenediamine tetraacetate (versenate, edathmil, or EDTA), a chemical familiar in biochemical research, was discovered to be effective in treating lead poisoning by Bessman and associates, and Belkman. Before chelation therapy was develOped, 66 per cent of severe lead poisoning cases were fatal, now with the early detection and treatment, less than 5 per cent are fatal.19 Other treatment measures include: (1) elimination of environmental lead sources, and (2) amelioration of nutritional or psychological factors responsible for pica. Removal of children from further exposure to lead as soon as early manifestations are observed or even at the stage of beginning encephalopathy is the most important factor in reducing mortality and the incidence of severe cortical damage. Prolonged recurrent exposure may lead to severe residual nervous system injury despite anti-lead therapy. The major threat of life appears to be increased intracranial pressure, which may occur shortly after the laIbid. 19Mark W. Oberle, "Lead Poisoning: A Preventable Childhood Disease of the Slums," Science, CLXV (September, 1969), 991. 16 onset of overt encephalOpathy.20 Although sequestration of lead with CaEDTA should be started promptly, radical attempts to lower intracranial pressure may be required to save a life. Techniques used with varying success have been lumbar puncture and craniotomy.21 Results of more recent work suggest that when no improvement is evident during therapy with EDTA, extensive surgical decompression of the skull can be life saving and may even reduce poten- tial residuals. Lonngerm Therapy Long term care is essential, and in many ways, is both the most difficult and most important aspect of treat- ment.22 The first rule is: no child ever returns to a leaded house.23 This requires the coordinated efforts of health and public authorities to effect the removal of hazardous lead sources, assistance of the mother in her search for safe housing, and, increasingly, mobilization of the community itself. Adequate care often requires brief hospitalization in a convalescent facility or foster home, 20Cohen and Ahrens, "Chronic Lead Poisoning," p. 274. lebid. 22American Academy of Pediatrics, "Prevention, Diagnosis, and Treatment of Lead Poisoning in Childhood," p. 296. ZBIbid. 17 thereafter, the child must be followed closely until he reaches school age. Where possible, enrollment in nursery school or Head Start Programs is advisable to provide stimulation for the child which may, for the preschool child, reduce his emotional needs for pica. During the first year of convalescence, intercurrent infections may contribute to the toxicity of lead. Some but not all, authorities feel that such episodes should be "covered" by brief courses of chelation therapy. It has also been re- ported that patients maintained on oral-d pencillamine therapy during the first three to six months of convales- cence do not experience toxic relapses during intercurrent infections.24 Phenobarbital and/or diphenyl hydantoin sodium (Dilantin) are generally adequate for the control of seizures that may follow encephalopathy.25 Recurrence of seizures without recurrent lead ingestion is usually indicative of a lapse in anticonvulsant medication. Both seizures and behavioral disturbances tend to abate during adolescence.26 24 25 Ibid., p. 297. Ibid. 26Ibid. CHAPTER III REVIEW OF THE LITERATURE In recent years, geographers have become more cognizant of social problems, but few geographical studies have been done on health problems. Clearly geographers should become involved in the great social issues and prob— lems of the day. One approach would be through the study of urban health problems. Original studies in medical geography undertaken by professional geographers are few.27 In 1950, Jacques May began publishing a series of maps that eventually made up the American Geographical Society's Atlas of Disease. The first six of these plates included "Map of World Distribution of Poliomyelitis," "Distribution of Cholera 1816-1850," "Distribution of Malaria Vectors," "Map of the World Distribution of Dengue and Yellow Fever," "Map of the World Distribution of Helminthiases," and "Map of 27These references are not meant to be exhaustive of research done on health problems by geographers. 18 19 the World Distribution of Plague."28 These comprised maps of the routes of major pandemics, geographic distribution of disease vectors, and a resume of the natural history of the vectors. In 1960, G. Melvyn Howe published a well-documented work on cancer mortality in Wales. He followed this a year later by another article of broader sc0pe, "The Geographical Variation of Disease Mortality in England and Wales in the mid-Twentieth Century," of which the purpose was to intro- duce the possibilities of geographical approach to the portrayal of biostatistical data.29 In 1962, Malcolm Murray supplemented Howe's study with "The Geography of Death in England and Wales."30 The purpose of this article was to illustrate the spatial 28Jacques May, "Map of the World Distribution of Poliomyelitis,” Geographical Review, XL (October, 1950), 646-48; idem, "Distribution of Cholera 1816—1850," 1b1d., XLI (ApriI, 1951), 272-73; idem, "Distribution of MaIar1a Vector," ibid., XLI (October, I951), 638-39; 1dem, "Map of the WorId Distribution of Dengue and Yellow Fever," ibid., XLII (April, 1952), 283-86; idem, "Map of World D1stribution of Plague," ibid., XLII (October, 1952), " 628-30; idem, "Map of WorId Distribution of Helm1nth1ases, ibid., XLII (January, 1952), 98-101. 296. Melvyn Howe, "The Geographical Distribution of Cancer Mortality in Wales, 1947-53," Institute of British Geographers, Publication No. 28 ILondon: Trans- Iations and Paper, 1960), pp. 199-214; idem, ”The Geo- graphical Variation of Disease Mortal1ty in England and Wales in Mid-Twentieth Century," Advancement of Science, XVII (1960-61), 415-25. 30Malcolm Murray, "The Geography of Death in England and Wales," Annals Association of American Geographers, LII (June, I962),7I30:49. 20 pattern of mortality variation in England and Wales through the medium of maps, and to suggest some possible reasons for the areal differences in mortality. In all three studies, maps of categories of causes of death constituted the focal approach and the pattern thus diSplayed were analyzed with reference to certain physical and cultural variations. In 1963, Dudley Stamp published four lectures delivered at London School of Hygiene and Medicine under ”Some Aspects of Medical Geography."31 The lectures dealt with "Climate and Disease," "Climate and Health," "The Mapping of Mortality-Morbidity," and "The Way Ahead " and their purpose was to discuss the geographical approach to the analysis of certain types of medical problems. In the same year Jacques May published The Ecology of Malnutrition in Five Countries of Eastern and Central EurOpe, in which he evaluated the national food resources of five countries of East-Central EurOpe.32 He attacked the national food balance by marshalling statistical and other data on food resources, diet types, and nutritional pat- terns in the individual countries to determine possible adequacy under various situations ranging from peace to war. 31Dudley Stamp, Some Aspects of Medical Geography, (London: Oxford University Press, 1964). 32Jacques M. May, The Ecology of Malnutrition in Five Countries of East CentraI Europe, Studies in Medical Geography, IV, 1962. 21 Hunter and Young published an article on "Diffu- 33 As sion of Influenza in England and Wales" in 1971. with Howe and Murray, maps constituted the focal approach and the patterns thus displayed were analyzed. In a study conducted in Mexico City in 1972, Fox attempted to show the relationship between the distribution 34 Bio- of ill health and a poor domestic environment. statistical data obtained from death certificates organ- ized by housing areas revealed a strong association be- tween crude death rates from both particular and certain elements in the home environment. In addition to these studies of Specific diseases, regional health studies have been done by a few geo- graphers. Deshler conducted a study on "Livestock Trypan- osomiasis and Human Settlement in Northeastern Uganda."3S He treated the impact of the disease on one cattle-keeping tribe's adjustment to the problem during three decades. 33John M. Hunter and Jonathan C. Young, "Diffusion of Influenza in England and Wales," Annals, Association of American Geographers, LXI (December, 1971), 637. 34David Fox, "Patterns of Morbidity and Mortality in Mexico City," Geographical Review, LXII (April, 1972), 151. 3SWalter Deshler, "Livestock Trypanosomiasis and Human Settlement in Northeastern Uganda," Geographical Review, L (July, 1960), 540. 22 In 1966, Hunter conducted a study on River Blind- ness in Nangodi, Ghana.36 Making use of aerial photographs and field investigation, Hunter concluded that 38 per cent of Nangodi had been deserted because of river blindness. In "Man and Malaria in Trinidad, Ecological Prospectives of a Changing Health Hazard," Fonaraff ex- amined the relationship between culture, disease and organism and the physical environment.37 Maps of malaria risk were presented to show the changing distribution of patterns of infection in reSponse to public health efforts in urban and rural land use. The spatial dimension of lead poisoning is a neg- lected aspect of research. Most of the research relating to lead poisoning has been performed by the medical pro- fession, in which the focus has been on incidence, etio- logy, treatment and prevention of lead poisoning. The majority of the data comes from the older northeastern cities, Philadelphia, Washington, D.C., Cleveland, Boston, Baltimore, Chicago, New Haven, and Portland, Maine. Lead poisoning has been described as "a disease of university 36John Hunter, "River Blindness in Nangodi, Northern Ghana: A Hypothesis of Cyclical Advance and Retreat," Geographical Review, LVI (July, 1966), 398. 37L. Schuyler Fonaroff, "Man and Malaria in Trinidad: Ecological Perspectives of a Changing Health Hazard," Annals, Association of American Geographers, LVIII (September, 1968), 527. 23 medical centers" because of the high incidence reported by these institutions which coexist in ghettos.38 Incidence Throughout the literature, the occurrence of lead poisoning appears to be parallel to the interest in the ‘publicity about the disease. Harrison noted that between 1935 and 1947, the average yearly reported incidence of childhood lead poisoning in Baltimore was 15 cases.39 From 1948 to 1956, approximately 40 cases yearly were reported. Having been one of the first cities to recognize lead poisoning in children as a public health problem, Baltimore reported a total of 293 cases between 1931 and 1951.40 Unlike other cities that have detected increasing numbers of cases, in recent years, Baltimore has reported a steady decline since 1958, when 133 cases were reported. In 1968, only 13 cases were reported. McLaughlin pointed out that the number of cases diagnosed and reported to the Board of Health in New York had steadily risen from one in 1950 to 41 80 in 1954. For the same city, Guinee reported a rise 38Paul Harris, Alvin H. Novack, and Leonard Fichtenbaum, "Lead Poisoning in an Inner-City Neighborhood,“ Connecticut Medicine, XXXV (August, 1971), 485. 39Harold E. Harrison, "Childhood Lead Poisoning," New York State Journal Medicine, LVI (December, 1956), 3938. 4011616. 41Mary Culhane McLaughlin, "Lead Poisoning in Children in New York City, 1950-1954," New York State Journal of Medicine, LVI (December, 1956), 3713. 24 from 151 cases in 1959 to nearly 2,500 cases in 1970.42 The high incidence areas of New York for 1963 are illus- trated in Figure 2. New Haven had the highest reported incidence of lead poisoning (22.5/100,000) in the United States in 1965.43 Lead poisoning remained fairly constant from 1962 through 1966 in Milwaukee, followed by a threefold in- crease in 1967 and a doubling of this in 1968. Lead was 7 per cent (74 cases) of the total poisonings (1,057) for the four-year period. The occurrence of lead poisoning cases for the four years was: l962-—no cases; l963--five cases; l964--eight cases; l965--five cases; 1967--l7 cases; and 1968-~34 cases.44 Detths attributed the abrupt rise in the number of lead poisonings in 1967 and 1968 to in- creased awareness of physicians and to better detection methods. Awakening of medical interest in the problem has been followed by similar results in Washington, D.C. Standard reported that more than 500 children were stricken 42"Children at Risk," Nature, CCVII (December. 1970), 1253. 43Harris et a1., "Lead Poisoning in an Inner-City Neighborhood," p._4857 44Tony M. Deeths and James T. Breeden, "Poisoning in Children--A Statistical Study of 1,057 Cases," Journal of Pediatrics, LXXVIII (February, 1971), 300. 25 CITY OF NEW YORK II Repornd gases 0‘ ‘."‘-‘V}\-\ K‘_ LEAD POISONING -.°. “N -- By Place Of Residence ~ .I New York City -|963 B R 0 N X [I 00% ./ 00000000 ./ “fififi / ........... .o.. ( .-_; :::: \ \ ",1 1111 \. .\ \- \- \- \ j é ! :3. . _,.I E r . .......... " \. | ‘ 0"...I.. . . . ‘ K W |. 'i ------- 3p 5% \ ,”1 NEJHW“ I ' '. -. .331? ‘;:.:.'.-n \'~’. ‘ ...... ! #355353. .2 ":::.'.'.:.'.':‘_--‘..'.a .\ } “33535555: . E55. 355‘» . L- , ‘- 'J'}::;’ \ .......... " "”- i . 3' ..... 1- . \ Y N "' as B ' ma‘c‘ ! I o. l V O 4"" LEGEND - \C rt-srw Afia‘“ High Incidence Ana: . IIoIafod Cam AFTER JACOUZINER AND RAYBIN, I962 Figure 2.--City of New York--Reported Cases of Lead Poisoning. 26 45 The Medical Com- with lead poisoning annually in D.C. mittee on Human Rights estimated that about 10 per cent of the 47,595 children living in the 22,000 substandard homes had been subjected to lead poisoning. Although only 45 clinical cases were diagnosed in 1968, the Medical Committee estimated that approximately 5,000 children had significant amounts of lead in their systems and many others were exposed to lead.46 During the 14 year period between 1939 and 1952, 20 cases of lead poisonings were diagnosed at the Childrenfis Memorial Hospital in Chicago.47 In 1953, alone, 21 cases of lead poisoning were uncovered in Chicago.48 During the 6 year period from January 1, 1959 through December 31, 1964, Reddick noted that a total of 22,989 cases of accidental poisonings were reported to the Poison Control Center of the Chicago Board of Health. The total number of cases of lead intoxication during the same 45Raymond L. Standard, "Lead Poisoning in Chil- dren," Medical Annals of D.C., XXXIX (July, 1970), 399. 461bid. 47A. L. Tanis, "Lead Poisoning in Children: In- cluding Nine Cases Treated with Edathamil Calcium Diso- dium," American Journal Diseases of Childhood, LXXXIX (March, 1955), 325. 48Robert B. Mellins and C. David Jenkins, "Epi- demiological and Psychological Study of Lead Poisoning in Children," Journal American Medical Association, CLVIII (May, 1955), 15. 27 period was 926 or 4 per cent of the total. In 1963, the first year the disease was made reportable, 203 cases of 49 lead poisoning were reported in Chicago. In 1968, the number of reported cases rose to 702.50 Along with the large number of reported cases of lead poisoning, there has been a decline in the number of fatalities. In Philadelphia, Ingalls reported that of the approximately 50 cases of lead poisoning reported yearly during the years 1955-1960 (Figure 3), 10 to 20 per cent of the diagnosed patients died within five years.51 In 1967-1968, 176 cases were reported and two deaths. In 1955, of the 21 cases of lead poisoning un- covered in Chicago, 20 per cent were fatal.52 From 1959 to 1961, lead poisoning accounted for 79 per cent of the deaths due to accidental poisoning in Chicago, while it accounted for only 4.7 per cent of the total number of 53 reported cases (Figure 4). In 1963, the fatality rate 49Lovett Reddick, "Plumbism Exists Today," Southern Medical Journal, LXIV (April, 1971), 446. 50Lin-Fu, "Childhood Lead Poisoning," p. 6. 51Theodore H. Ingalls, Emil A. Tiboni, and Milton Werrin, "Lead Poisoning in Philadelphia, 1955-1960," Archives of Environmental Health, III (November, 1961), 90. 52Mellins and Jenkins, "Epidemiological and Psychological Study of Lead Poisoning in Children," p. 16. S3Reddick, "Plumbism Exists Today," p. 447. 28 —oo— .owmalwmma “mucmwuwm mo mwucmpwmmm mandaoomHasm ha mcacomwom puma mo mommo mam mo mm: uommlu.m musmam .m :mumII.v mqmde 75 Data on the histories of pica by census tracts are sum— marized in Table 5. The percentage of children with pica in a census tract ranged from 18 per cent in Census Tract 8 to 50 per cent in Census Tract 19. It should be noted that the number of children in some of the census tracts are very small, thereby causing an unrepresentative result. The nature of objects ingested was listed for children with pica during the three month period. It was found that the objects ingested fell into seven major cate- gories. Details of the categories and the corresponding percentages of children with pica in each are listed in Table 6. Out of the nine census tracts, it should be noted that only one child was reported as having pica for plasten The prevalence of oral activities such as thumb sucking, finger sucking or using a pacifier and pica were determined, and characteristic patterns for the prevalence of these activities were found (Figure 12). Oral activi- ties fluctuated between 5 and 23 per cent for all age groups and tended to cease at the age of fifty-four months. Pica was found to have an almost linear fall from 48 per cent at twenty-four months of age to 10 per cent at forty- two months of age. Pica then rose at forty-eight months to 14 per cent and ceased at fifty-four months of age. The questionnaire sought information about a number of factors that might be of predictive value in identifying the child with an increased body burden of TABLE 5.--History of Pica in 314 Children. 76 $52235 ehiggéen Pica % nga % 2 23 7 30 16 69 6 26 8 30 18 70 7 11 2 18 9 82 8 32 10 31 22 69 13 54 20 37 34 63 15 48 16 33 34 63 18 16 7 44 9 67 19 6 3 50 3 50 20 98 25 26 73 74 Total 314 98 216 77 TABLE 6.-—Distribution of Children With Pica According to the Type of Object Ingested. Nature of Object No. % Tobacco: cigarette butts, filters 40 43 Paper: toilet paper, writing paper 26 29 Matches: live and spent 11 12 Writing materials: crayons, pencils, chalk 13 14 Dirt: ashes, house dirt 7 8 Plaster: wall 1 1 Other 10 10 Total 108 117* * Some children ingested more than one object. 78 Pica o——o 100 Finger sucking, thumb sucking, pacifer...’ B 8 80 m.~ nIH 8 8 0 60 z m H CH 0) \“7/\ SE: 40 H :1: u 20 .v’ .¥’_’___ 0 i 4 J 1 4 1 J I2—I7 18-23 24-29 30—35 36-1I 42‘11 43—53 54—60 AGE (in Months) Figure 12.--The Prevalence of Finger Sucking, Thumb Sucking or Using a Pacifier and Pica for 314 Children, 1 to 5 Years of Age. 79 lead. It is generally felt that families with problems, such as, severed marriage, welfare or ADC recipients, or large numbers of children living at home, "impair the ability of some mothers to perform many of their child 111 These families are believed to have rearing tasks." higher rates of lead poisoning. Consequently, information was sought about the following indicators of family charac- teristics or problems: intact marriage, divorced, separ- ated, widowed, single, and welfare or ADC recipients (Table 7). The characteristics have been summarized by census tracts. In Census Tract 13, the area predicted to be the highest risk, 24 per cent of the families had only one parent and 42 per cent were receiving ADC or welfare. In Census Tracts 2, 15, 18, and 19, areas of second high- est risk, 10, 63, 55, and 25 per cent, respectively, of the families had one parent, and 50, 77, 82, and 25 per cent, respectively, were receiving ADC or welfare. In Census Tract 20, the third highest risk area, 22 per cent of the families had one parent, and 34 per cent were re- ceiving ADC or welfare. In the lowest risk area, Census Tracts 6, 7, and 8 had 20, 62, and 39 per cent, respec- tively, of the families with one parent; and 40, 63, and 48 per cent, respectively, were receiving ADC or welfare. 111J. Wister Meigs and Elaine Whitmire, "Epidemio- logy of Lead Poisoning in New Haven Children--Operational Factors," Connecticut Medicine, XXXV (August, 1971), 373. 80 TABLE 7.-~Characteristics of 214 Families by Census Tracts. Marital ADC-~Welfare Census Tracts Status No. % No. % 2 Intact ll 90 6 50 Separated l 10 6 Intact 12 8O 6 40 Single 1 7 Divorced 2 l3 7 Intact 3 38 5 63 Divorced 4 50 Separated l 12 8 Intact 14 61 ll 48 Single 2 9 Divorced 3 l3 Separated 4 17 13 Intact 29 76 16 42 Single 4 10 Divorced l 3 Separated 3 8 Widowed l 3 15 Intact ll 37 23 77 Single 5 l7 Divorced 4 13 Separated 8 22 Widowed 2 7 l8 Intact 5 45 9 82 Single 4 37 Divorced l 9 Separated l 9 l9 Intact 3 75 l 25 Single 1 25 20 Intact 53 73 25 34 Single 5 7 Divorced 10 14 Separated 4 5 Widowed l l 81 Inasmuch as the number of families in some of the census tracts is very small, the percentage is somewhat distorted. For the entire study population, 66 per cent of the fami- lies had both parents, 10 per cent were separated, 11 per cent were divorced, 10 per cent were single, and 2 per cent were widowed (Table 8). Forty-eight per cent of the total study population were receiving ADC or welfare. The major prediSposing factor to chronically in- creased body burden of lead is habitual exposure to bad ~housing. While it is not known precisely how many children in Lansing have been exposed to lead paint, the age of the majority of residential indicates that almost all would contain lead-based paint (Table 9). The distribution and condition of houses by census tracts are shown in the table. Going from highest to lowest risk, 55 per cent of the houses in Census Tract 13 were less than 50 per cent good (based on assessment by the City Assessor Office). In Census Tracts 2, 15, 18, and 19, the second order of high- est risk, 25, 40, 45, and 100 per cent, respectively, of the houses were less than 50 per cent good. Of the 214 families, no houses were built after 1940, and no houses were more than 89 per cent good. When considering the age and condition of the housing, one other major factor should be included, and that is, income. Needless to say, the income, in most instances, determines the condition of the house. The 82 TABLE 8.—-Summary Characteristics of Total Sample Population. No. % Marital Status Intact 142 66 Separated 22 10 Divorced 24 12 Single 22 10 Widowed 4 2 Total 214 100 Sources of Income ADC--Welfare 102 48 Not on ADC-~Welfare 112 52 Additional Sources Social Security 9 Veteran Benefits 12 Railroad Retirement Pension 2 Medicaid 2 Food Stamps 5 Other 4 83 TABLE 9.--Distribution of 214 Homes by Age Group and Condition of Home (Expressed in Percentage Good). Census Year Home Built % Good Tract