|
|
Volume 4: No. 1, January 2007
ORIGINAL RESEARCH
Case Management Protocol and Declining Blood Lead Concentrations Among Children
Nedra S. Whitehead, PhD, MS, Richard Leiker, MS
Suggested citation for this article: Whitehead, NS, Leiker, R. Case management protocol and declining blood lead concentrations among children. Prev Chronic Dis
[serial online] 2007 Jan [date cited]. Available from: http://www.cdc.gov/pcd/issues/2007/
jan/06_0023.htm.
PEER REVIEWED
Abstract
Introduction
Blood lead concentrations among children aged 6 years and younger become a concern at 10 µg/dL
(0.48 μmol/L) or higher. The authors’ objective was to determine whether initial blood lead concentrations of 10–19 µg/dL
(0.48–0.96 μmol/L)
declined among children aged 3 years and younger and whether the magnitude of decline was associated with the case management
protocol of the state or local childhood lead poisoning prevention program.
Methods
The authors analyzed childhood blood lead surveillance data from 1994
through 1995 and case management protocols from six states that reported the results of all blood lead tests. The study included 2109 children aged 2 years or younger who had a venous blood lead concentration of 10–19 µg/dL
(0.48–0.96 μmol/L) and a follow-up venous blood lead test within 3 to 12 months.
Results
Overall, blood lead concentrations increased by 0.25 µg/dL (0.01 μmol/L) between the time of the initial elevated blood lead test and the follow-up test, but concentrations declined by 1.96 µg/dL
(0.09 μmol/L) among children covered by a case management protocol that included a home visit and by 0.92 µg/dL
(0.04 μmol/L) among those covered by a protocol that included
a lead source investigation. The decline remained significant after we adjusted for the child’s age.
Conclusion
These findings suggest that childhood lead prevention programs should consider focusing their efforts on home visits and lead source investigations.
Back to top
Introduction
Children are exposed to lead from multiple sources, including lead-based paint and lead-contaminated dust. This exposure can have chronic consequences. Preschool children with blood lead concentrations greater than 9 µg/dL
(0.43 μmol/L) have lower intelligence and more performance problems on average than do children
who are unexposed to lead (1,2). Research by Bellinger et al (1991)
and Ruff et al (1996) suggests that scores for children aged 2 years on measures of cognitive performance drop one point for every 1-µg/dL
(0.05-μmol/L) increase in blood lead concentration (1,2). Although the decreases in cognitive performance are small individually, in the aggregate they may result in more children with behavioral problems and lower intelligence. Childhood lead
exposure can also result in adult chronic health problems (e.g., adverse pregnancy outcomes [3,4], hypertension [5,6]).
In 1991, the Centers for Disease Control and Prevention (CDC) designated blood lead concentrations of 10 µg/dL
(0.48 μmol/L) or higher as the level of concern for children aged 6 years and younger. Children were not considered to need environmental or medical intervention unless their blood lead concentration was 20 µg/dL
(0.97 μmol/L) or higher (7). An estimated 890,000
children aged 6 years and younger had blood lead concentrations of 10 µg/dL
(0.48 μmol/L) or greater in the United States from 1991 through 1994 (8). Although blood lead concentrations among young children have declined since 1994, exposure to lead continues to be a significant problem (9).
Blood lead concentrations of exposed, untreated children increase until children are about aged 2 years and decline thereafter (10). Behavioral and environmental changes to reduce lead exposure are necessary to lower blood lead concentrations before children are aged 2 years. Lead accumulates in bone during chronic exposure and may be released when bone is reabsorbed during pregnancy or
lactation (11,12). This release increases maternal blood lead concentrations associated with fetal neurological damage (13,14).
Childhood lead poisoning prevention programs have various case management protocols for children with blood lead concentrations of 10–19 µg/dL
(0.48–0.96 μmol/L), but the effect of these case management protocols on children’s blood lead concentrations is unknown. We analyzed childhood blood lead surveillance data from six states to examine changes in blood lead
concentrations among children aged 2 years and younger to determine whether there was any relationship with case management protocol. We examined the following questions:
- Does blood lead concentration decline after an initial venous blood lead test result of 10–19 µg/dL
(0.48–0.96 μmol/L)?
- If so, is the size of the decline associated with state or local case management protocol?
- Does the effect of the case management protocol differ if the initial blood lead concentration is between 10–14 µg/dL
(0.48–0.71 μmol/L) or between 15–19 µg/dL (0.72–0.96 μmol/L)?
- Does the effect of case management protocol remain after controlling for a child’s demographic characteristics?
Back to top
Methods
We defined a case of borderline elevated blood lead concentration as a venous blood lead concentration of 10–19 µg/dL
(0.48–0.96 μmol/L), regardless of the case definition used by state and local lead poisoning prevention programs. The case management protocol for a state or county was defined as the method of contact required under the protocol (i.e., mail, telephone, or home
visit) and the type of service to be delivered under the protocol (i.e., educational materials on lead exposure prevention alone or lead source investigation) for children with a given blood lead concentration. Each child
with blood lead concentrations of 10–19 µg/dL (0.48–0.96 μmol/L) was assigned a method of contact and a type of service according to information on case management protocol provided by
the coordinator of each state lead poisoning prevention program. One state, Wisconsin, provided county-level information. Children were assumed to have received the services called for under the case management protocol of their state or county of residence.
Children’s demographic information and blood lead test data came from CDC’s childhood blood lead database, which is compiled from state childhood blood lead surveillance data (15). Test results are submitted by laboratories and physicians to state surveillance programs, which link the laboratory tests of each child to ensure that duplicate results are deleted and sequential tests are
accurately identified. We limited our analysis to six states that 1) had laws requiring that the results of all blood lead tests on children be reported to the state health department, 2) submitted blood lead surveillance data from 1994 and 1995 to CDC, and 3) agreed to have their data used for our analysis. These states were Iowa, Montana, New Mexico, Ohio (only tests performed after April
1995, when universal reporting began, were included), Rhode Island, and Wisconsin.
In 1996, guidelines for blood lead screening changed. Under the new
guidelines, targeted screening of children in high risk areas and populations
was recommended instead of universal screening — a change that altered the
population of children who were tested. We limited our analysis to children who
had an initial venous blood lead test concentration of 10–19 µg/dL
(0.48–0.96 μmol/L) before they were aged 2 years and who had at least
one follow-up venous blood test 3 to 12 months after their initial test. These parameters were selected to ensure sufficient time for interventions to affect blood lead concentrations, to examine the long-term effects of the interventions, and to allow for varied case management protocols. Although a follow-up test within this
period was recommended for all children with a venous blood lead concentration of 10–19 µg/dL
(0.48–0.96 μmol/L), the timing of the follow-up test varied by case management protocol. The test could be either a venous or a capillary test (7). We limited our analysis to venous tests because greater variability in capillary blood test results made it difficult to identify
small changes in blood lead levels. Among the six states, 121,862 children had a blood lead test result in the database, and 4606 (3.8%) children had an initial elevated level between 10–19 µg/dL
(0.48–0.96 μmol/L) and at least one follow-up test. Of these children, 2109 (46%) met our study criteria. Our data set included all available test results as well as demographic
and intervention data for children who met our study criteria.
We computed the change in blood lead concentration for a child as the difference between the blood lead concentration at the first elevated venous test and the concentration at the first venous follow-up test completed 3 to 12 months after the initial elevated test. We calculated mean changes as the average of individual changes for the group and used paired t tests to test for
significant changes. We stratified our analysis by blood lead concentration because we expected the magnitude of any decline in blood lead concentration to be related to the initial concentration.
We used Kruskal-Wallis tests to compare mean changes in blood lead concentrations,
analysis of variance (ANOVA) to compare the mean number of months needed for blood lead concentrations to decline to less than 10 µg/dL
(0.48 μmol/L), and the Mantel-Haenszel chi-square test to determine differences in the proportion of children whose blood lead concentration was less than 10 µg/dL
(0.48 μmol/L) at the end of follow-up. We examined the relationship between
case management protocol and changes in blood lead concentration over the
entire follow-up period and controlled for the age of the child with generalized
linear modeling. Quadratic splines with knots at 20, 50, and 80 percentiles for each variable allowed the relationship between a child’s age at the initial test, or during the time between tests, and blood lead concentration to differ for different ages or time spans. All the venous blood test results available for a child were used in generalized equalizing equation modeling with
autoregressive correlation to examine the longitudinal relationship between case management protocol and blood lead concentration. We controlled for age at the initial and follow-up tests. We used SAS Version 8
(SAS Institute, Inc, Cary, NC) for all analyses (16).
Back to top
Results
The children in this study were served by childhood lead poisoning prevention programs that provided parental education by mail (78%),
telephone (21%), or home visits (<1%) when a child’s blood lead concentration was 10–14 µg/dL
(0.48–0.71 μmol/L).
Forty-eight percent of children in the study were served by childhood lead
poisoning prevention programs that also provided parental education by mail when
a child’s blood lead concentration was 15–19 µg/dL (0.72–0.96 μmol/L). The other 52% were
covered by childhood lead poisoning prevention programs that provided home
visits. Eighty-four percent of the children were covered by programs that
provided education alone and 16% by programs that provided investigations of the
source of lead exposure (Table 1).
Forty percent of children in the study were aged 13 months and younger when they had their first elevated blood lead test result (Table 1). A public agency paid for the initial blood lead test of 33% of the children; 11% had private payers, and payment source was unknown for 56%. Race and ethnicity were known for 68% of the children. Of
all children in the study, 29% of the children were white, 21% were black, and
18% were Hispanic. Approximately one half of the children were from Wisconsin.
On average, blood lead concentrations increased by 0.25 µg/dL (0.01 μmol/L) between the first elevated venous blood lead test and the first follow-up test done 3 to 12 months after the initial elevated test. The direction and magnitude of change in blood lead concentration varied by the child’s age at the initial elevated test, whether a public or private entity
paid for the test, the child’s race or ethnicity, and state of residence. Blood lead levels declined, on average, among older children, those whose test was paid for by private funds, those who were not white or Hispanic, and residents of states other than Ohio and Wisconsin. The sex of the child was not associated with changes in blood lead concentrations
(Table 1).
Overall, blood lead concentrations declined most among children whose case
management protocol called for a home visit
(Table 2). Blood lead concentrations decreased by 1.96 µg/dL
(0.09 μmol/L)
in these children and by 0.72 µg/dL (0.03 μmol/L) among children in families receiving a telephone call as follow-up. In contrast, blood lead concentrations increased
1.18 µg/dL (0.06 μmol/L) among children receiving mail follow-up.
Table 3 shows that blood
lead concentrations declined by 0.92 µg/dL (0.04 μmol/L), or 6%, on average among children covered by a protocol that included a lead source investigation but rose by 0.36 µg/dL
(0.02 μmol/L),
or 4%, among children covered by protocols that provided only mailed educational materials.
The contrast between protocols was even more striking for children whose initial blood lead concentration was 10–14 µg/dL
(0.48–0.71 μmol/L). Table 2 shows that lead concentrations rose by 1.49 µg/dL
(0.07 μmol/L),
13.5%, among children whose parents received mailed materials but declined by 2.20 µg/dL
(0.11 μmol/L), 18.8%, among those who received a home visit.
Also among children with initial blood lead concentration of 10–14 µg/dL, lead
source investigation protocols were associated with an average decline of 1.76 µg/dL
(0.08 μmol/L) in lead concentration, whereas education-only protocols were associated with an average increase of 1.07 µg/dL
(0.05 μmol/L) (Table 3).
The association with type of contact was less marked for children whose initial blood lead concentration was 15–19 µg/dL
(0.72–0.96 μmol/L), and there was no overall difference between blood lead concentrations among children receiving
mailed educational materials and those receiving a lead source investigation (Table 3). Blood lead concentrations increased by 0.48
µg/dL (0.02 μmol/L) among children who received mailed materials but declined by 1.95 µg/dL
(0.09 μmol/L) among those who received home visits (Table 2). Blood lead concentrations declined by 0.79 µg/dL
(0.04 μmol/L) among children who received
mailed educational materials only and by 0.72 µg/dL (0.03 μmol/L) among those who received a lead source investigation (Table 3). The association between
type of case management protocol and changes in blood lead concentration persisted even after we controlled for a child’s age at the first elevated test result and follow-up tests (Tables 2,3). Blood lead concentrations remained lower at the time of later tests among children who received telephone contact or home visits than among those contacted by mail (Table 2). Concentrations also
remained lower among those who received a lead source investigation than among those who received
mailed educational materials only (Table 3). The results were similar when the analysis was limited to children aged 15 months or younger at the time of their initial blood lead test (data not shown).
Among children with initial blood lead concentrations of 15–19 µg/dL
(0.72–0.96 μmol/L) who received a home visit, blood lead concentrations of those who received
mailed educational materials declined by 2.49 µg/dL (0.12 μmol/L), a larger decline than that of those who received lead source investigations 0.72 µg/dL
(0.03 μmol/L) (data not shown). The difference remained
after we adjusted for a child’s age but was not significant at later tests.
We did not control for race, ethnicity, and payment source in these models because of missing data; only 23% of records included information on these variables. When we fit models including race and payment source, we found that home visits and lead source investigations among children with initial blood lead concentrations of 10–14 µg/dL
(0.48–0.71 μmol/L) were
still associated with a significant decline in blood lead concentrations between the time of initial test and first follow-up test, but telephone contact was not significant (data not shown). Including these variables did not change any longitudinal effects significantly.
Blood lead concentrations declined to less than 10 µg/dL (0.48 μmol/L) by the last reported test among 43% of children whose initial blood lead concentration was 10–14 µg/dL
(0.48–0.71 μmol/L) and among 23% of children whose initial blood lead concentration was 15–19 µg/dL
(0.72–0.96 μmol/L)
(Table 4). On average, the time required for blood
lead concentrations to drop to less than 10 µg/dL (0.48 μmol/L) was 12 months for children with a concentration of 10–14 µg/dL
(0.48–0.71 μmol/L) and 13 months for those with an initial concentration of 15–19 µg/dL
(0.72–0.96 μmol/L). Home visits were associated with the highest proportion of children with blood lead concentrations of
less than 10 µg/dL (0.48 μmol/L) by the last reported follow-up test and with the shortest average time required for blood lead concentrations to decline to less than 10 µg/dL
(0.48 μmol/L).
Back to top
Discussion
We found that home visit protocols were associated with a larger decline in blood lead concentrations than mail or telephone contact protocols, regardless of a child’s initial blood lead concentration. Mailed educational materials alone were not associated with lower blood lead concentrations.
There are several possible limitations to our study. One is that we may have underestimated the effects of case management protocol. Another is that tested children may not have actually received the services called for by the lead poisoning prevention program in their area. We also had no information on the details of interventions and how these may differ among programs. State laws require
the reporting of blood lead tests, but some results, especially those below 10 µg/dL
(0.48 μmol/L) or conducted by out-of-state laboratories, may not have been reported or linked to an appropriate child. We used the first venous test performed at least 3 months after the index test of 10–19 μg/dL, but we included children who had at least one follow-up test up to 12 months.
Blood lead concentrations among children who had more time between the initial test and the follow-up test would have more time to decline, and this effect could bias our results. The analyses that controlled for the timing of tests, however, should not be affected by this limitation.
The effect of other limitations is less clear. We had no information on many variables, such as iron or calcium intake, that affect blood lead concentrations. Demographic characteristics were missing for many children. We cannot determine how results may have differed if we had been able to control for race and payment source, but results of analyses that included these variables were similar
to ones that did not. For these factors to affect our results, however, they would have to be associated with both the case management protocol of the state or county childhood lead poisoning prevention program and with changes in a child’s blood lead concentration. Although many factors are associated with an initial elevated blood lead concentration, few have been found to affect changes
in blood lead concentration (16-20). Our study was limited to states that require all blood lead test results be reported to the state health department and may not apply to states not included in the analysis.
Surveillance data result from tests performed at the request of a child’s parents or physician, and circumstances for these children may differ from circumstances of children who are not tested. This limitation may affect the applicability of our findings to other children. Parents of children who had an elevated blood lead test result but who did not take their children for follow-up
tests may be less likely to implement measures to control lead exposure than parents of children who did receive follow-up tests. If this is true, we would expect all case management protocols to be less effective in children overall than we found among children in our study.
The total amount of lead stored in tissues in a child’s body can affect blood lead concentrations and obscure the efficacy of interventions. Lead is released during bone turnover until all the stored lead has been released from tissues. Rust et al estimated that among children aged 2 years and younger, bone lead stores could elevate blood lead concentrations for up to 1 year after all
sources of lead exposure were removed (21). Bone lead stores could not be estimated for children in this study and may have caused us to underestimate the efficacy of all case management protocols. Differences in bone lead stores, however, could account for our results only if children who received mail or education interventions had higher bone lead stores on average than those of the same age
and initial blood lead concentration who received home visits or lead source investigations.
Our study has several strengths in relation to other studies of interventions
to reduce blood lead concentrations. We had a large sample, which allowed us to
detect small effects on blood lead concentrations, and a diverse study
population in terms of race and ethnicity, population density, and geographic
region. Our blood lead tests were linked by child and allowed us to compare
changes in an individual’s blood lead concentration instead of an average for a group.
We identified five randomized trial studies that examined the effectiveness of interventions to reduce blood lead concentrations among children who had concentrations of less than 20 µg/dL
(0.97 μmol/L) (17,18,22,23). These interventions included professional house cleaning (17,22), provision of household cleaning supplies and instructions (23), vacuuming
with high efficiency particulate (HEPA) air filters (18), and provision of
an individualized care plan that included multiple home visits and parental teaching on lead exposure prevention (24). Only one study intervention was effective: repeated professional house cleaning resulted in a 2.1 µg/dL
(0.1 μmol/L) decrease in blood lead concentration (22). In four of the studies, however, the controls received a home visit that included information about prevention
of lead poisoning or identification of lead hazards; this information was likely similar to information provided by lead poisoning prevention programs (17,18,22,24). The changes in mean blood lead concentration among these control groups varied
after 3 months: −5.9 µg/dL (–0.28 μmol/L) (17); −1.0 µg/dL
(−0.05 μmol/L) (18), +0.1 µg/dL (<0.01 μmol/L) (22), and
−6.2 µg/dL (−0.3 μmol/L) (24). Rhoads et al included information on accident prevention and provided safety equipment in addition to information on lead hazards and lead poisoning prevention. The presence of safety and accident information may have lessened the impact of the lead poisoning prevention information (22). Hilts et al conducted their study near an
active lead smelter; this location increased the likelihood of lead exposure. Aschengrau et al had only 24 children in randomized groups and included older children whose blood lead levels may already have begun to decline. The comparison group in the study by Brown et al received one or two educational home visits. In the remaining study, controls received a brochure on lead poisoning prevention
(23). The blood lead concentrations of these children declined slightly [0.60 µg/dL
(0.03 μmol/L)], but the average age at recruitment was 20 months, so the decline may
be attributable to the natural decline as children age.
All of these other studies measured the change in group mean blood lead concentrations. We measured the change in blood lead concentrations for individual children. The decline in blood lead concentrations among children in our study who received home visits [−1.96 µg/dL
(0.09 μmol/L)], however, was within the range of changes in blood lead concentrations among these control
groups.
Schultz et al, in a study of children followed by a local lead poisoning prevention program, examined the average changes in blood lead concentrations before and after the program implemented home education visits among children who had initial blood lead concentrations of 20–24 µg/dL
(0.97–1.16 μmol/L) (25). These authors found that blood lead concentrations declined by 3.9 µg/dL
(0.19 μmol/L) on average among children who received home visits but increased by 1.0 µg/dL
(0.05 μmol/L) among children who received no follow-up. They may have found a larger decline in blood lead concentrations than we did because the children in their study had higher initial blood lead concentrations than those in our study.
The decline in blood lead concentrations among children covered by a case
management protocol that included a home visit was larger and faster than predicted by Neimuth and Schultz for children not receiving interventions (26). For children with the age and initial blood lead concentration ranges of this study, Niemuth and Schultz predicted changes at 12-month follow-up tests that ranged from
a 7% increase for children aged 6 months with an initial blood lead concentration of 10 µg/dL
(0.48 μmol/L) to an 8.2% decrease for children aged 24 months with an initial blood lead concentration of
15 µg/dL (0.72 μmol/L) (26). We found a 19% decline among children whose initial blood lead concentration was 10–14 µg/dL
(0.48–0.71 μmol/L) and who
were covered by a case management protocol that included a home visit and a 12% decline among those whose initial blood lead concentration was 15–19 µg/dL
(0.72–0.96 μmol/L). Mailed educational materials were associated with a 10% increase in blood lead concentrations; this increase was the same or higher than predicted for children receiving no treatment.
Roberts et al estimated the time that would be required for blood lead concentrations to decline to less than 10 µg/dL
(0.48 μmol/L) among children who received no intervention. In our study, the time required for initial blood lead concentrations of 10–14 µg/dL
(0.48–0.71 μmol/L) to decline to less than 10 µg/dL (0.48 μmol/L) among children covered by
home visit protocols was similar to that estimated by Roberts et al for children with blood lead concentrations in this range who received no intervention (27). Among children whose initial blood lead concentration was 15–19 µg/dL
(0.72–0.96 μmol/L) and who received a home visit, however, blood lead concentrations declined to less than 10 µg/dL
(0.48 μmol/L) in 10
months — 4 months faster than was estimated by Roberts et al (27).
Some clinicians have questioned the value of following children with blood lead concentrations of less than 15 µg/dL
(0.72 μmol/L) (28). Although a systematic evaluation of the effect of different types of programs is needed, our results suggest that blood lead concentrations of less than 20 µg/dL
(0.97 μmol/L) can be significantly reduced with protocols that include home
visits and lead source investigations. This reduction is valuable because recent research has suggested that even children with blood lead concentrations of less than 10 µg/dL
(0.48 μmol/L) have identifiable cognitive deficits associated with lead exposure because stored lead has long-term effects (16,29). Other research has found that strong state policies requiring lead abatement in
housing result in fewer children exposed to lead and fewer children with elevated blood lead concentrations (30,31). Home investigations for children with borderline elevated blood lead concentrations, combined with strong lead abatement policies, could lower current and future lead exposure among children.
Back to top
Acknowledgments
The authors thank Dr Hoyt Wilson, Division of Reproductive Health, CDC, for his statistical assistance. Mr. Leiker receives salary support from
CDC Cooperative Agreement US7/CCU-022875.
Back to top
Author Information
Corresponding Author: Nedra S. Whitehead, Research Triangle Institute (RTI) International, Social and Statistical Sciences, 2951 Flowers Rd, Suite 119, Atlanta, GA 30341. Telephone: 770-986-5051. E-mail: nwhitehead@rti.org.
Author Affiliations: Richard Leiker, Oregon Childhood Lead Poisoning Prevention Program, Environmental and Occupational Epidemiology Section, Oregon Health Services, Office of Disease Prevention and Epidemiology, Portland, Ore.
Back to top
References
- Bellinger D, Sloman J, Leviton A, Rabinowitz M, Needleman HL, Waternaux C.
Low-level lead exposure and children's cognitive function in the preschool
years. [Published erratum in: Pediatrics 1994;93(2):A28]. Pediatrics
1991;87(2):219-27.
-
Ruff HA, Markowitz ME, Bijur PE, Rosen JF.
Relationships among blood lead levels, iron deficiency, and cognitive development in two-year-old children. Environ Health Perspect 1996;104(2):180-5.
-
Hernandez-Avila M, Peterson KE, Gonzalez-Cossio T, Sanin LH, Aro A, Schnaas L, et al.
Effect of maternal bone lead on length and head circumference of newborns and 1-month-old infants. Arch Environ Health 2002;57(5):482-8.
-
Rothenberg SJ, Kondrashov V, Manalo M, Jiang J, Cuellar R, Garcia M, et al.
Increases in hypertension
and blood pressure during pregnancy with increased bone lead levels. Am J Epidemiol 2002;156(12):1079-87.
- Glenn BS, Stewart WF, Links JM, Todd AC, Schwartz BS.
The longitudinal association of lead with blood pressure. Epidemiology 2003;14(1):30-6.
- Gerr F, Letz R, Stokes L, Chettle D, McNeill F, Kaye W.
Association between bone lead concentration and blood pressure among young adults. Am J Ind Med 2002;42(2):98-106.
- Roper WL, Houk VN, Falk H, Binder S. Preventing lead poisoning in young children: a statement by the Centers for Disease Control--October 1991. Atlanta
(GA): Centers for Disease Control and Prevention; 1991.
- Centers for Disease Control and Prevention (CDC).
Update: blood lead levels--United States, 1991-1994.
[Published erratum in: MMWR Morb Mortal Wkly Rep 1997;46(26):607]. MMWR Morb
Mortal Wkly Rep 1997;46(7):141-6.
- Centers for Disease Control and Prevention (CDC).
Blood lead levels in young children--United States and selected states, 1996-1999. MMWR Morb
Mortal Wkly Rep 2000;49(50):1133-7.
-
Dietrich KN, Succop PA, Berger OG, Hammond PB, Bornschein RL.
Lead exposure and the cognitive development of urban preschool children: the Cincinnati Lead Study cohort at age 4 years. Neurotoxicol Teratol 1991;13(2):203-11.
- Gulson BL, Jameson CW, Mahaffey KR, Mizon KJ, Korsch MJ, Vimpani G.
Pregnancy increases mobilization of lead from maternal skeleton. J Lab Clin Med 1997;130(1):51-62.
- Gulson BL, Mahaffey KR, Jameson CW, Mizon KJ, Korsch MJ, Cameron MA, et al.
Mobilization of lead from the skeleton during the postnatal period is larger
than during pregnancy. J Lab Clin Med 1998;131(4):324-9
- Emory E, Ansari Z, Pattillo R, Archibold E, Chevalier J.
Maternal blood lead effects on infant intelligence at age 7 months. Am J Obstet Gynecol 2003;188(4):S26-32.
- Gonzalez-Cossio T, Peterson KE, Sanin LH, Fishbein E, Palazuelos E, Aro A, et al.
Decrease in birth weight in relation to maternal bone-lead burden. Pediatrics 1997;100(5):856-62.
- National Childhood Blood Lead Surveillance Database. Atlanta (GA): Centers
for Disease Control and Prevention, National Center for Environmental
Health;[cited 2006 Oct 1]. Available from: http://www.cdc.gov/nceh/lead/surv/database/database.htm
- SAS Institute, Inc. SAS Language Reference, Version 6. 1st Ed. Cary (NC): SAS Institute, Inc; 1990.
- Lanphear BP, Dietrich K, Auinger P, Cox C.
Cognitive deficits associated with blood lead concentrations <10 microg/dL in
US children and adolescents. Public Health Rep 2000;115(6):521-9.
- Aschengrau A, Hardy S, Mackey P, Pultinas D.
The impact of low technology lead hazard reduction activities among children with mildly elevated blood lead levels. Environ Res 1998;79(1):41-50.
- Hilts SR, Hertzman C, Marion SA.
A controlled trial of the effect of HEPA vacuuming on childhood lead exposure. Can J Public Health 1995;86(5):345-50.
- Jordan CM, Yust BL, Robison LL, Hannan P, Deinard AS.
A randomized trial of education to prevent lead burden in children at high
risk for lead exposure: efficacy as measured by blood lead monitoring. Environ Health Perspect 2003;111(16):1947-51.
- Staes C, Matte T, Copley CG, Flanders D, Binder S.
Retrospective study of the impact of lead-based paint hazard remediation on
children's blood lead levels in St. Louis, Missouri. Am J Epidemiol 1994;139(10):1016-26.
- Rust SW, Kumar P, Burgoon DA, Niemuth NA, Schultz BD.
Influence of bone-lead stores on the observed effectiveness of lead hazard
intervention. Environ Res 1999;81(3):175-84.
- Rhoads GG, Ettinger AS, Weisel CP, Buckley TJ, Goldman KD, Adgate J, et al.
The effect of dust lead control on blood lead in toddlers: a randomized trial. Pediatrics 1999;103(3):551-5.
- Lanphear BP, Winter NL, Apetz L, Eberly S, Weitzman M.
A randomized trial of the effect of dust control on children's blood lead levels. Pediatrics 1996;98(1):35-40.
- Brown MJ, McLaine P, Dixon S, Simon P.
A randomized, community-based trial of home visiting to reduce blood lead levels in children. Pediatrics 2006;117(1):147-53.
- Schultz B, Pawel D, Murphy A.
A retrospective examination of in-home educational visits to reduce childhood lead levels. Environ Res 1999;80(4):364-8.
- Niemuth NA, Wood BJ, Schultz BD.
Estimated change in blood lead concentration in control populations. Arch Environ Health 2001; 56(6):542-51.
- Roberts JR, Reigart JR, Ebeling M, Hulsey TC.
Time required for blood lead levels to decline in nonchelated children. J
Toxicol Clin Toxicol 2001;39(2):153-60.
- Block B, Szekely K, Escobar M.
Difficulties in evaluating abnormal lead screening results in children. J Am Board Fam Pract 1996;9(6):405-10.
- Canfield RL, Henderson CR Jr, Cory-Slechta DA, Cox C, Jusko TA, Lanphear
BP.
Intellectual impairment in children with blood lead concentrations below 10
microg per deciliter. N Engl J Med 2003;348(16):1517-26.
- Sargent JD, Dalton M, Demidenko E, Simon P, Klein RZ.
The association between state housing policy and lead poisoning in children. Am J Public Health 1999;89(11):1690-5.
- Brown MJ, Gardner J, Sargent JD, Swartz K, Hu H, Timperi R.
The effectiveness of housing policies in reducing children's lead exposure. Am J Public Health 2001;91(4):621-4.
Back to top
|
|
