April 7, 1993, Vol 269, No. 13 >

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ARTICLE | April 7, 1993

Lead-Contaminated Soil Abatement and Urban Children's Blood Lead Levels FREE

Michael Weitzman, MD; Ann Aschengrau, ScD; David Bellinger, PhD; Ronald Jones; Julie Shea Hamlin, MPH; Alexa Beiser, PhD

[+] Author Affiliations

These findings were reported to the Environmental Protection Agency in July 1992. This article has not been subjected to the agency's peer and administrative review and therefore may not necessarily reflect the views of the agency, and no official endorsement should be inferred.

Reprint requests to Department of Pediatrics, Rochester General Hospital, 1425 Portland Ave, Rochester, NY 14621 (Dr Weitzman).

JAMA. 1993;269(13):1647-1654. doi:10.1001/jama.1993.03500130061033

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ABSTRACT

ABSTRACT | REFERENCES

Objective. —To test the hypothesis that a reduction of 1000 ppm or more of lead in soil accessible to children would result in a decrease of at least 0.14 μmol/L (3 μg/dL) in blood lead levels.

Setting. —Urban neighborhoods with a high incidence of childhood lead poisoning and high soil lead levels.

Design. —Randomized controlled trial of the effects of lead-contaminated soil abatement on blood lead levels of children followed up for approximately 1 year after the intervention.

Patients. —A total of 152 children less than 4 years of age with venous blood lead levels of 0.34 to 1.16 μmol/L (7 to 24 μg/dL). Children were largely poor and had a mean age at baseline of 32 months, a mean blood lead level of 0.60 μmol/L (12.5 μg/dL), and a median surface soil lead level of 2075 ppm.

Interventions. —Children were randomized to one of three groups: the study group, whose homes received soil and interior dust abatement and loose paint removal; comparison group A, whose homes received interior dust abatement and loose paint removal; and comparison group B, whose homes received only interior loose paint removal.

Main Outcome Measures. —Change in children's blood lead levels from preabatement levels to levels approximately 6 and 11 months after abatement.

Results. —The mean decline in blood lead level between preabatement and 11 months after abatement was 0.12 μmol/L (2.44 μg/dL) in the study group (P=.001), 0.04 μmol/L (0.91 μg/dL) in group A (P=.04), and 0.02 μmol/L (0.52 μg/mL) in group B (P=.31). The mean blood lead level of the study group declined 0.07 μmol/L (1.53 μg/dL) more than that of group A (95% confidence interval [CI], -0.14 to -0.01 μmol/L [-2.87 to -0.19 μg/dL]) and 0.09 μmol/L (1.92 μg/dL) more than group B (95% CI, -0.16 to -0.03 μmol/L [-3.28 to -0.56 μg/dL]). When adjusted for preabatement lead level, the 11-month mean blood lead level was 0.06 μmol/L (1.28 μg/dL) lower in the study group as compared with group A (P=.02) and 0.07 μmol/L (1.49 μg/dL) lower than in group B (P=.01 ). The magnitude of the decline independently associated with soil abatement ranged from 0.04 to 0.08 μmol/L (0.8 to 1.6 μg/dL) when the impact of potential confounders, such as water, dust, and paint lead levels, children's mouthing behaviors, and other characteristics, was controlled for.

Conclusions. —These results demonstrate that lead-contaminated soil contributes to the lead burden of urban children and that abatement of lead-contaminated soil around homes results in a modest decline in blood lead levels. The magnitude of reduction in blood lead level observed, however, suggests that lead-contaminated soil abatement is not likely to be a useful clinical intervention for the majority of urban children in the United States with low-level lead exposure.(JAMA. 1993;269:1647-1654)

REFERENCES

ABSTRACT | REFERENCES

References 4, 7-12, 14-16,19, 20, 23, 26-28.

Needleman HL, Gatsonis CA. Low-level lead exposure and the IQ of children. JAMA . 1990;;263: 673-678.

Weitzman M, Glotzer D. Lead poisoning. Pediatrics Rev . 1992;;13:461-468.

Centers for Disease Control. Preventing Lead Poisoning in Young Children: A Statement by the Centers for Disease Control . Atlanta, Ga: US Dept of Health and Human Services; October 1991;.

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, Ga: US Dept of Health and Human Services, Public Health Service; 1988;.

Environmental Defense Fund. Legacy of Lead: America's Continuing Epidemic of Childhood Lead Poisoning . Washington, DC: Environmental Defense Fund; 1990;.

Barltrop D, Meek F. Effect of particle size on lead absorption from the gut. Arch Environ Health . 1979;;34:280-285.

Sayre JW, Charney E, Vostal J, Pless JB. House and hand dust as a potential source of childhood lead exposure. AJDC . 1974;;127:167-170.

Charney E, Sayre JW, Coulter M. Increased lead absorption in inner city children: where does the lead come from? Pediatrics . 1980;;65:226-231.

Charney E, Kessler B, Farfel M, Jackson D. Childhood lead poisoning: a controlled trial of the effect of dust-control measures on blood lead levels. N Engl J Med . 1983;;309:1089-1093.

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.

Bornschein RL, Succop PA, Kratt KM, Clark CS, Peace B, Hammond PB. Exterior surface dust lead, interior house dust lead and childhood lead exposure in an urban environment. In: Hemphill DD, ed. Trace Substances in Environmental Health , XX: Proceedings of University of Missouri's 20th Annual Conference. Columbia: University of Missouri; 1987;:322-332.

Environmental Protection Agency. Air Quality Criteria for Lead . Washington, DC: Environmental Protection Agency; 1977;. Publication 600/ 8-77-017; chapt 12 :36.

Rabin R. Warnings unheeded: a history of child lead poisoning. Am J Public Health . 1989;;79:1668-1674.

Yaffe Y, Flessel CP, Wesolowski JJ, del Rosario A, Guirguis GN, Matias V. Identification of lead sources in California children using the stable isotope ratio technique. Arch Environ Health . 1983;; 38:237-245.

Mielke HW, Anderson JC, Berry KJ, Mielke PW, Chaney RL, Leech M. Lead concentrations in inner-city soils as a factor in the child lead problem. Am J Public Health . 1983;;73:1366-1369.

Duggan MJ, Inskip MJ. Childhood exposure to lead in surface dust and soil: a community health problem. Public Health Rev . 1985;;13:1-54.

Chisolm JJ. Removal of lead paint from old housing: the need for a new approach. Am J Public Health . 1986;;26:236-237.

Clark CS, Bornschein RL, Succop P, et al. Pathways to elevated blood lead and their importance in control strategy development. In: Lindberg SE, Hutchinson TC, eds. International Conference: Heavy Metals in the Environment . New Orleans, La: CEP Consultants Ltd; 1987;:159-161.

Landrigan PJ, Gehlbach SH, Rosenblum BF, et al. Epidemic lead absorption near an ore smelter: the role of particulate lead. N Engl J Med . 1975;; 292:123-129.

Barltrop D, Strehlow CD, Thornton I, Webb JS. Absorption of lead from dust and soil. Postgrad Med J . 1975;;51:801-804.

Schneider DJ, Lavenhar MA. Lead poisoning: more than a medical problem. Am J Public Health . 1986;;76:242-244.

Jones R, Guitirrez L, Rabin R, Gonzales M, Weitzman M. The geography of childhood lead poisoning and new preventive strategies. In: Stone EM, Donahue CL, eds. Mothers, Infants, and Children at Risk . Waltham: Massachusetts Health Data Consortium; 1989;:121-127.

Rabinowitz M, Leviton A, Needleman H, Bellinger D, Wateraux C. Environmental correlates of infant blood lead levels in Boston. Environ Res . 1985;;38:96-107.

Colton TC. Statistics in Medicine . Boston, Mass: Little Brown & Co Inc; 1974;:122-123.

Miller D, Paschal D, Gunter E, Stroud P, D'Angelo J. Determination of lead in blood using electrothermal atomization atomic absorption spectrometry with a l'vov platform and matrix modifier. Analyst . 1987;;112:1701-1704.

Roels HA, Buchet JP, Lauwerys RR, et al. Exposure to lead by the oral and the pulmonary routes of children living in the vicinity of a primary lead smelter. Environ Res . 1980;;22:81-94.

Angle CR, Marcus A, Cheng IH, Mclntire MS. Omaha childhood blood lead and environmental lead: a linear total exposure model. Environ Res . 1984;; 35:160-170.

Mielke H, Blake B, Burroughs S, Hassinger N. Urban lead levels in Minneapolis: the case of the Hmong children. Environ Res . 1984;;34:64-76.

Rabinowitz M, Bellinger D. Soil lead-blood lead relationship among Boston children. Bull Environ Contam Toxicol . 1988;;44:791-797.

Bornschein R, Hammond P, Dietrich K, et al. The Cincinnati Prospective Study of low-level lead exposure and its effects on child development: protocol and status report. Environ Res . 1985;;38:4-18.

McMichael A, Baghurst P, Robertson E, Vimpani G, Wigg N. The Port Pirie Cohort Study: blood lead concentrations in early childhood. Med J Aust . 1985;;143:499-503.

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Country-Specific Mortality and Growth Failure in Infancy and Yound Children and Association With Material Stature

Use interactive graphics and maps to view and sort country-specific infant and early dhildhood mortality and growth failure data and their association with maternal