Published online January 4, 2006
PEDIATRICS Vol. 117 No. 1 January 2006, pp. 147-153 (doi:10.1542/peds.2004-2880)
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My File Cabinet
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Brown, M. J.
Right arrow Articles by Simon, P.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Brown, M. J.
Right arrow Articles by Simon, P.
Related Collections
Right arrow Therapeutics & Toxicology
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?

ARTICLE

A Randomized, Community-Based Trial of Home Visiting to Reduce Blood Lead Levels in Children

Mary Jean Brown, ScD, RNa, Pat McLaine, RN, MPHb, Sherry Dixon, PhDb and Peter Simon, MD, MPHc

a Lead Poisoning Prevention Branch, Division of Emergency and Environmental Health Services, National Center for Environmental Health, Centers for Disease Control and Prevention, Atlanta, Georgia
b National Center for Healthy Housing, Columbia, Maryland
c Department of Family Health, Rhode Island Department of Health, Providence, Rhode Island


    ABSTRACT
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
OBJECTIVE. The objective of this study was to measure the effectiveness of intensive case management to reduce blood lead levels (BLLs) in children. Lead poisoning remains a common, preventable pediatric condition despite advances in reducing children's BLLs in the United States. Substantial evidence implicates lead paint–contaminated house dust as the most common high-dose source of lead in children's environments. Housekeeping and parental supervision also may contribute to risk for lead exposure.

METHODS. We conducted a community-based, randomized trial of comprehensive education and home visiting for families of children with BLLs 15 to 19 µg/dL. BLLs after 1 year of follow-up were compared for intervention group children, whose families received individualized education that was designed to address specific risks factors in a child's environment, and comparison group children, whose families received customary care, usually 1 or 2 educational visits. Environmental samples were collected at baseline and after 1 year of follow-up for intervention group children and compared with those of comparison group children, collected only at the end of study.

RESULTS. During the follow-up period, parents of intervention group children (n = 92) successfully decreased dust lead levels and significantly improved parent-child interaction and family housekeeping practices compared with comparison group children (n = 83). Overall geometric mean BLLs declined by 47%, and the difference in BLL by group was not significant (9 vs 8.3 µg/dL for intervention versus comparison group children, respectively.) After 1 year, nearly half of enrolled children had BLLs ≥10 µg/dL.

CONCLUSIONS. Until a reservoir of lead-safe housing is created, programs that educate families to reduce environmental exposure are needed. Although providing families with quantitative information regarding lead contamination may have a role in short-term efforts to prevent lead exposure, these null findings suggest that it has little benefit once BLLs are elevated.


Key Words: lead poisoning • home visiting • case management

Abbreviations: BLL—blood lead level • NCATS—Nurse Child Assessment Satellite Teaching Scale • GM—geometric mean • CI—confidence interval

The serious consequences of lead exposure during childhood have been reviewed systematically since 1943, when Byers and Lord1 first presented data on school failure for 20 children who had been hospitalized for lead ingestion in early infancy. In the 60 years after this publication, a compelling body of data that demonstrates that lead exposure in early childhood compromises children's later intellectual development and life achievement has been accumulated.211 No blood lead level threshold below which children are safe from the adverse effects of lead exposure has been identified.12,13

Efforts to reduce blood lead levels (BLLs) in the United States have been a resounding public health success.14 However, an unacceptable number of children are exposed to lead each year. Specific populations and regions experience disproportionately high levels of lead poisoning, particularly young, black, and central-city residents.1517

Substantial evidence implicates lead paint–contaminated house dust, ingested during normal mouthing behaviors, as the major source of lead exposure for young children in the United States.1822 Interventions that are designed to reduce lead contamination in house dust and limit children's access to residential lead hazards usually are implemented after identification of a lead-poisoned child. The efficacy of these interventions remains an open question. Initial retrospective reports of parental education and empowerment were encouraging.23 However, because these were uncontrolled trials with results that depended on retrospective or repeated measure designs, their scientific merit was limited. A number of studies have evaluated house cleaning and parental education interventions to control exposure to leaded house dust. In a randomized trial of the efficacy of regular home cleaning, investigators found that cleaning by professional cleaners, accompanied by maternal education, is safe and partially effective in reducing BLLs.24 However, in 2 trials in which dust control was performed by families, 1 study concluded that education was not effective in preventing lead exposure, and the other found that although 19% of children who received an intensive education later had an elevated BLL versus 27% of control group children, education alone cannot prevent lead burden.25,26 Dust cleanup as a 1-time, low-cost strategy in housing with existing lead paint hazards has proved disappointing as a primary prevention strategy.27 Other factors that are thought to be associated with increased risk for lead poisoning among children include nutritional status, particularly for iron and calcium; the perception that the risk is minor; poor housekeeping and personal hygiene; and inadequate parent-child interaction.28

Here we present the findings of a randomized, community-based trial that was designed to measure the effectiveness of intensive case management to address the behavioral and environmental factors that are thought to affect lead exposure compared with standard case management. This study was approved by the Rhode Island Department of Health, Harvard School of Public Health, and the Centers for Disease Control and Prevention human subjects committees.


    METHODS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
All children who were identified through routine blood lead testing as having venous BLLs 15 to 19 µg/dL and reported to the Rhode Island Department of Health between July 1999 and June 2002 were referred to the study. Families of children who qualified for the study because (1) the child was <28 months of age, (2) the child had a venous BLL of 15 to 19 µg/dL, and (3) the family spoke English or Spanish were invited to participate. A random-numbers table was used to assign cases to either the intervention or the comparison group, sequentially by the study coordinator (M.J.B.). Group assignments were sealed into envelopes and unknown to either study personnel or the families until after parental consent was obtained.29 The nurses who provided follow-up to comparison group children were blinded to whether any given child was a study participant. Nurses who provided care to intervention group children were not blinded as to the child's status.

Intervention Group
Children received a series of 5 home visits during the 1-year follow-up period. Nurses (1) collected interior dust and soil samples using a standardized protocol; (2) evaluated parent-child interaction using the Nurse Child Assessment Satellite Teaching Scale (NCATS), which measures the mother-infant pair sensitivity to cues and the clarity of the mother's communication; and (3) identified occupational or recreational exposure to lead sources and other factors that are thought to influence lead exposure or absorption using a standardized questionnaire first developed by the US Department of Housing and Urban Development and the Centers for Disease Control and Prevention.30 A detailed and individualized nursing care plan directed parent teaching and other services. Families were given the results of all environmental and blood lead testing as soon as these were available.

Comparison Group
Children received customary care, in most cases, in 1 or 2 educational visits by an outreach worker. These visits focused on standard health education about lead poisoning and its prevention but did not include environmental sampling, education tailored to individual circumstances, or standardized assessment of nutrition or parent-child interaction. Data for comparison group children were collected at the end of the follow-up period, when nurses (1) collected interior dust and soil samples, (2) evaluated parent-child interaction, and (3) identified occupational or recreational exposure to lead sources using the tools listed above. Families were given the results of BLL tests and environmental sample results as soon as they were available.

Blood Lead Analysis
Venous blood samples were collected by children's pediatric health care providers and measured by graphite furnace atomic absorption spectroscopy that was conducted by 1 laboratory that had proficiency in blood lead testing and adhered to the Clinical Laboratory Improvement Amendments.

Environmental Lead Analysis
Dust wipes were digested using a method described by the United States Department of Housing and Urban Development.31 Soil was dried, sieved to a particle size of <250 µm, homogenized, and digested using a modified National Institute for Occupational Safety and Health 7082 procedure. Dust wipe and soil digestates were analyzed by flame atomic absorption spectroscopy according to EPA SW846-7420 EPA 239.1. The Hematology and Environmental Laboratory of the University of Cincinnati performed all sample preparation and analysis. The laboratory is accredited by the National Industrial Hygiene Association as an Industrial Hygiene Laboratory and is recognized under the National Lead Laboratory Accreditation Program as an Environmental Lead Laboratory. Consequently, the laboratory participates in the Proficiency Analytical Testing Program and the Environmental Lead Proficiency Analytical Testing Program. The laboratory is certified through the State of New York as a National Environmental Laboratory Accreditation Conference laboratory and participates in the New York proficiency program for environmental sample analytes, including lead.

Data Analysis
Statistical analyses were performed using SAS version 8.02. Because BLLs and dust lead levels were not normally distributed, log transformation was used. BLLs and dust lead levels below the limit of detection were substituted by the limit of detection divided by {surd}2 based on the log-normal distribution of BLLs and dust lead levels. Paired t tests were used to test for a change in mean or geometric mean (GM) within group blood or dust lead values from one sampling time to another. Wilcoxon signed rank test was used to test for a median change in intervention group children's blood and dust lead values from one sampling time to another. Two-sample t tests were used to test for equality of mean (eg, NCATS score) or GM values for intervention versus comparison group children's blood or dust lead values. Wilcoxon rank sum tests were used to test for equality of median values for 2 groups. McNemar's test was used to test for a change in percentage of children with elevated BLLs as well as for a change in the percentage of families with more frequent housekeeping from one sampling time to another. Analysis of variance was used to test for equality of mean or GM values for >2 groups. Cochran-Mantel-Haenszel row-mean-score statistic was used to test for equality of an ordinal response variable in 2 groups. Regression analysis was used to examine predictors of an outcome of interest. Nested models were used to examine predictors of blood or dust lead levels when multiple observations from the same child were included. Survival-type modeling was done using product-limit survival estimates, and a likelihood ratio test was used to test the between-group difference in time from baseline to BLL <10 µg/dL.


    RESULTS
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Of the 241 families with children who were eligible, 175 (73%) consented to participate, and these children were randomly assigned: 83 children to the comparison group and 92 to the intervention group. For the 66 children whose families refused participation, work and school responsibilities were the most frequently cited reasons for nonparticipation. Parents of 2 enrolled children refused the first and all subsequent visits; the families of 9 other children refused to participate at some time during the study, and 2 children were lost to follow-up. Another 9 children moved out of state and were dropped from the study. The odds of not completing the study did not differ significantly between comparison and intervention group children (odds ratio [OR]: 1.4; 95% confidence interval [CI]: 0.6–3.6). Intervention and comparison children also did not differ on factors that are known to affect risk for elevated BLLs (Table 1).


View this table:
[in this window]
[in a new window]

 
TABLE 1 Characteristics of Study Population

 
Dust lead levels significantly decreased, and these decreases were maintained through the follow-up period for the intervention group children. The most significant decreases occurred during the first 3 months of case management. Although decreases were sustained across the 12-month follow-up period and the percentage reduction doubled from 3 to 12 months, few measurements showed statistically significant changes between 3 and 12 months of follow-up. We observed this pattern in homes of all intervention group children, regardless of whether the family moved during the study (data not shown).

Baseline dust lead levels for the intervention group children did not differ significantly from those of the comparison group children collected 1 year after enrollment except that for floors identified as in poor condition. For these floors, dust lead levels of intervention group children were higher than those of comparison group children. However, dust lead levels of the intervention group children, collected 1 year after children were identified, were significantly lower than dust levels of the comparison group children (Table 2).


View this table:
[in this window]
[in a new window]

 
TABLE 2 GM Dust Lead Loadings: Comparison and Intervention Group Homes

 
Reported housekeeping practices at baseline for intervention group children did not differ significantly from those for comparison groups after 1 year of follow-up. After 1 year of participation, intervention group families were significantly more likely than at baseline to report cleaning window sills and wells in the kitchen, child's bedroom, and living room and more likely to vacuum the living room and child's bedroom floor. These differences reflected a change in the reported frequency of damp cleaning for sills (from monthly to every 2 weeks) and for wells (from less than monthly to nearly every 2 weeks). In addition, in the intervention group, the level of cleaning observed by the nurse improved significantly from baseline to the 1-year visit (P = .03).

Parent-child interaction scores did not differ significantly between intervention and comparison group families at the time it was first administered. Intervention group children showed significant improvements over time in NCATS scores. After 1 year of follow-up, NCATS scores for the intervention group were significantly higher than those for the comparison group. Adjusting for child's age when the test was administered did not affect these differences (Table 3).


View this table:
[in this window]
[in a new window]

 
TABLE 3 Comparison of Mean NCATS Scores According to Group

 
Both baseline and 12-month BLLs were measured for 145 (83%) of the 175 children enrolled in the study. The GM BLL at enrollment was 16.5 µg/dL (range: 15–19 µg/dL). The greatest reduction in BLLs occurred within 3 months after baseline, when the GM level fell by 37% to 10.3 µg/dL (interquartile range: 9–14 µg/dL; n = 125). By the end of the 12-month follow-up period, the GM BLL of participant children was 8.7 µg/dL (interquartile range: 7–12 µg/dL; n = 145), a 47% reduction from the baseline mean BLL.

The GM BLL did not differ significantly between intervention and comparison group children at 3, 6, or 12 months after baseline. In addition, the number of children whose last available BLL was ≥10 µg/dL did not differ between the groups: 42 (51%) in the comparison group versus 46 (51%) in the intervention group children. The percentage of children with any BLL ≥20 µg/dL also did not differ between groups (9 [11%] vs 7 [8%], comparison versus intervention group, respectively). Finally, no difference existed between the 2 groups in the time from baseline level to BLL <10 µg/dL (Fig 1).


Figure 1
View larger version (8K):
[in this window]
[in a new window]

 
FIGURE 1 Comparison of GM BLLs: intervention group versus comparison group.

 

    DISCUSSION
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Mouthing and other normal behaviors for children who are younger than 2 years result in high risk for exposure to lead in house dust. However, resources often are not available to remove lead paint permanently from children's environments, and legitimate concern exists that inexpert removal of lead paint hazards will result in more widespread contamination.3235 As a result, there has been a protracted search for inexpensive, low-technology interventions that would reduce BLLs by reducing house dust lead levels and mitigating other factors that are thought to influence lead absorption, particularly for children who have elevated BLLs and are not candidates for chelation therapy.

The few randomized trials of parent education and rigorous housekeeping to reduce BLLs once they are elevated have found either only modest improvements (a reduction of BLLs of 17% in the intervention group) or no difference in children's BLLs between children who received and did not receive the intervention.24,25 Furthermore, concern exists that families could not on their own successfully reduce environmental lead contamination and maintain lower dust lead levels over time.36 In 1 study of education to prevent lead burden in children, the likelihood of an elevated BLL was reduced by 34% in intervention compared with control group children, but the effect was of borderline significance.26 In addition, although dust samples were collected in both intervention and control group homes, whether the decrease in risk for elevated BLLs is the result of changes in dust lead measurements over time was not reported.26

In this study, we found that within a primarily low-income, urban, minority population living in old, deteriorated housing, families who were informed of the dust lead levels and apprised of their success in lowering these levels over time were capable of the sustained effort that this required, whereas families who were educated about the dangers of lead dust but not given objective data about the extent of the contamination or feedback on their efforts to reduce it were not. We also found that families were willing to participate actively in efforts to reduce environmental lead levels; when families who moved out of state are excluded, fewer than 5% of families who were enrolled in this study dropped out before the end of their participation period.

The nurse case managers also helped families move toward a more supportive interaction and communication pattern with their children. This intriguing finding requires additional research for several reasons. First, higher NCATS parents' scores correlate significantly with subsequent measures of children's cognitive abilities, although the effect of improvements in the scores has not been examined over time.37 Second, in experimental animal models, enrichment of the laboratory environment has increased brain mass across the animals' lifespan and, more recently, in rat models reversed the cognitive and molecular deficits that were induced by lead exposure during infancy.38

Until a reservoir of lead-safe housing is created, programs that educate families how to reduce dust lead levels are needed. However, although we demonstrated that a home visiting program that provides families with quantitative information regarding lead contamination can enable parents to reduce significantly dust lead levels, we could not demonstrate that this reduced BLLs of moderately poisoned children more than a less intensive strategy that did not result in decreased dust lead levels. In addition, after 1 year, nearly half of the enrolled children still had BLLs ≥10 µg/dL, the level targeted for elimination by the end of the decade.

It may be that the customary care provided to the children in the comparison group was sufficient to educate parents about the dangers of lead exposure and methods to reduce or limit children's access to residential hazards. However, given that dust lead levels at enrollment for intervention group children did not differ significantly compared with those of comparison group children collected at the end of the study, we have no evidence that the change in BLL was related to changes in the level of residential contamination. In addition, if customary care effectively reduced BLLs, then we would not expect nearly half of enrolled children to have BLLs ≥10 µg/dL a year after enrollment. It seems more likely that these findings are the result of developmental changes, primarily decreased hand-to-mouth behaviors as the children aged, coupled with bone lead mobilization as exposure to exogenous lead sources decreased, factors that presumably occurred equally in both groups. In a recent report of 3 lead-poisoned children, researchers estimated that up to 90% of lead in blood may be the result of mobilized skeletal lead depending on the child's age and exposure history.39

These findings also indicate that the benefits of programs that rely solely on interventions to reduce environmental lead contamination after children are exposed are limited. The nation should focus on developing and testing primary prevention strategies that protect children from becoming lead poisoned.


    ACKNOWLEDGMENTS
 
This work was sponsored in part by Centers for Disease Control and Prevention grant TS 275 14/14 and Maternal and Child Health Bureau grant 5T76 MC 00001 (formerly MCJ201).

Our thanks go to Kristine Campagna, Beth Graziano, RN, and Sue Ferreira, RN, VNA, of Care New England; Crystal Evans, National Center for Lead Safe Housing; and Dr Tom Matté and Tim Morta, Centers for Disease Control and Prevention, without whom this work could not have been conducted. We deeply appreciate the time and effort of the families who participated.


    FOOTNOTES
 
Accepted Jun 27, 2005.

Address correspondence to Mary Jane Brown, ScD, RN, Lead Poisoning Prevention Branch, Centers for Disease Control and Prevention, 4770 Buford Hwy, NE (MS-F40), Atlanta, GA 30341. E-mail: mjb5{at}cdc.gov

The findings and conclusions in this report are those of the author(s) and do not necessarily represent the views of the funding agency.

The authors have indicated they have no financial relationships relevant to this article to disclose.


    REFERENCES
 TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

  1. Byers RK, Lord EE. Late effects of lead poisoning on mental development. Am J Dis Child. 1943;66 :471 –494
  2. Bellinger D, Leviton A, Waternaux C, Needlemand H, Rabinowitz R. Longitudinal analyses of prenatal and postnatal lead exposure and early cognitive development. N Engl J Med. 1987;316 :1037 –1043[Abstract]
  3. Dietrich K, Krafft K, Bornschein R, et al. Low-level fetal lead exposure effect on neurobehavioral development in early infancy. Pediatrics. 1987;80 :721 –730[Abstract/Free Full Text]
  4. Bornschein R, Hammond P, Dietrich K, et al. The Cincinnati prospective study of low-level lead exposure and its effect on child development: protocol and status report. Environ Res. 1985;38 :4 –18[Medline]
  5. World Health Organization. Environmental Health Criteria 165: Inorganic Lead. Geneva, Switzerland: World Health Organization; 1995
  6. Needleman HL, Gatsonis CA. Low level lead exposure and the IQ of children: a meta-analysis of modern studies. JAMA. 1990;263 :673 –678[Abstract/Free Full Text]
  7. Needleman HL, Schell A, Bellinger D, Leviton A, Allred E. The long term effects of exposure to low doses of lead in childhood: an 11 year follow-up report. N Engl J Med. 1990;311 :83 –88
  8. White R, Diamond R, Proctor S, et al. Residual cognitive deficits 50 years after lead poisoning during childhood. Br J Ind Med. 1993;50 :613 –622[Web of Science][Medline]
  9. Bellinger D. Interpreting the literature of lead and child development: the neglected role of the experimental system. Neurotoxicol Teratol. 1995;17 :201 –212[CrossRef][Web of Science][Medline]
  10. Dyer F. Clinical presentation of the lead poisoned child on mental ability tests. J Clin Psychol. 1993;49 :94 –101[Web of Science][Medline]
  11. Shaheen S. Neuromaturation and behavior development: the case of childhood lead poisoning. Dev Psychol. 1984;20 :542 –550[CrossRef][Web of Science]
  12. Lanphear BP, Dietrich K, Auinger P, Cox C. Cognitive deficits associated with blood lead concentrations <10 µg/dL in US children and adolescents. Public Health Rep. 2000;115 :521 –529[CrossRef][Web of Science][Medline]
  13. Canfield RL, Henderson CR, Cory-Slechta DA, et al. Intellectual impairment in children with blood lead concentrations below 10 µg/dL. N Engl J Med. 2003;348 :1517 –1526[Abstract/Free Full Text]
  14. Pirkle J, Brody D, Gunter E, et al. The decline in blood lead levels in the United States: the National Health and Nutrition Examination Surveys (NHANES). JAMA. 1994;272 :284 –291[Abstract/Free Full Text]
  15. Centers for Disease Control and Prevention. Blood lead levels in young children—United States and selected states, 1996–1999. MMWR Morb Mortal Wkly Rep. 2000;49 :1133 –1137[Medline]
  16. Sargent J, Brown MJ, Freeman J, et al. Childhood lead poisoning in Massachusetts communities: its association with sociodemographic and housing characteristic. Am J Public Health. 1995;85 :528 –534[Abstract/Free Full Text]
  17. Brown MJ, Shenassa E, Tips N. Small Area Analysis for Childhood Lead Poisoning. Washington, DC: Alliance to End Childhood Lead Poisoning; 2001
  18. Sayre J, Charney E, Vostal J, Pless B. House and hand dust as a potential source of childhood lead exposure. Am J Dis Child. 1974;127 :167 –170[Abstract/Free Full Text]
  19. Clark S, Bornschein R, Succop P, Roda S, Peace B. Urban lead exposures of children in Cincinnati, Ohio. Chem Speciation Bioavail. 1991;3 :163 –171
  20. Lanphear BP, Weitzman M, Winter N, et al. Lead contaminated house dust and urban children's blood lead levels. Am J Public Health. 1996;86 :1416 –1421[Abstract/Free Full Text]
  21. Lanphear B, Matte T, Rogers J, et al. The contribution of lead contaminated house dust and residential soil to children's blood lead levels: a pooled analysis of 12 epidemiologic studies. Environ Res. 1998;79 :51 –68[Medline]
  22. Lanphear B, Hornung R, Ho M, et al. Environmental lead exposure during early childhood. J Pediatr. 2002;140 :40 –47[CrossRef][Web of Science][Medline]
  23. Schultz B, Pawel D, Murphy A. A retrospective examination of in-home educational visits to reduce childhood lead levels. Environ Res. 1999;80 :364 –368[Medline]
  24. Rhoads G, Ettinger A, Weisel C, et al. The effect of dust lead control on blood lead in toddlers: a randomized trial. Pediatrics. 1999;103 :551 –555[Abstract/Free Full Text]
  25. Lanphear B, Howard C, Eberly S, et al. Primary prevention of childhood lead exposure: a randomized trial of dust control. Pediatrics. 1999;103 :772 –777[Abstract/Free Full Text]
  26. Jordan CM, Yust BL, Robison LL, Hannon P, DEinard AS. A randomized trial of education to prevent lead burden in children. Environ Health Perspect. 2003;111 :1947 –1951[Web of Science][Medline]
  27. Tohn ER, Dixon SL, Wilson JW, Galke WA, Clark CS. An evaluation of one-time professional cleaning in homes with lead-based paint hazards. App Occup Environ Hyg. 2003;18 :138 –143[CrossRef]
  28. Bornschein R, Succop P, Dietrich K, Clark C, Que Hee S, Hammond P. The influence of social and environmental factors on dust lead, hand lead and blood lead levels in young children. Environ Res. 1984;38 :108 –118[CrossRef]
  29. Pocock S. Clinical Trials: A Practical Approach. Chichester, United Kingdom: Wiley; 1995
  30. US Department of Housing and Urban Development. Evaluation of the HUD Lead-Based Paint Hazard Control Grant Program in Private Housing: Overall Design and Data Collection Forms and Procedures. Washington, DC: US Department of Housing and Urban Development; 1994
  31. US Department of Housing and Urban Development. Guidelines for the Evaluation and Control of Lead-Based Paint Hazards in Housing. Washington, DC: US Department of Housing and Urban Development; 1995
  32. Amitai Y, Graef J, Brown MJ, Gerstle R, Kohn N, Chochrane P. Hazards of deleading homes of children with lead poisoning. Am J Dis Child. 1987;141 :758 –760[Abstract/Free Full Text]
  33. Inskip MJ, Hutton M. Lead-based paint in the dwellings: the potential for contamination of the home environment during renovation. Environ Geochem Health. 1987;9 :86 –92
  34. Farfel M, 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[Abstract/Free Full Text]
  35. Amitai Y, Brown MJ, Graef J, Cosgrove E. Residential deleading: effects on the blood lead levels of lead-poisoned children. Pediatrics. 1991;88 :893 –897[Abstract/Free Full Text]
  36. 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[Abstract]
  37. Barnard KE, Hammon MA, Booth CL, Bee HL, Mitchell SK, Spieker SJ. Measurement and meaning of parent-child interaction. In: Morrison FJ, Lord CE, Keating DP, eds. Applied Developmental Psychology. Vol 3. New York, NY: Academic Press; 1984:39 –80
  38. Guilarte T, Toscano C, McGlothan J, Weaver S. Environmental enrichment reverses cognitive and molecular deficits induced by developmental lead exposure. Ann Neurol. 2003;53 :50 –56[CrossRef][Web of Science][Medline]
  39. Gwiazda R, Campbell C, Smith D. A noninvasive isotopic approach to estimate the bone lead contribution to blood in children: implications for assessing the efficacy of lead abatement. Environ Health Perspect. 2005;113 :104 –110[Web of Science][Medline]

PEDIATRICS (ISSN 1098-4275). ©2006 by the American Academy of Pediatrics

Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Facebook Facebook   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter    What's this?


This article has been cited by other articles:


Home page
PediatricsHome page
H. J. Binns, C. Campbell, M. J. Brown, and for the Advisory Committee on Childhood Lead Poiso
Interpreting and Managing Blood Lead Levels of Less Than 10 {micro}g/dL in Children and Reducing Childhood Exposure to Lead: Recommendations of the Centers for Disease Control and Prevention Advisory Committee on Childhood Lead Poisoning Prevention
Pediatrics, November 1, 2007; 120(5): e1285 - e1298.
[Abstract] [Full Text] [PDF]


This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow E-mail this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to My File Cabinet
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Brown, M. J.
Right arrow Articles by Simon, P.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Brown, M. J.
Right arrow Articles by Simon, P.
Related Collections
Right arrow Therapeutics & Toxicology
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?