Childhood Lead Poisoning, New York City, 1988

Kenneth Daniel Melissa H. Sedlis, M.D. Lisa Polk Solo Dowuona-Hammond Barbara McCants Bureau of Lead Poisoning Control New York City Department of Health Thomas D. Matte, M.D., M.P.H. Lead Poisoning Prevention Branch Division of Environmental Hazards and Health Effects Center for Environmental Health and Injury Control

Summary In 1988, a total of 796 cases of childhood lead poisoning were identified through surveillance by the New York City Bureau of Lead Poisoning Control (BLPC), an estimated 0.3 cases identified per 100 children screened. Sixty-two percent of the case-group children had blood-lead levels between 25 and 34 ug/dl. One- and two-year-old children accounted for 61% of cases. Of the children in the case group, 59% were black and 27% were Hispanic. From 1986 through 1989, the annual number of children screened increased by 27%, while the annual number of new cases fell by 30%. Because of incomplete screening, false negative results, and lack of information on children with lower but potentially harmful levels of blood lead (10-24 ug/dl), the magnitude of excessive lead absorption in New York City children is underestimated. These surveillance data indicate that lead poisoning among children is a persistent public health problem in New York City. INTRODUCTION

Lead poisoning among children is a widespread and persistent public health problem in the United States (1). Although lead is also toxic to adults and affects virtually all organ systems, adverse effects on cognitive development and behavior in children (2-5) are of special concern. In 1984, an estimated 200,700 U.S. children living in standard metropolitan statistical areas (SMSAs) had blood-lead levels of greater than or equal to 25 ug/dl (1), CDC's current definition of an elevated blood-lead level for use in screening programs for children (6). Growing evidence indicates that levels of blood lead in the range of 10-15 ug/dl and above have adverse neurobehavioral effects in children (3-5); in 1984, an estimated 3 million children in SMSAs had blood-lead levels of greater than or equal to 15 ug/dl (1).

The main source of lead exposure among lead-poisoned children in urban areas is lead-based paint (1,7). Children may ingest lead directly from paint chips, but an important route of exposure is the normal mouthing of hands or objects such as toys, resulting in the ingestion of small amounts of lead paint-contaminated housedust and soil (8). Children living in deteriorating housing built before 1950 are at high risk for excessive lead exposure via this route (1), and poor, black children in urban areas are disproportionately affected by lead poisoning (9).

Organized programs to screen children for lead poisoning were started in Chicago and other large cities in the late 1960s and expanded during the 1970s with federal support (10). Since that time, state and local childhood lead-poisoning prevention programs (CLPPPs) have remained the principal means by which lead-poisoned children are detected and lead-paint hazards are identified and abated. The New York City Bureau of Lead Poisoning Control (BLPC), created in 1970, is the largest CLPPP in the country (1). In this report, the characteristics of lead-poisoning cases identified through surveillance by BLPC for 1988 are described, and time-trends in overall case counts from 1986 through 1989 are reported. METHODS

BLPC has the responsibility for screening children for lead poisoning, facilitating and monitoring screening conducted by health-care providers, inspecting dwellings of lead-poisoned children for lead-based paint, and ensuring that lead-paint hazards are abated when identified. This report is based on BLPC's computerized registry of childhood lead-poisoning cases, which are identified in three ways. First, BLPC monitors screening and diagnostic tests for lead poisoning performed by city-operated and affiliated clinics and hospitals and by some private providers. Second, BLPC staff conduct "door-to-door" household screening, usually in targeted, high-risk neighborhoods. Finally, cases are identified through mandatory reporting of blood-lead levels of greater than or equal to 25 ug/dl by private laboratories to BLPC.

Two screening methods are used by providers reporting to BLPC. In approximately 60% of screening tests, portable hematofluorometers are used to measure zinc protoporphyrin (ZPP) (11) on site from capillary blood samples. Children who screen positive, defined as ZPP of greater than or equal to 35 ug/dl, are evaluated with a venous blood-lead measurement. In the second screening method, capillary blood samples are collected on lead-free filter paper. These are submitted to the New York City Bureau of Laboratories and analyzed for free erythrocyte protoporphyrin (FEP) (12) and for blood lead (13) if the FEP is greater than or equal to 35 ug/dl. Children with blood-lead measurements of greater than or equal to 25 /g divided by l, as indicated by the filter-paper method, are recalled for a venous blood-lead measurement. Case-group children are defined as children with venous blood-lead levels of greater than or equal to 25 ug/dl and ZPP or FEP levels of greater than or equal to 35 ug/dl. In addition, children's capillary blood-lead levels of greater than or equal to 70 ug/dl and FEP of greater than or equal to 110 ug/dl or with capillary blood-lead levels of greater than or equal to 50 ug/dl and FEP of greater than or equal to 250 ug/dl are tentatively registered as cases, pending the venous blood-lead level.

Because laboratory tests for lead toxicity reported to BLPC include follow-up tests, estimates of the number of persons screened are obtained by multiplying the number of tests by 0.92, the estimated proportion of tests that are screening tests (BLPC, unpublished data). These estimates were used in this report to compute "case-detection rates"--cases per 100 persons screened. Age- and race-specific estimates of persons screened were not available. Age- and race-specific enrollment data were available for city clinics and hospitals where a previous study showed that approximately 75% of active patients 9 months through 6 years of age were screened at least annually (BLPC, unpublished data). These data were used to compute case/enrollment ratios for children 9 months through 5 years of age seen at such facilities. RESULTS

In 1988, an estimated 229,365 New York City children had screening tests for lead poisoning that were reported to BLPC. Among these children, 694 new cases of lead poisoning were detected (Table 1). Private laboratories reported an additional 102 new cases to BLPC. Screening conducted at city clinics and hospitals accounted for 375 cases (47% of all cases identified). BLPC door-to-door screening identified less than 10% of cases but yielded the highest case-detection rate (1.17 cases per 100 children screened).

In most new cases (61%), the children had blood-lead levels between 25 and 34 ug/dl (Figure 1). Thirteen percent had blood-lead levels of greater than or equal to 50 ug/dl, levels that may be associated with overt symptoms (14). In addition to these new cases, in 545 cases identified before 1988, the children had at least one blood-lead level of greater than or equal to 25 ug/dl measured in 1988. These "previous/active" cases included children still undergoing treatment, children whose homes had not yet undergone abatement for lead-based paint, and children whose blood-lead levels remained elevated after household abatement.

In 1988, 1- and 2-year-old children accounted for 61% of all lead-poisoning cases (Figure 2). The age distribution for all cases was closely paralleled by that for cases identified at city clinics and hospitals. The case/enrollment ratio in the latter group peaked among 2-year-olds at 0.3 cases per 100 children enrolled.

More than three-fourths of all cases identified occurred among black (59%) or Hispanic (28%) children (Table 2). A similar racial distribution was noted among cases identified at city clinics and hospitals, where the case/enrollment ratio among black children (0.23 cases per 100 enrolled) was nearly four times that among white children (0.06 cases per 100 enrolled). The highest case/enrollment ratio (0.30) was observed in the "other" racial/ethnic category. Asians and Pacific Islanders accounted for 41% of "other" children enrolled at city clinics and hospitals; the BLPC case registry does not include a separate category for Asians or Pacific Islanders.

BLPC data indicated that the number of children screened annually was 27% greater in 1989 than in 1986, the first full year in which current lead-poisoning criteria were used (Figure 3). During this same period, the annual number of new cases decreased by 30%, from 1,284 to 897; however, a 15% increase in the number of children screened from 1988 through 1989 was associated with a 13% increase in new cases. The number of previously identified cases in which the child had measured blood-lead levels of greater than or equal to 25 ug/dl decreased each year during the period. DISCUSSION

BLPC data indicate that childhood lead poisoning is a persistent public health problem in New York City, as it is in many other cities (1). Because of certain limitations of BLPC data, the magnitude of excessive lead absorption among children in New York City is underestimated. First, not all children in the high-risk age group (9 months through 5 years of age) are screened. The screening coverage for children receiving care from non-city-affiliated providers is unknown, but it probably is lower than the estimated 75% coverage at city-affiliated facilities. In most new cases (87%) identified by BLPC, the children had blood-lead levels that were toxic but too low to cause overt symptoms. Such cases would not be detected without screening. Second, the principal screening methods that were used miss a substantial proportion of children with elevated blood-lead levels. Estimated false-negative rates for FEP and ZPP screening range from 30% (CDC, unpublished data) to greater than 50% (15). Third, the current CDC case definition of lead poisoning (6) excludes children with blood-lead levels between 10 and 24 ug/dl. Recent research has linked such levels with adverse effects in children (5), and the CDC case definition will soon be revised to reflect these findings.

An advantage of the fixed-site screening methods used in New York City is that large numbers of children can be screened efficiently by primary-care providers during routine pediatric care. However, high-risk children with limited access to primary care may be missed by such screening. The BLPC experience suggests that door-to-door screening in selected neighborhoods may be a useful, though time-consuming, way of detecting cases missed by fixed-site screening.

BLPC surveillance data are consistent with national data showing that children ages 6 months through 2 years are at highest risk of lead poisoning (9). Toddlers are especially liable to ingest lead in contaminated environments because of normal mouthing behavior and increased hand contact with dirt and dust (8). Children in this age group are also more susceptible than older children to lead-related neurobehavioral toxicity (3).

The predominance of black and Hispanic children in the case group in New York City is partly attributable to the racial and ethnic composition of children served by city-affiliated clinics and hospitals. The distribution of cases by racial/ethnic group probably also reflects an increased risk of lead poisoning among black and Hispanic children, suggested by higher ratios of cases to enrolled children in those groups compared with whites. Data from the Second National Health and Nutrition Examination Survey indicate that black children have a higher prevalence of elevated blood-lead levels than white children, regardless of age, household income, or degree of urbanization (9). In 1984, black children accounted for an estimated 60% of children in SMSAs with blood lead-levels greater than 25 ug/dl (1).

The decrease in annual case counts over time is consistent with the experience of CLPPPs nationally (1). Previous screening and abatement activities have addressed lead paint hazards in only a small proportion of homes with leaded paint and therefore cannot account entirely for this trend. For example, in 1984, approximately 422,800 New York City children 6 months through 5 years of age lived in housing constructed before 1950, most of which still contains leaded paint (1). Intensive education efforts and decreased contributions to blood-lead levels from other sources, especially leaded gasoline (16), probably account for some of the decrease in lead poisoning cases.

Although surveillance data indicate that blood-lead levels and the incidence of lead poisoning are decreasing, recent research has identified adverse health effects at blood-lead levels previously thought to be safe (5). As a result, the recognized public health burden of lead poisoning among children remains large. More intensive screening and abatement efforts are needed to eliminate blood-lead levels greater than or equal to 25 ug/dl in New York City children. Addressing the larger numbers of children with toxic blood-lead levels less than 25 ug/dl will require a still greater commitment of resources.

References

1. Agency for Toxic Substances and Disease Registry. The nature

and extent of lead poisoning in children in the United States: a report to Congress. Atlanta, Georgia: US Department of Health and Human Services, 1988.

2. Needleman HL, Schell A, Bellinger D, Leviton A, Allred EN. The long-term effects of exposure to low doses of lead in childhood, an 11-year follow-up report. N Engl J Med 1990;322:83-8.

3. McMichael AJ, Baghurst PA, Wigg NR, Vimpani GV, Robertson EF, Roberts RJ. Port Pirie cohort study: environmental exposure to lead and children's abilities at the age of four years. N Engl J Med 1988;319:468-75.

4. Bellinger D, Leviton A, Waternaux C, Needleman H, Rabinowitz M. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development. N Engl J Med 1987;316:1037-43.

5. Mushak P, Davis JM, Crocetti AF, Grant LD. Prenatal and postnatal effects of low-level lead exposure: integrated summary of a report to the US Congress on childhood lead poisoning. Environ Res 1989;50:11-36.

6. CDC. Preventing lead poisoning in young children, a statement by the Centers for Disease Control. Atlanta, Georgia: US Department of Health and Human Services, 1985.

7. Clark CS, Bornschein RL, Succop P, Que Hee SS, Hammond PB, Peace B. Condition and type of housing as an indicator of potential environmental lead exposure and pediatric blood lead levels. Environ Res 1985;38:46-53.

8. Bellinger D, Leviton A, Rabinowitz M, Needleman H, Waternaux C. Correlates of low-level lead exposure in urban children at 2 years of age. Pediatrics 1986;77:826-33.

9. Mahaffey KR, Annest JL, Roberts J, Murphy RS. National estimates of blood lead levels: United States, 1976-1980: association with selected demographic and socioeconomic factors. N Engl J Med 1982;307:573-9. 10. Lin-Fu JS. Lead poisoning and undue lead exposure in children: history and current status. In: Needleman HL, ed. Low level lead exposure: the clinical implications of current research. New York: Raven Press, 1980:5-16. 11. Blumberg WE, Eisinger J, Lamola AA, Zuckerman DM. The hematofluorometer. Clin Chem 1977;23:270-4. 12. Davidow B, Slavin G, Piomelli S. Measurement of free erythrocyte protoporphyrin in blood collected on filter paper as a screening test to detect lead poisoning in children. Ann Clin Lab Sci 1976;6:209-13. 13. Joselow NM, Bogden JD. A simplified micro method for the collection and determination of lead in blood using a paper disk-in-Delves cup technique. Atom Absorpt Newsl 1972;11:99-101. 14. Piomelli S, Rosen JF, Chisolm JJ, Graef JW. Management of childhood lead poisoning. J Pediatr 1984;105:523-32. 15. Mahaffey KR, Annest JL. Association of erythrocyte protoporphyrin with blood lead levels and iron status in the Second National Health and Nutrition Examination Survey, 1976-1980. Environ Res 1986;41:327-38. 16. Annest JL, Pirkle JL, Makuc D, Neese JW, Bayse DD, Kovar MG. Chronological trend in blood lead levels between 1976 and 1980. N Engl J Med 1983;308:1373-7.

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