OBJECTIVES. To evaluate trends in children's blood lead levels and the extent of blood lead testing of children at risk for lead poisoning from national surveys conducted during a 16-year period in the United States.
METHODS. Data for children aged 1 to 5 years from the National Health and Nutrition Examination Survey III Phase I, 1988–1991, and Phase II, 1991–1994 were compared to data from the survey period 1999–2004.
RESULTS. The prevalence of elevated blood lead levels, ≥10 μg/dL, among children decreased from 8.6% in 1988–1991 to 1.4% in 1999–2004, which is an 84% decline. From 1988–1991 and 1999–2004, children's geometric mean blood lead levels declined in non-Hispanic black (5.2–2.8 μg/dL), Mexican American (3.9–1.9 μg/dL), and non-Hispanic white children (3.1 μg/dL to 1.7 μg/dL). However, levels continue to be highest among non-Hispanic black children relative to Mexican American and non-Hispanic white children. Blood lead levels were distributed as follows: 14.0% were <1.0 μg/dL, 55.0% were 1.0 to <2.5 μg/dL, 23.6% were 2.5 to <5 μg/dL, 4.5% were 5 to <7.5 μg/dL, 1.5% were 7.5 to <10 μg/dL, and 1.4% were ≥10 μg/dL. Multivariable analysis indicated that residence in older housing, poverty, age, and being non-Hispanic black are still major risk factors for higher lead levels. Blood lead testing of Medicaid-enrolled children increased to 41.9% from 19.2% in 1988–1991. Only 43.0% of children with elevated blood lead levels had previously been tested.
CONCLUSIONS. Children's blood lead levels continue to decline in the United States, even in historically high-risk groups for lead poisoning. To maintain progress made and eliminate remaining disparities, efforts must continue to test children at high risk for lead poisoning, and identify and control sources of lead. Coordinated prevention strategies at national, state, and local levels will help achieve the goal of elimination of elevated blood lead levels.
The adverse health effects of lead are well documented,1,2 and no threshold for adverse effects has been specified.3–5 Because overt clinical symptoms are rare at blood lead levels (BLLs) of <70 μg/dL, blood lead testing is necessary to identify asymptomatic children with elevated BLLs of ≥10 μg/dL. The United States Department of Health and Human Services and the Centers for Disease Control and Prevention (CDC) have targeted BLLs of ≥10 μg/dL for elimination in the United States by 2010.6 Childhood lead poisoning prevention programs have focused on young children aged <6 years, because these children are especially vulnerable to the adverse health effects of lead. The nervous systems of young children are still developing and the hand-to-mouth behaviors common at these ages increase their risk for ingesting lead in their environment.
Nationally, BLLs in children have been declining.7–11 Some children, however, continue to be at greater risk for exposure to lead than others.12–14 Since 1976, blood lead data from the National Health and Nutrition Examination Surveys (NHANES) have been used to characterize children's BLLs. Children at highest risk are non-Hispanic black, live in housing built before 1950, and their families are poor.15,16 From 1991–1994, Medicaid enrollees accounted for 60% of US children who had elevated BLLs, yet only 19% of Medicaid-enrolled children had a blood lead test before their participation in the NHANES III.17,18 The decline in the prevalence of elevated BLLs over time has been most pronounced among children belonging to high-risk groups, especially non-Hispanic black children. They experienced a 72% decline in the prevalence of elevated BLLs between the 1991–1994 and 1999–2002 NHANES.7 Nevertheless, the geometric mean BLL remained higher for non-Hispanic black children compared with Mexican American and non-Hispanic white children in the 1999–2004 NHANES (2.8 vs 1.9 and 1.7 μg/dL, respectively) (Table 1), indicating that differences in risk for exposure to lead still exist as seen from previous reports of NHANES data: 1976–1980, 1988–1991, and 1999–2002.7–10
With increasing evidence that adverse health effects occur at BLLs of <10 μg/dL,5,19–21 little is known about the distribution of and risk factors associated with BLLs of <10 μg/dL. Although in at least 1 study, well-established risk factors associated with BLLs of ≥10 μg/dL were also predictive of BLLs of ≥5 μg/dL.22 However, this study also found that for a number of children with BLLs 5 to 9 μg/dL, multiple sources of lead exposure seemed likely given the prevalence of these levels among children without obvious risk factors.22 In this study, we augmented previous work by updating information on the distribution of children's BLLs, the extent of blood lead testing of children at risk for lead poisoning, and risk factors for higher BLLs among children 1 to 5 years of age from 2 separate NHANESs (1988–1994 and 1999–2004).
The National Center for Health Statistics of the CDC conducts the NHANES, which measure health and nutrition in a representative sample of the US noninstitutionalized civilian population aged 3 months and older by using a multistage probability design. Since 1999, the NHANES has been inclusive of all ages and has been a continuous survey as previously described.23 Beginning in 1999, ∼5000 people were recruited annually to participate in the NHANES. Of these ∼5000 individuals, ∼550 were children between the ages of 1 to 5 years. A medical examination included blood lead testing as part of the laboratory component and a household interview contained questions on health, demographics and nutritional characteristics, as well as whether a child had been previously tested for lead poisoning, and health insurance status, including Medicaid enrollment. Participants ages 1 year and older were eligible for blood lead testing. A family member provided questionnaire responses for children <16 years of age. The NHANES III (1988–1994) design and the blood lead component have been described previously.9,15–16,24
Whole blood samples were drawn into prescreened ethylenediaminetetraacetic acid-anticoagulated evacuated tubes by venipuncture of all participants.24 The analysis of lead was conducted in the Inorganic Toxicology Laboratory, Division of Laboratory Sciences, National Center for Environmental Health, CDC, Atlanta, Georgia. Blood lead samples were stored frozen at −20°C or lower until analyzed. The laboratory methods used to analyze blood lead in the NHANES III have been described in detail previously.9,16 During the survey years of 1999–2002, the blood samples were measured for lead by graphite furnace atomic absorption spectrometry (CDC method No. ITB002A) by using a modification of the method of Miller et al.25 During the survey years of 2003–2004, the blood samples were measured for lead by inductively coupled plasma mass spectrometry (CDC method No. ITB001A) by using a modification of the method of Nixon et al.26 The blood lead limit of detection (LOD) for graphite furnace atomic absorption spectrometry and inductively coupled plasma mass spectrometry is 0.3 μg/dL. Analytical quality control was monitored by using 4 concentrations of bench quality control material and 2 levels of “blind” quality control materials.
This analysis included data from the NHANES III, Phase 1 (1988–1991), NHANES III, Phase 2 (1991–1994), and the first 6 years of the current NHANES (1999–2004) for children 1 to 5 years of age.
We reported only 3 categories of race/ethnicity (non-Hispanic white, non-Hispanic black, and Mexican American) in the race/ethnicity section of the tables, because there were small numbers of children in the other Hispanic, other race, and multiracial categories. For all other sections of the tables, results were included for all participants in the survey.
Because responses for “year housing was built” used different categories between the NHANES III and the NHANES 1999–2004, we defined the most closely similar categories as highest risk (built before 1946 [NHANES III] and before 1950 [NHANES 1999–2004]), medium risk (built between 1946 and 1973 [NHANES III] and 1950 and 1977 [NHANES 1999–2004]), and low risk (built 1974 and after [NHANES III]) and 1978 and after [NHANES 1999–2004]). Observations for which information was not available about when the housing unit was built were defined as “not known;” this category was reported in the tables but was not used in any statistical comparisons.
The poverty income ratio (PIR) (defined as the ratio of total family income to the poverty threshold for the year of the interview) was stratified as ≤1.3 (corresponding to low income) and >1.3 (corresponding to middle to high income). These categories were selected in part to be consistent with major government food assistance programs that use a PIR of 1.3 to determine eligibility.15 The Medicaid status variable was defined as whether a child was enrolled in Medicaid (yes) or not enrolled in Medicaid (no).
Statistical analysis was conducted by using SAS 9.1.3 (SAS Institute, Inc, Cary, NC) and SUDAAN 9.0 (Research Triangle Institute, Research Triangle Park, NC). NHANES-specific sample weights were used for all analyses to adjust for the differential probabilities of selection, nonresponse, and noncoverage. All statistical test results were evaluated by using an overall significance level of P < .05. BLLs were not rounded before statistical analysis. Because of small proportions, the arcsine method was used to construct 2-sided confidence intervals (CIs).27,28 We computed geometric mean BLLs by taking the antilog of the mean of log10 of the BLLs.
We also analyzed BLLs by examining their distribution across 6 categories: <1.0, 1.0 to <2.5, 2.5 to <5, 5 to <7.5, 7.5 to <10, and ≥10 μg/dL. These categories were selected to provide a relatively fine breakdown of BLLs of <10 μg/dL. These fine breakdowns show the changes in distributions across these categories in subpopulations between NHANESs as well as the status of these subpopulations within the current NHANES. Because no BLL has been identified as safe for children, the use of several fine cut points of <10 μg/dL also allows assessment at several levels that may be of interest. For example some analyses have used a cut point of 5 μg/dL. Less than 1 μg/dL was chosen as a cut point, because the LOD in BLL measurements in the current NHANES is 0.3 μg/dL. These cut points may be more easily understood than statistically derived cut points (eg, quartiles).
We evaluated differences in geometric means and proportions for 1999–2004 by computing the t statistic, by using the Bonferroni method to adjust for multiple comparisons across categories of race-ethnicity and housing risk. For 1999–2004, we evaluated the differences in the categorical BLL variable across levels of age, race-ethnicity, PIR, Medicaid status, and housing risk, by using the χ2 test of independence. For 1999–2004, we also evaluated differences in the proportion of children with BLLs of <1 μg/dL (lowest category) and the proportion of children with BLLs of ≥10 μg/dL (highest category) across the covariates mentioned previously. We evaluated changes over time for geometric means and proportions by using a 2-tailed t test to test for differences between the periods of 1988–1991 and 1999–2004, by using the Bonferroni method to adjust for multiple comparisons within variables. We used a comparable approach to assess changes over time for overall geometric means and overall prevalence of elevated BLLs in the current NHANES data, assessing change from the 1999–2000 period to the 2003–2004 period.
To assess risk factors associated with higher BLLs, we also fit multivariable logistic and linear regression models by using the RLOGIST and LINEAR procedures in SUDAAN. Multivariable logistic regression was used to assess various risk factors associated with an elevated BLL (≥10 μg/dL). Multivariable linear regression was used to assess risk factors associated with higher BLLs. The dependent variables were the probability of having a BLL of ≥10 μg/dL for the logistic model and a natural log-transformed BLL for the linear model. For both modeling approaches, the main effects were fitted that included gender of the child (male, female [referent]), age of the child (1–2 years, 3–5 years [referent]), race/ethnicity (non-Hispanic black, Mexican American, non-Hispanic white [referent]), PIR (≤1.3, >1.3 [referent]), housing risk (high risk, medium risk, low risk [referent]), and NHANES (NHANES 1999–2004, NHANES III 1991–1994, NHANES III 1988–1991 [referent]). Gender of child was not a predictor of BLLs in the logistic model nor in the linear model and thus was not included in the final models. We also evaluated all possible 2-way interaction terms for the final main effects model by adding them, 1 at a time, to the model and assessing their statistical significance. None of the 2-way interaction terms achieved statistical significance in either the logistic or linear analyses. No 3-way interactions were evaluated.
Geometric means and distribution of BLLs across 6 blood lead categories both overall and by analytical variables, for NHANES III Phase I (1988–1991), NHANES III Phase 2 (1991–1994), and NHANES 1999–2004 are presented in Tables 1 to 3. Overall, the distribution of BLLs for US children shifted toward lower BLL categories from the 1988–1991 period to the 1999–2004 period, as evidenced by the lower geometric mean for the latter period (P < .0001). The overall prevalence of BLLs of ≥10 μg/dL declined dramatically, from 8.6% in 1988–1991 to 1.4% in 1999–2004, a decrease of 84%. Among the race/ethnicity groups examined, the prevalence of BLLs of ≥10 μg/dL declined 84% in Mexican American children, 82% in non-Hispanic black children, and 78% in non-Hispanic white children between the 1988–1991 period and 1999–2004 period.
Distribution of BLLs
In the 1999–2004 period, 14.0% of children ages 1 to 5 years had BLLs of <1.0 μg/dL, 55.0% had BLLs of 1.0 to <2.5 μg/dL, 23.6% had BLLs of 2.5 to <5 μg/dL, 4.5% had BLLs of 5 to <7.5 μg/dL, 1.5% had BLLs of 7.5 to <10 μg/dL, and 1.4% had BLLs of ≥10 μg/dL (Table 1). Differences in the distribution of BLLs across the 6 BLL categories were statistically significant across strata of age, race/ethnicity, income, Medicaid status, and housing risk (Table 1). A higher percentage of children with BLLs of ≥10 μg/dL were non-Hispanic black (3.4% vs 1.2% for Mexican American and 1.2% for non-Hispanic white children), 1 to 2 years of age (2.4% vs 0.9% for 3 to 5 years of age), and enrolled in Medicaid (1.9% vs 1.1% for not enrolled in Medicaid); however, none of these differences achieved statistical significance (P > .05).
Children with BLLs of <1 μg/dL were more likely to be non-Hispanic white (17.6% vs 4.0% for non-Hispanic black children [P < .0001] and 10.9% for Mexican American children [P < .01]); not enrolled in Medicaid (17.6% vs 5.8% for enrolled in Medicaid; P < .0001), and from higher income (PIR > 1.3) families (19.9% vs 6.7% for being from low income families [PIR ≤ 1.3]; P < .0001). The geometric mean BLL was higher for non-Hispanic black children compared with non-Hispanic white children (P < .001) and Mexican American children (P < .0001); lower income children compared with higher income children (P < .0001); children enrolled in Medicaid compared with those not enrolled in Medicaid (P < .0001); and children living in high-risk housing compared with those living in medium-risk (P < .0001) and low-risk housing (P < .0001) (Table 1).
Figure 1 provides a visualization of the distribution of BLLs using the categories defined for the analysis for each of the 3 race/ethnicity groups (non-Hispanic white, Mexican American, non-Hispanic black) for the 3 most recent cycles of the NHANES. By the 1999–2004 survey, the distributions of BLLs for non-Hispanic white and Mexican American children were similar. Although the geometric mean BLL for non-Hispanic black children in the 1999–2004 survey was still higher than those of non-Hispanic white children and Mexican American children (Tables 1–3), the prevalence of elevated BLLs in non-Hispanic black children declined dramatically between NHANES III Phase I and the current NHANES, as noted above. The prevalence of BLLs of ≥10 μg/dL in most of the high-risk groups (low income, Medicaid eligible, and high-risk housing) also declined dramatically. Likewise, the distributions of BLLs by markers of poverty status (PIR and Medicaid enrollment status) were lower (Tables 1–3) by 1999–2004, although the prevalence in all categories for lower income children did not decline to the same extent as did prevalences for higher-income children. Similarly, BLLs for children living in high-risk housing also were lower, although not to the same extent as for children living in low- and medium-risk housing.
For the 1999–2004 NHANES, the overall geometric means were 2.2 μg/dL (95% CI: 2.0–2.5) for 1999–2000, 1.7 μg/dL (95% CI: 1.6–1.8) for 2001–2002, and 1.8 μg/dL (95% CI: 1.6–1.9) for 2003–2004. The difference in geometric mean for 2003–2004 compared with 1999–2000 was statistically significant (P < .05). Prevalences of elevated BLLs (≥10 μg/dL) were 2.2% (95% CI: 1.2–3.4) in 1999–2000, 1.1% (95% CI: 0.6–2.0) in 2001–2002, and 1.2% (95% CI: 0.4–2.4) in 2003–2004. The relative SEs of the prevalence estimates for 2001–2002 and 2003–2004 was between 30% and 40% (data not shown). The prevalence of elevated BLLs for 2003–2004 did not differ statistically from that for 1999–2000 (P > .05).
Multivariable Regression Results
Results of the multivariable logistic and linear regression analyses are presented in Table 4. All risk factors associated with BLLs of ≥10 μg/dL in bivariable analyses (Tables 1–3) (being ages 1–2 years, being non-Hispanic black, having a PIR of ≥1.3, and living in a moderate-risk [built ∼1950–1977] or high-risk house [built before 1950]) were statistically significant in the multivariable logistic model. For housing risk, the odds of having a BLL of ≥10 μg/dL was 1.8 times higher in children living in a moderate-risk house compared with a low-risk house (built ∼1978 and later) and 5.9 times higher in children living in a high-risk house compared with a low-risk house. The decline in the proportion of children with BLLs of ≥10 μg/dL across the 3 NHANES study periods was also statistically significant, with children in the NHANES III 1991–1994 being 60% less likely to have a BLL of ≥10 μg/dL than children in the NHANES III 1988–1991; children in the NHANES 1999–2004 were 90% less likely to have a BLL of ≥10 μg/dL than children in the NHANES III 1988–1991. Likewise, in the multivariable linear model, all risk factors associated with higher geometric mean BLLs in bivariate analyses (Table 1–3) (the same risk factors as in the logistic models) were statistically significant. Non-Hispanic black children had higher BLLs than non-Hispanic white children, whereas Mexican American children had BLLs comparable to non-Hispanic white children across all 3 surveys. The increasingly negative linear regression coefficients (β) corresponding to later NHANES study periods (Table 4) reflected the decline seen in mean population BLLs from 1988 to 2004.
With all main effects in the model, data from 4817 sampled children (67% of the total number originally available for analysis) were available to compute estimates. These data included 321 sampled children with BLLs of ≥10 μg/dL (70% of the total number with BLLs of ≥10 μg/dL available for analysis). This smaller number of observations was primarily due to missing data on the year the housing was built. This categorical variable was missing for 14% in NHANES III 1988–1991, 16% in NHANES III 1991–1994, and 38% in NHANES 1999–2004. To assess the impact of the smaller samples that had missing information on the year housing was built, we used 2 strategies: (1) we compared the bivariable results from Tables 1 through 3 ⇑⇑⇑ to a bivariable analysis by using the 4817 children included in the multivariable analysis, and (2) we computed multivariable regression models that omitted the housing risk variable. In the bivariable analysis, the percentage of children with BLLs of ≥10 μg/dL were affected more by the smaller sample (with these percents tending to be smaller than in the original bivariable analysis) than were geometric means, with differences being more evident for NHANES 1999–2004. However, inferences from the bivariable analysis using the smaller sample were comparable to the original bivariable analysis for both percent of children with BLLs of ≥10 μg/dL and for geometric means. In the regression analyses that excluded housing risk, the primary impact on the logistic model was a reduced odds ratio for children ages 1 to 2 years compared with children ages 3 to 5 years. However, inferences were comparable to those from the models containing year housing built. In the linear models, excluding year housing built from the model reduced the model R2 from 0.36 to 0.27, but had little impact on the computed main effects compared with the models containing year housing built. These analyses indicate that the year housing built category is an important predictor for elevated BLLs. However, missing data on this variable did not impact inferences for other risk factors.
Children Previously Tested for Lead
Because the information on previous lead testing was first obtained in the NHANES 1988–1991, the percentage of 1- to 5-year-old children tested increased by 274% from 8.9% to 33.3% (P < .0001) (Table 5). For non-Hispanic black children, the percentage tested increased from 21.0% in 1988–1991 to 43.6% in 1999–2004 (P < .0001). In Mexican American children, the percentage tested increased dramatically, from 1.2% in 1988–1991 to 28.0% in 1999–2004 (P < .0001). Among children enrolled in Medicaid in 1988–1991, 19.2% of children had had a blood lead test at some point before the NHANES examination; in 1999–2004 this percentage had increased to 41.9% (P < .001). Among the small percentage of children with elevated BLLs (≥10 μg/dL) in the NHANES, the percentage previously tested was 43.0% in 1999–2004, compared with 30.1% in 1988–1991; however, this difference was not statistically significant (P > .05).
BLLs in US children continue to decrease most likely as a result of an intense coordinated effort to control or eliminate lead sources in children's environments by government officials, health care and social service providers, and the communities most at risk. Although disparities have lessened, the mean BLLs and distribution of BLLs continue to be higher for low-income children, non-Hispanic black children, and children living in older housing stock (built before 1950). The analysis also indicated that the vast majority of US children still have some low-level exposure to lead. Given that no “safe” BLL in children has been identified,3–5 primary prevention of lead poisoning will play an important role in continuing lead control efforts.
Since the 1970s, the NHANES have provided valuable information on children's BLLs and risk factors for elevated BLLs in the United States. Because these surveys are based on a nationally representative sample, estimates can be generalized only to the US population; the sample is not designed to provide estimates for smaller geographic areas or specific populations where the risk of elevated BLLs is high. For example, 1 inner-city prevalence study in 2001 found that nearly 33% of children in 1 community had elevated BLLs12 much higher than the national prevalence of 1.6% reported here. Therefore, it may not be appropriate to assume that local BLLs would be similar to the NHANES estimates. State and local surveillance data are needed to monitor local trends. For this reason, the CDC funds childhood lead poisoning prevention programs to include surveillance of BLLs. Data from CDC-funded surveillance programs consistently have shown that the risk for exposure to lead is not evenly distributed through the pediatric population.8,13,29 When health care providers are determining which children to test for lead poisoning, they should assess whether a child has any known risk factors for lead poisoning.30–32
The percentage of children who have had a previous BLL test increased almost fourfold in the NHANES 1999–2004 compared with NHANES III Phase 1 (1988–1991). More importantly, markedly larger percentages of highest-risk children (eg, Medicaid-enrolled children, children from low-income families, and children from the NHANES with elevated BLLs) reported having had a previous blood lead test in the NHANES 1999–2004 compared with NHANES III Phase 1, although the increase was not statistically significant in children with elevated BLLs. Since 1997, the CDC has recommended that states develop plans to target testing to children at high risk (state testing plans can be accessed at www.cdc.gov/nceh/lead). The CDC and the Centers for Medicare and Medicaid Services also recommend that states link blood lead surveillance and Centers for Medicare and Medicaid Services claims data to identify children and areas where testing is inadequate.33
The data suggest that the recommendation for targeted rather than universal blood lead testing for preschool children has not resulted in a decrease in testing among children at highest risk. Nevertheless, fewer than half of children enrolled in Medicaid had been tested for lead poisoning. Federal regulations require that all children enrolled in Medicaid must receive a blood lead screening test at ages 12 and 24 months. All children aged 36 to 72 months who have not previously been screened must also receive a blood lead test. The American Academy of Pediatrics30 and the CDC's Advisory Committee for Childhood Lead Poisoning Prevention31 concur. No state is exempt from this testing requirement. A limitation of the testing prevalence estimates is that they are parent reported and may be biased. However, testing may be improved by monitoring testing by various providers and working to improve testing rates. For example, testing of children enrolled in Medicaid varies by the child's usual place of health care. A recent Rhode Island study found that although the percentage of enrolled children tested was high (80% had at least 1 blood lead test), testing varied by provider site: 68% for office-based physicians, 86% for neighborhood health centers, 86% for hospital-based clinics, and 91% for staff-model health maintenance organizations.34
Children can be exposed to lead from multiple sources. Because leaded house paint is a common high-dose source of exposure for children living in the United States, the focus of US public health efforts should continue to be on reducing exposure to leaded house paint and the dust and soil it contaminates.35–38 However, there are other less-common sources of lead in the United States that also have high-lead content. Some CDC-funded childhood lead poisoning prevention programs have documented that lead in consumer products, imported toys, imported and traditional medicines and house wares, and “take-home” exposure for children whose parents work with lead have been identified for as many as 15% to 30% of children with elevated BLLs.39,40 The single most important step to reduce children's BLLs is to identify and remove or control lead sources.41
Lead poisoning and other public health issues arising from environmental problems are often complex, costly, controversial, and require creative solutions. It is critical to incorporate human health concerns into environmental policy-making, as public health problems arise from, and solutions must be sought, beyond the health sector (eg, environmental, social, commercial, economic, and political sectors).42 The challenge is to develop strategies that can prevent children and adults from ever becoming poisoned by lead. Successful efforts combine epidemiologic surveillance, source identification and reduction, regulatory enforcement, and a long-term government commitment to eliminating lead as a public health threat, especially to children.
Children's BLLs continue to decline in the United States, even in historically high-risk groups for lead poisoning. To maintain progress made as well as eliminate remaining disparities, efforts must continue to test children at high risk for lead poisoning and identify and control lead sources that can poison children. Coordinated prevention strategies that are implemented at national, state, and local levels will help achieve the goal of elimination of elevated BLLs.
- Accepted November 11, 2008.
- Address correspondence to Robert L. Jones, PhD, Centers for Disease Control and Prevention, National Center for Environmental Health, 4770 Buford Hwy, Atlanta, GA 30341. E-mail:
The findings and conclusions in this report are those of the author(s) and do not necessarily represent the views of the Centers for Disease Control and Prevention or the Agency for Toxic Substances and Disease Registry.
The authors have indicated they have no financial relationships relevant to this article to disclose.
What's Known on This Subject
The analysis of national trends in blood lead exposure is well documented for the NHANES before 1999. The evaluation of how well children at high risk (aged 1–5 years) are being screened for lead exposure after 1998 is limited.
What This Study Adds
This study evaluates and reports the national trends in BLLs and the extent of blood lead testing in children for the period of 1988–2004 in various risk groups.
- ↵Agency for Toxic Substances and Disease Registry (ATSDR). Toxicological Profile for Lead. Atlanta, GA: ATSDR; 1999
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