|
|
||||||||
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.
| INTRODUCTION |
|---|
|
|
|---|
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.
| METHODS |
|---|
|
|
|---|
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.
| RESULTS |
|---|
|
|
|---|
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).
|
| DISCUSSION |
|---|
|
|
|---|
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.
| Acknowledgments |
|---|
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.
| Footnotes |
|---|
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.
| References |
|---|
|
|
|---|
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;237:12791284.
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 1995:5.35.41, 7.57.64. Publication HUD-1539-LBP.
4. Vostal JJ, Taves E, Sayre JW, Charney E. Lead analysis of house dust: a method for the detection of another source of lead exposure in inner city children. Environ Health Perspect. 1974;7:9197.[Medline]
5. Lanphear BP. The paradox of lead poisoning prevention. Science. 1998;281:617618.
6. Schlenker TL, Fritz CJ, Mark D, et al. Screening for pediatric lead poisoning. Comparability of simultaneously-drawn capillary and venous blood samples. JAMA. 1994;271:13461348.[Abstract]
7.
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;80:12401245.
8. Schwartz J, Levin R. The risk of lead toxicity in homes with lead paint hazard. Environ Res. 1991;54:17.[Medline]
9. McMichael AJ, Baghurst PA, Robertson EF, Vimpani GV, Wigg NR. The Port Pirie cohort study. Blood lead concentration in early infancy. Med J Aust. 1985;143:499503.[Medline]
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;15:3744.[Medline]
11. Clark S, Bornschein R, Succop P, Roda S, Peace B. Urban lead exposures of children in Cincinnati, Ohio. Chem Speciation Bioavailability. 1991;3:163171.
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;67:125148.[Medline]
13.
Lanphear BP, Weitzman M, Eberly S. Racial differences in urban children's environmental exposures to lead. Am J Public Health. 1996;86:14601463.
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |