Children's Blood Lead Research Articles

Exposure of U.S. Children to Residential Dust Lead, 1999–2004: I. Housing and Demographic Factors

BackgroundLead-contaminated house dust is a major source of lead exposure for children in the United States. In 1999–2004, the National Health and Nutrition Examination Survey (NHANES) collected dust lead (PbD) loading samples from the homes of children 12–60 months of age.ObjectivesIn this study we aimed to compare national PbD levels with existing health-based standards and to identify housing and demographic factors associated with floor and windowsill PbD.MethodsWe used NHANES PbD data (n = 2,065 from floors and n = 1,618 from windowsills) and covariates to construct linear and logistic regression models.ResultsThe population-weighted geometric mean floor and windowsill PbD were 0.5 μg/ft2 [geometric standard error (GSE) = 1.0] and 7.6 μg/ft2 (GSE = 1.0), respectively. Only 0.16% of the floors and 4.0% of the sills had PbD at or above current federal standards of 40 and 250 μg/ft2, respectively. Income, race/ethnicity, floor surface/condition, windowsill PbD, year of construction, recent renovation, smoking, and survey year were significant predictors of floor PbD [the proportion of variability in the dependent variable accounted for by the model (R2) = 35%]. A similar set of predictors plus the presence of large areas of exterior deteriorated paint in pre-1950 homes and the presence of interior deteriorated paint explained 20% of the variability in sill PbD. A companion article [Dixon et al. Environ Health Perspect 117:468–474 (2009)] describes the relationship between children’s blood lead and PbD.ConclusionMost houses with children have PbD levels that comply with federal standards but may put children at risk. Factors associated with PbD in our population-based models are primarily the same as factors identified in smaller at-risk cohorts. PbD on floors and windowsills should be kept as low as possible to protect children.

Exposure of U.S. Children to Residential Dust Lead, 1999–2004: II. The Contribution of Lead-Contaminated Dust to Children’s Blood Lead Levels

BackgroundThe U.S. Centers for Disease Control and Prevention collected health, housing, and environmental data in a single integrated national survey for the first time in the United States in 1999–2004.ObjectivesWe aimed to determine how floor dust lead (PbD) loadings and other housing factors influence childhood blood lead (PbB) levels and lead poisoning.MethodsWe analyzed data from the 1999–2004 National Health and Nutrition Examination Survey (NHANES), including 2,155 children 12–60 months of age with PbB and PbD measurements. We used linear and logistic regression models to predict log-transformed PbB and the odds that PbB was ≥ 5 and ≥ 10 μg/dL at a range of floor PbD.ResultsThe population-weighted geometric mean (GM) PbB was 2.0 μg/dL (geometric standard error = 1.0). Age of child, race/ethnicity, serum cotinine concentration, poverty-to-income ratio, country of birth, year of building construction, floor PbD by floor surface and condition, windowsill PbD, presence of deteriorated paint, home-apartment type, smoking in the home, and recent renovation were significant predictors in either the linear model [the proportion of variability in the dependent variable accounted for by the model (R2) = 40%] or logistic model for 10 μg/dL (R2 = 5%). At floor PbD = 12 μg/ft2, the models predict that 4.6% of children living in homes constructed before 1978 have PbB ≥ 10 μg/dL, 27% have PbB ≥ 5 μg/dL, and the GM PbB is 3.9 μg/dL.ConclusionsLowering the floor PbD standard below the current standard of 40 μg/ft2 would protect more children from elevated PbB.

Blood Lead Levels: Rhoads and Brown Respond

Rothenberg states that the level of concern for blood lead in children should be lowered from 10 μg/dL, but he provides little cogent rationale for doing so. As basic science support, he cites studies that a) exposed isolated neurons to a 3 μM solution of lead (Ishihara et al. 1995), a concentration that is 5,000 times the plasma levels expected in a child with a blood lead level (BLL) of 5 μg/dL (Manton et al. 2001); b) a study of squirrel monkeys exposed in utero to maternal BLLs in the 20- to 70-μg/dL range (Newland et al. 1996); and c) a study of occupationally exposed workers with a median BLL of 17.1 μg/dL that contains no data on neurologic effects of lead (Murata et al. 2003). Rothenberg’s choice of these citations emphasizes how little basic science work has been done on neuro-developmental effects at the very low levels of lead under discussion. There was a 90% decrease in U.S. childhood BLLs from the late 1970s to the late 1990s (Pirkle et al. 1994). If the regression coefficients relating BLLs 135. To our knowledge, no such effect has been noted in the education literature, nor is it evidenced, for instance, among the increasing proportion of U.S. students admitted to U.S. graduate programs (Basken 2006). What measures can be used to look more formally for this IQ improvement? IQ itself is problematic because the Flynn effect and adjustments in test instruments make secular changes in IQ hard to interpret. The teaching content in science and math has likely shifted over this period. Therefore, in our editorial (Brown and Rhoads 2008) we cited reading scores that measure a key skill that has been identified repeatedly as being affected by lead exposure among other factors. Campbell et al. (2000) reported that reading scores, examined with a suitable time lag in large nationally representative samples of children, were virtually unchanged over the critical period of declining lead levels. Rothenberg is correct that modest gains in math and science were recorded, but these changes could easily have other explanations, and they do nothing to explain the absence of any signal in reading scores. Although there may be other explanations for this absence, the simplest explanation of this paradox is that the published regression coefficients relating BLLs < 10 μg/dL to cognitive measures, all of which come from observational studies, are biased. This possibility is suggested by the steepening of the IQ curve at low lead levels [Centers for Disease Control and Prevention (CDC) 2005b]. Regardless of one’s view of the above evidence, it is important to recognize that virtually all of the progress made in eliminating childhood lead poisoning has been through primary prevention—the control or elimination of lead sources before children are exposed. This approach has lowered the proportion of 1- to 5-year-old children with BLLs > 10 μg/dL from well above 50% 30 years ago to 1.6% in 1999–2002 (CDC 2005a). The percentage is almost certainly lower today. Primary prevention has been proven to work and deserves the continuing attention that we described in our editorial (Brown and Rhoads 2008). Primary prevention can, and should, include increased attention to controlling exposures from lead paint hazards, imported foods, medicines, cosmetics, and toys. Renewed emphasis on screening with a lower BLL of concern would be expensive, intrusive to families, and hard to justify in the absence of proven, practical strategies for reducing lead levels in identified children. Further, it would likely deflect needed resources away from the primary prevention effort. The CDC, in collaboration with federal, state, and local agencies, has outlined and begun to implement a comprehensive, society-wide effort to prevent lead exposure in children while maintaining efforts to identify and treat children with elevated BLLs (CDC 2005b). The CDC has also developed specific recommendations for health care and social service providers, scientists, and public health practitioners who are interested in actively participating in these primary prevention efforts by providing valuable leadership and expertise (Binns et al. 2007; CDC 2005b). By working together with federal, state, and local agencies to foster expansion of primary prevention services, these child advocates can accelerate achieving our mutual goal—lead-safe environments for the nation’s children.

Tracking Childhood Exposure to Lead and Developmental Disabilities

Elevated levels of lead detected in the blood are associated with harmful effects on children's learning and behavior. The goal of the current Environmental Public Health Tracking Project was to examine the relationship between selected developmental disabilities and childhood blood lead levels in a population-based sample. Using extant datasets from the Florida Department of Health, Childhood Lead Poisoning Prevention Program, and the Florida Department of Education, we were able to isolate a linked dataset of children who were tested for lead poisoning and attended public schools. Special education categories served as a proxy for developmental disabilities; the prevalence of these disabilities in the sample of children with blood lead levels was compared with that in children who attended the same schools but were not tested for lead poisoning. Results indicated that children screened for lead poisoning were more likely to be receiving services for behavior problems, mental retardation, learning disabilities, or a speech-language impairment than other children attending the same schools. Implications for using administrative datasets to examine this relationship are discussed.

Blood Lead Levels in Children

Blood Lead Levels in Children

Lead in housing paints: An exposure source still not taken seriously for children lead poisoning in China

After prohibitions on lead gasoline additives, which have proved to be a public health accomplishment world wide, many countries focus on other exposure source of children lead poisoning. Removing lead from paints is one of the important measures. Although there have been regulatory limits on lead in paints in China, evidence reported in this article indicates that lead-based paints were very common in new paints available for housing and in existing residential paints. Twenty-nine of 58 new paint samples (50%) had lead content equal to or exceeding 600 ppm, including 14 (24%) equal to or exceeding 5000 ppm. The highest sample contained 153,000 ppm lead, about 15% of the paint weight. Thirty-two new paints (55%) contained “soluble” lead exceeding 90 ppm, the current lead limit on paints in China. Of the existing paints, 16 of 28 samples of existing paint (57%) collected from 24 kindergartens and primary schools had lead concentrations equal to or exceeding 600 ppm, including six samples (21%) equal to or exceeding 5000 ppm. The highest concentration sample contained 51,800 ppm lead, accounting for 5.2% of the paint weight. It has been shown in many areas that paint lead is a major exposure source for lead poisoning in children. This is particularly true after the phasing out of lead from gasoline. Effective limitation on lead content in new paint, and lead hazard control measures directed towards existing paint, could reduce children blood lead levels (BLLs). There has been a lead standard for paints in China since 1986 and a stricter limit was introduced in recent years. Governments should take it seriously and enforce regulations, commit a long-term challenge to eliminate paint lead as it is the threat to current and the next generation.

Windblown Lead Carbonate as the Main Source of Lead in Blood of Children from a Seaside Community: An Example of Local Birds as “Canaries in the Mine”

BackgroundIn late 2006, the seaside community in Esperance, Western Australia, was alerted to thousands of native bird species dying. The source of the lead was thought to derive from the handling of Pb carbonate concentrate from the Magellan mine through the port of Esperance, begun in July 2005. Concern was expressed for the impact of this process on the community.ObjectiveThis study was designed to evaluate the source of Pb in blood of a random sample of the community using Pb isotope ratios.MethodsThe cohort comprised 49 children (48 < 5 years of age) along with 18 adults (> 20 years of age) with a bias toward higher blood lead (PbB) values to facilitate source identification.ResultsMean PbB level of the children was 7.5 μg/dL (range, 1.5–25.7 μg/dL; n = 49; geometric mean, 6.6 μg/dL), with four children whose PbB was > 12 μg/dL. The isotopic data for blood samples lay around two distinct arrays. The blood of all children analyzed for Pb isotopes contained a contribution of Pb from the Magellan mine, which for young children ranged from 27% up to 93% (mean, 64%; median, 71%). Subtraction of the ore component gave a mean background PbB of 2.3 μg/dL. Several children whose PbB was > 9 μg/dL and most of the older subjects have complex sources of Pb.ConclusionsThe death of the birds acted as a sentinel event; otherwise, the exposure of the community, arising from such a toxic form of Pb, could have been tragic. Isotopic data and mineralogic and particle size analyses indicate that, apart from the recognized pathway of Pb exposure by hand-to-mouth activity in children, the inhalation pathway could have been a significant contributor to PbB for some of the very young children and in some parents.

Airborne lead carbonate as the main source of lead in blood of children from a seaside community: An example of “canaries” in the mine

Airborne lead carbonate as the main source of lead in blood of children from a seaside community: An example of “canaries” in the mine

Yearly measurements of blood lead in Swedish children since 1978: The declining trend continues in the petrol-lead-free period 1995–2007

Background We have measured blood lead concentrations (B-Pb) in Swedish children, yearly since 1978. As reported previously, a substantial decrease of B-Pb was found for the period 1978–1994 (2440 children measured), as an effect of gradual reduction of lead in petrol. In another report focusing on the petrol-lead-free period 1995–2001, we noted that B-Pb seemed to stabilize at an average level close to 20 μg/L. Objective We here analyze data from the extended petrol-lead-free period 1995–2007. Methods B-Pb was measured in 1268 children, aged 7–11 years, from the municipalities of Landskrona and Trelleborg in southern Sweden, yielding 1407 measurements on B-Pb (since 139 children were measured in two different calendar years). Results We observed statistically significant decreases of the average concentrations during the recent years. The average B-Pb reduction rate was close to 5%/yr in the petrol-lead-free period 1995–2007; a similar reduction rate was estimated for the period with gradual reduction of lead in petrol, 1978–1994. The most recent geometric mean of B-Pb was 13.1 (range, 6.9–29.1) μg/L in Trelleborg (sample year 2005) and 13.2 (5.7–58.5) μg/L in Landskrona (2007). A declining B-Pb time trend was observed during the recent years among children who lived in near smelter, urban, and rural residential areas, respectively. B-Pb was influenced by the variables sex (boys had higher B-Pb), parents’ smoking habits (children with one or both parents smoking had higher B-Pb), and potentially lead-exposing hobbies (for example, shooting air guns). Conclusion Children's B-Pb levels can continue to decline markedly more than a decade after lead in petrol has been phased out in a country.

Association of Prenatal and Childhood Blood Lead Concentrations with Criminal Arrests in Early Adulthood

BackgroundChildhood lead exposure is a purported risk factor for antisocial behavior, but prior studies either relied on indirect measures of exposure or did not follow participants into adulthood to examine the relationship between lead exposure and criminal activity in young adults. The objective of this study was to determine if prenatal and childhood blood lead concentrations are associated with arrests for criminal offenses.Methods and FindingsPregnant women were recruited from four prenatal clinics in Cincinnati, Ohio if they resided in areas of the city with a high concentration of older, lead-contaminated housing. We studied 250 individuals, 19 to 24 y of age, out of 376 children who were recruited at birth between 1979 and 1984. Prenatal maternal blood lead concentrations were measured during the first or early second trimester of pregnancy. Childhood blood lead concentrations were measured on a quarterly and biannual basis through 6.5 y. Study participants were examined at an inner-city pediatric clinic and the Cincinnati Children's Hospital Medical Center in Cincinnati, Ohio. Total arrests and arrests for offenses involving violence were collected from official Hamilton County, Ohio criminal justice records. Main outcomes were the covariate-adjusted rate ratios (RR) for total arrests and arrests for violent crimes associated with each 5 μg/dl (0.24 μmol/l) increase in blood lead concentration. Adjusted total arrest rates were greater for each 5 μg/dl (0.24 μmol/l) increase in blood lead concentration: RR = 1.40 (95% confidence interval [CI] 1.07–1.85) for prenatal blood lead, 1.07 (95% CI 0.88–1.29) for average childhood blood lead, and 1.27 (95% CI 1.03–1.57) for 6-year blood lead. Adjusted arrest rates for violent crimes were also greater for each 5 μg/dl increase in blood lead: RR = 1.34 (95% CI 0.88–2.03) for prenatal blood lead, 1.30 (95% CI 1.03–1.64) for average childhood blood lead, and 1.48 (95% CI 1.15–1.89) for 6-year blood lead.ConclusionsPrenatal and postnatal blood lead concentrations are associated with higher rates of total arrests and/or arrests for offenses involving violence. This is the first prospective study to demonstrate an association between developmental exposure to lead and adult criminal behavior.

Decreased Brain Volume in Adults with Childhood Lead Exposure

BackgroundAlthough environmental lead exposure is associated with significant deficits in cognition, executive functions, social behaviors, and motor abilities, the neuroanatomical basis for these impairments remains poorly understood. In this study, we examined the relationship between childhood lead exposure and adult brain volume using magnetic resonance imaging (MRI). We also explored how volume changes correlate with historic neuropsychological assessments.Methods and FindingsVolumetric analyses of whole brain MRI data revealed significant decreases in brain volume associated with childhood blood lead concentrations. Using conservative, minimum contiguous cluster size and statistical criteria (700 voxels, unadjusted p < 0.001), approximately 1.2% of the total gray matter was significantly and inversely associated with mean childhood blood lead concentration. The most affected regions included frontal gray matter, specifically the anterior cingulate cortex (ACC). Areas of lead-associated gray matter volume loss were much larger and more significant in men than women. We found that fine motor factor scores positively correlated with gray matter volume in the cerebellar hemispheres; adding blood lead concentrations as a variable to the model attenuated this correlation.ConclusionsChildhood lead exposure is associated with region-specific reductions in adult gray matter volume. Affected regions include the portions of the prefrontal cortex and ACC responsible for executive functions, mood regulation, and decision-making. These neuroanatomical findings were more pronounced for males, suggesting that lead-related atrophic changes have a disparate impact across sexes. This analysis suggests that adverse cognitive and behavioral outcomes may be related to lead's effect on brain development producing persistent alterations in structure. Using a simple model, we found that blood lead concentration mediates brain volume and fine motor function.

Status of children's blood lead levels in Pakistan: Implications for research and policy

Data on blood lead levels, sources of lead and health effects were reviewed among children in Pakistan. A systematic review was conducted of published studies found through PubMed, an index of Pakistani medical journals PakMediNet and unpublished reports from governmental and non-governmental agencies in Pakistan. With the exception of a few studies that had adequate sample sizes and population-based samples, most studies were small and used convenience sampling methods to select study subjects. Overall, blood lead levels declined from 38 microg/dl in 1989 to 15 microg/dl in 2002. The major sources of lead that directly or indirectly resulted in lead exposure of children included: leaded petrol; father's occupation in lead-based industry; leaded paint; traditional cosmetics; and remedies. Apart from leaded petrol, there was no information regarding the level of lead in other sources such as paints and the household environment. Very little information was available regarding the adverse health effects of lead among children. The phasing out of leaded petrol was a commendable mitigation measure undertaken in July 2001 in Pakistan. A comprehensive assessment is now needed urgently to explore other sources of lead contributing to adverse health effects, and to plan intervention options with the ultimate goal of reducing the burden of disease due to lead exposure.

Reduction of elevated blood lead levels in children in North Carolina and Vermont, 1996-1999.

BackgroundFew studies have examined factors related to the time required for children’s blood lead levels (BLLs) ≥ 10 μg/dL to decline to < 10 μg/dL.ObjectivesWe used routinely collected surveillance data to determine the length of time and risk factors associated with reducing elevated BLLs in children below the level of concern of 10 μg/dL.MethodsFrom the North Carolina and Vermont state surveillance databases, we identified a retrospective cohort of 996 children < 6 years of age whose first two blood lead tests produced levels ≥ 10 μg/dL during 1996–1999. Data were stratified into five categories of qualifying BLLs and analyzed using Cox regression. Survival curves were used to describe the time until BLLs declined below the level of concern. We compared three different analytic methods to account for children lost to follow-up.ResultsOn average, it required slightly more than 1 year (382 days) for a child’s BLL to decline to < 10 μg/dL, with the highest BLLs taking even longer. The BLLs of black children [hazard ratio (HR) = 0.84; 95% confidence interval (CI), 0.71–0.99], males (HRmale = 0.83; 95% CI, 0.71–0.98), and children from rural areas (HRrural = 0.83; 95% CI, 0.70–0.97) took longer to fall below 10 μg/dL than those of other children, after controlling for qualifying BLL and other covariates. Sensitivity analysis demonstrated that including censored children estimated a longer time for BLL reduction than when using linear interpolation or when excluding censored children.ConclusionChildren with high confirmatory BLLs, black children, males, and children from rural areas may need additional attention during case management to expedite their BLL reduction time to < 10 μg/dL. Analytic methods that do not account for loss to follow-up may underestimate the time it takes for BLLs to fall below the recommended target level.

An epidemiological survey on saturnism among children due to lead pollution released from township enterprise

To understand the current situations of saturnism and blood lead levels of children resided in village and circumjacent areas, and to know its relations with sex, age and other factors on children' s health as to providing some evidences for prevention and control. An epidemiological survey was conducted for finding out the pollution sources and for a better understanding of the surrounding environment. All 221 children under 14 years old, from the lead pollution villages and surrounding establishments were enrolled, and their blood lead levels were detected by graphite atomizer absorption spectrophotometer method. Symptoms of the saturnism were investigated through a standardized questionnaire. SPSS13.0 software was administrated for data analysis. High blood lead level identification rate was 66.06% (146/221), and saturnism rate 32.13% (71/221). The children's blood lead levels among group 1, group 2, group 3 in this village and jade factory were (161.20 +/- 32.94), (176.60 +/- 43.62), (258.00 +/-106.08) and (238.01 +/- 55.20) microg/L respectively and the significant differences were observed through Kruskal-Wallis test (chi2 = 51.84, df= 3, P<0. 01). The blood lead levels of children from group 3 in this village and the jade factory were higher than those of other two groups. No correlation was found between children's age and blood lead level (r = 0.10, P = 0.13). There was a significant difference in blood lead levels between boys and girls (t' = 3.83, P<0.01). With the children's blood lead levels rising, the occurrence rate of main saturnism symptoms was significantly increased. This survey suggested that the pollution source was a coarse lead smelter. The blood lead level should ke overwhelmingly increased among children who live nearby the higher level of lead blood, that living nearby the lead smeltery,might result in stautnism and negative effect on children's healthy.

Unexplained decline in the prevalence of anemia among US children and women between 1988–1994 and 1999–2002

We used data from the 1988–1994 and 1999–2002 National Health and Nutrition Examination Surveys to examine recent anemia changes in US children and women. We calculated the prevalence of anemia [hemoglobin &lt;11.0 g/dL (&lt;24 m), &lt;11.1 g/dL (24–59 m), &lt;12.0 g/dL (women)], iron deficiency anemia (anemia + abnormal value ≥2: serum ferritin, transferrin saturation, erythrocyte protoporphyrin) and high blood lead (≥10 μg/dL) and anemia in children 12–59 m and women 20–49 y. In women we also calculated the prevalence of folate deficiency (erythrocyte folate &lt;317.2 nmol/L) and anemia and high C‐reactive protein (&gt;10 mg/L) and anemia. Multiple logistic regression was used to compare total and type‐specific anemia between surveys, controlling for race, age and sex. Anemia declined significantly in children (from 8.0% to 3.6%, OR=0.4; 95% CI: 0.3, 0.7) and women (10.8% to 6.9%, 0.6; 0.4, 0.7). The prevalence of iron deficiency anemia did not change significantly in children (1.5% vs. 1.2%, 0.7; 0.4, 1.5) or women (4.9% vs. 4.1%, 0.8; 0.6, 1.1). Folate deficiency and anemia declined significantly in women (4.1% to 0.5%, 0.1; 0.1, 0.2), but none of the types of anemia explained the decline in total anemia when included in multivariate models. Anemia declined significantly in US women and children between 1988–1994 and 1999–2002, but the decline was not associated with changes in iron or folate deficiency, inflammation or blood lead.

Testing Lead’s Limits: Time for Another Reassessment of Guidelines?

Cohort data during the 1980s linked blood lead levels of at least 10 μg/dL with low cognitive test scores in children, prompting the decision by the Centers for Disease Control and Prevention to redefine the action level for elevated blood lead from 25 to 10 μg/dL. Now, new data add to the growing evidence that the 10-μg/dL level may not be protective [EHP 116:243–248; Jusko et al.]. The investigators recruited children aged 24–30 months who had been previously enrolled in a dust control study. All the children were born between July 1994 and January 1995 and lived in Rochester, New York, with parents expressing no plans to relocate. To reduce the possibility of misclassification of exposure, blood samples were collected for measuring blood lead on up to 8 occasions (at ages 6, 12, and 18 months, and annually from age 2 through 6 years). The children were given the Wechsler Preschool and Primary Scale of Intelligence during their 6-year visit by an examiner trained in neurobehavioral testing and blinded to each child’s blood lead level. These assessments were made at an age when IQ is measured reliably and is a significant predictor of IQ scores and educational and occupational success during adolescence and adulthood. The data analysis employed a regression model that controlled for family income; maternal education, race, prenatal smoking, and Stanford-Binet IQ score; child’s birth weight; breastfeeding; crowding in the home; and quality of childrearing (using the Home Observation for Measurement of the Environment Inventory). The average blood lead level was 7.2 μg/dL, and lead concentrations for more than half the children never exceeded the 10 μg/dL mark. Even at these concentrations, blood lead levels were inversely related to IQ scores. The association was most pronounced for the Full-Scale and Performance IQ scores. Children whose blood lead levels measured in the 5- to 9.9-μg/dL range had significantly lower IQ scores than children with levels below 5 μg/dL. A descriptive analysis of peak exposure throughout early childhood suggested an inverse association between maximal blood lead level and IQ at blood lead levels less than 3 μg/dL; levels as low as about 2 μg/dL were associated with significant IQ declines. These findings, reinforced by previous data gathered by the same research team, support the need for a further reassessment of standard guidelines for responding to blood lead in infants and children.

The Relationship between Children's Blood Lead Level and Postural Stability

The Relationship between Children's Blood Lead Level and Postural Stability Children, especially younger, are recognized as very susceptible to environmental lead exposure. In order to assess the effect of lead on spontaneous postural sway, we studied 327 children 4-13 years old, living in 4 cities in Upper Silesia an industrial region of Poland. Lead concentration in blood was measured by absorption atomic spectrometry (AAS) and posturography was performed using CATSYS 2000 - SWAY 7.0 equipment. Children's postural sway characteristics decreased with age. Particular variables had higher values for boys than girls and were positively associated with blood lead levels. There was an association between postural sway characteristics and smoking habits of mother, usage of aminoglycosides and paracetamol. Posturography seems to be a useful tool for assessment of lead exposure effects on the nervous system at low blood lead levels.

Risk for Elevated Blood Lead Levels in 3- and 4-Year-Old Children

We conducted a study to evaluate the relation between environmental, demographic, and medical risk factors and late-onset childhood lead poisoning, defined as children who were poisoned at age 3 or older. We performed a retrospective case-control study of 262 children whose test results showed non-elevated (<10 microg/dl) blood lead levels (BLLs) before age 2 but levels > or =10 microg/dl after age 3 and of 300 control children who had non-elevated BLL test results before age 2 and also after age 3. The target population was children receiving care at MetroHealth Medical Center in Cleveland, OH. We modeled the association between demographic and clinical risk factors and BLLs > or =10 microg/dl after age 3. Covariates considered were race, gender, body mass index, immunization status, mean corpuscular volume, hematocrit, red cell volume distribution width (RDW), red blood count, hemoglobin, baseline BLL result, and time between the baseline and second BLL test. Case children were more likely to be male (P < 0.0001), black (P = 0.0189) and to have a high RDW defined as > or =14.5 % (P = 0.0083). On the basis of the final model, children with BLLs 7-9 microg/dl before age 2 and again after a follow-up BLL test (<21 months) were more likely to become lead poisoned than were control children. The risk of black children developing lead poisoning increased over time, regardless of the child's first BLL test result. Although national recommendations are to test children's blood lead levels at ages 1 and 2, children living in high-risk areas with such risk factors should have a blood lead test at these older ages.

Nonlinear association between soil lead and blood lead of children in metropolitan New Orleans, Louisiana: 2000–2005

Metropolitan New Orleans is unique because it has a universal blood lead (BL) screening dataset ( n = 55,551) from 2000–2005 spatially coupled with a soil lead (SL) dataset ( n = 5467) completed in 2000. We evaluated empirical associations between measurements of SL and BL exposure responses of children in New Orleans by stratifying the databases by Census Tracts and statistically analyzing them with permutation methods. A consistent curvilinear association occurred annually between SL and BL with robust significance ( P-values < 10 − 23 ). The mathematical model of the pooled BL datasets for 2000–2005 is: BL = 2.038 +0.172 × (SL) 0.5 (agreement ( ℜ) of 0.534, an r 2 of 0.528, and a P-value of 1.0 × 10 − 211 ) indicating that chance alone cannot explain the association. Below 100 mg/kg SL children's BL exposure response is steep (1.4 μg/dL per 100 mg/kg), while above 300 mg/kg SL the BL exposure response is gradual (0.32 μg/dL per 100 mg/kg). In 1995, the BL prevalence was 37% ≥ 10 μg/dL for the most vulnerable poor and predominantly African-American children. In the era of universal screening the prevalence of elevated BL is 11.8% ≥ 10 μg/dL for the general population of children. The SL map describes community variations of potential BL exposure. If health effects occur at BL ≥ 2 μg/dL, then 93.5% of the children in New Orleans are at risk. These results reinforce the proposal that prevention of childhood Pb exposure must include SL remediation as demonstrated by a New Orleans pilot project and a proactive Norwegian government program.

The Prevalence of Blood Lead Levels ≥5μg/dl among 1 to 21 Year Old U.S. Population and Trends from 1988–1994 through 1999–2002

Elevated blood lead in children is defined as ≥10ug/dl. In light of data suggesting adverse health effects at blood lead levels (PbB) <10ug/dl, lowering the current definition has been recommended. To ascertain the population level impact of such a change, we calculated the prevalence and distribution of PbB ≥5μg/dl in 1 to 21 year old population in the United States. Furthermore, we characterized changes in PbB between 1988–1994 and 1999–2002. We analyzed data from the National Health and Nutrition Examination Survey (NHANES) III (n=10,755) and NHANES 1999–2002 (n=8,013). Between 1988–1994 and 1999–2002, the geometric mean PbB declined from 2.88μg/dl to 1.94μg/dl in children 1 to 5 years, 1.80 μg/dl to 1.36μg/dl in children 6 to 11 years, and 1.24μg/dl to 1.02μg/dl in children and adolescents 12 to 21 years of age. Also, the prevalence of PbB ≥5μg/dl declined from 25.7% to 8.8%, 12.8% to 3.0%, and 7.5% to 1.2% in these age groups, respectively. In 1999–2002, a disproportionately higher prevalence of PbB ≥5μg/dl was present among children 1 to 5 and 6 to 11 years old who were non-Hispanic blacks, had lower household income, were not home owners, and lived in older housing. Among 12 to 21 year olds, having lower income levels, male sex, and no health insurance were each associated with a higher prevalence of PbB ≥5μg/dl. Despite an overall decline in PbB, a substantial proportion of children (approximately 2.4 million) may be at risk for adverse health effects from lead exposure.