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© 2001 American Public Health Association
RESEARCH |
At the time of the study, Vijayalakshmi Potula was with the Department of Environmental Health, Harvard School of Public Health, Boston, Mass. Margaret Hegarty-Steck is with Lead-Safe Cambridge, Cambridge Community Development Department, Cambridge, Mass. Howard Hu is with the Department of Environmental Health, Harvard School of Public Health, and Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Mass.
Correspondence: Requests for reprints should be sent to Vijayalakshmi Potula, PhD, Epidemiology and Surveillance Branch, Agency for Toxic Substances and Disease Registry, Executive Park, Building 4, 1600 Clifton Rd, Mail Stop E-31, Atlanta, Ga 30333.
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INTRODUCTION |
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 TOP INTRODUCTION METHODSRESULTSDISCUSSIONReferences |
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In the United States, 42 million dwellings contain lead paint and 1.8 million children live in homes with deteriorating lead paint. Fifty-two percent of all residential housing units have lead paint at concentrations of 0.7 mg/cm2 or higher.1 These community exposures to lead may cause adverse effects in children, such as alterations in heme synthesis and neuropsychological deficits resulting in decreased IQ, behavioral changes, and impaired school performance.2
The goal of this pilot study was to use data from a federally sponsored lead-based-paint hazard control program to compare the correlation of various measures of paint lead and dust lead with elevated blood lead levels among children living in homes built before the 1940s, after controlling for demographic factors.
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METHODS |
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TOPINTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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Study Population and Data Collection
All children were from families who volunteered to participate in the Lead-Safe Cambridge Program. This residential lead hazard control program is administered by the City of Cambridge (Massachusetts) Community Development Department in partnership with the Cambridge Hospital; it receives funding from the US Department of Housing and Urban Development (HUD).
Lead Sampling Protocol and Analysis
Leaded paint inspection and sampling3 was performed in accordance with the Massachusetts Lead Law on interior painted components, common areas in multifamily units, and exterior painted components. Interior dust samples were collected from the floors, interior windowsills, and window wells. Sample preparation and collection were performed by the method of Vostal et al.4 The dust wipe method used in the present study measures lead loading as micrograms of lead per unit of surface area,3 a measure that is better than dust lead concentrations (i.e., micrograms of lead per gram of dust)5 for predicting children's blood lead levels. All dust samples were analyzed according to Environmental Protection Agency SW-846 Method 7420 for flame atomic absorption spectrophotometry. Blood lead screening6 was conducted in participants' homes by appointment, and blood samples were collected by finger-stick by a registered nurse from Lead-Safe Cambridge. Blood lead samples were sent to the State Laboratory Institute (participants in the Wisconsin and New York lead proficiency testing programs) at the Massachusetts Department of Public Health for lead analysis by graphite furnace atomic absorption spectrophotometry (Perkin-Elmer, Boston, Mass). Typical accuracy and precision (relative standard deviation [%]) values for the blood lead measurements in quality control analyses were ±1 µg/dL and 2% to 3%, respectively.
Data analysis in this cross-sectional study focused on blood lead as a dependent variable, with age, tenure status (owner occupied or rental), sex, race/ethnicity, and environmental lead values as independent variables. A multivariate linear regression model was constructed, beginning with a model including all the potential predictors and proceeding by backward elimination with a cutoff of P < .05.
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RESULTS |
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TOPINTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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The children (59 subjects from 44 homes) were aged 6 months to 6 years (mean age = 2.7 years) and living in housing built before the 1940s. Of the 59 children, 50 (85%) were from families who rented their homes, 24 (41%) were White, and 30 (51%) were girls.
The mean blood lead level in the children (n = 59) was 9.74 µg/dL. Thirty percent of the children (n = 18) had blood lead levels greater than the Centers for Disease Control and Prevention standard of 10 µg/dL. Paint and dust samples had high mean lead levels, with many values exceeding health-based standards. Mean paint lead levels (mg/cm2) were 5.04, 5.77, and 7.03 for interior, common, and exterior areas, respectively. Mean dust lead levels (µg/ft2) were 183.14, 221.85, and 11 670.9 for floors, windowsills, and window wells, respectively.
In the final multivariate regression model of blood lead that began with age, race/ethnicity, sex, tenure status, and all the environmental variables, the variables that remained after backward elimination (P < .05) were interior window trough dust lead and lower age (Table 1
). The total R2 of the model was 0.39 (n = 20).
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DISCUSSION |
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TOPINTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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This study found interior dust lead and lower age to be the strongest predictors of blood lead in children. Regardless of a building's condition, window wells are reservoirs for lead dust, with concentrations that are typically several orders of magnitude higher than those in other locations.7,8 Blood lead levels among children typically rise until the age of 18 to 27 months, plateau, and then decline as the mouthing of foreign objects decreases.2,9–11 The roles of leaded dust in window wells and of mouthing behaviors in children aged 18 to 27 months12,13 present a compelling case for addressing windows as a primary prevention measure.
This pilot study has several limitations. First, the sample population screened for the study was small, and it consisted of an urban population of predominantly African American and Hispanic children living in deteriorating older housing. Hence, the results may not be generalizable to other groups. Second, we did not include soil lead or nutritional and other factors that could act as potential confounders. Despite these limitations, however, this pilot study reveals the importance of more complete abatement of lead dust on window units and more effective cleanup to remove lead-bearing dust, particularly in homes where younger children live. In addition, the study demonstrates the feasibility of performing research with data from abatement projects supported by HUD.
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Acknowledgments |
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Support for this research was provided by NIEHS grants T32 ES07069 and P42-ES05947 and NIEHS center grant 2 P30 ES00002. Lead-Safe Cambridge Program funding was provided by the US Department of Housing and Urban Development Office of Lead Hazard Control and administered through the City of Cambridge Community Development Department.
We gratefully acknowledge the research assistance of Catherine M. Mitchell, Alicia A. Morris, Marissa Barr, Julie Nassif (from the State Laboratory Institute), and Soma Datta. Julie McCoy provided editorial assistance with the manuscript.
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Footnotes |
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Note. This article's contents are solely the responsibility of the authors and do not necessarily represent the official views of the National Institute of Environmental Health Sciences (NIEHS), National Institutes of Health.
V. Potula planned the study, analyzed the data, and wrote the paper. M. Hegarty-Steck directed the Lead-Safe Cambridge Program, which examined all participants and conducted the sample analysis. H. Hu supervised the design and data analysis and contributed to the writing of the paper.
Accepted for publication May 21, 2001.
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References |
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TOPINTRODUCTIONMETHODSRESULTSDISCUSSIONReferences |
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1. The Nature and Extent of Lead Poisoning in Children in the United States: A Report to Congress. Atlanta, Ga: Agency for Toxic Substances and Disease Registry, Public Health Service; July 1988.
2. Baghurst PA, McMichael AJ, Wigg NR, et al. Environmental exposure to lead and children's intelligence at the age of seven years. N Engl J Med. 1992;237:1279–1284.
3. Guidelines for the Evaluation and Control of Lead-Based Paint Hazards in Housing. Washington, DC: US Dept of Housing and Urban Development, Office of Lead-Based Paint Abatement and Poisoning Prevention; July 1995:5.3–5.41, 7.5–7.64. Publication HUD-1539-LBP.
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5. Lanphear BP. The paradox of lead poisoning prevention. Science. 1998;281:617–618.
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Schlenker TL, Fritz CJ, Mark D, et al. Screening for pediatric lead poisoning. Comparability of simultaneously-drawn capillary and venous blood samples. JAMA. 1994;271:1346–1348.
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Farfel MR, Chisolm J. Health and environmental outcomes of traditional and modified practices for abatement of residential lead-based paint. Am J Public Health. 1990;80:1240–1245.
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10. Dietrich KN, Berger OG, Succop PA, Hammond PB, Bornschein RL. The developmental consequences of low to moderate prenatal and postnatal lead exposure. Intellectual attainment in the Cincinnati Lead Study Cohort following school entry. Neurotoxicol Teratol. 1993;15:37–44.[Medline]
11. Clark S, Bornschein R, Succop P, Roda S, Peace B. Urban lead exposures of children in Cincinnati, Ohio. Chem Speciation Bioavailability. 1991;3:163–171.
12. Aschengrau A, Belser A, Bellinger D, Copenhafer D, Weitzman M. The impact of soil lead abatement on urban children's blood lead levels, phase II: results from the Boston Lead-in-Soil Demonstration Project. Environ Res. 1994;67:125–148.[Medline]
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Lanphear BP, Weitzman M, Eberly S. Racial differences in urban children's environmental exposures to lead. Am J Public Health. 1996;86:1460–1463.
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