Low-Level Environmental Lead Exposure
Lead is a confirmed neurotoxin, but questions remain about lead-associated intellectual deficits at blood lead levels < 10 µg/dL and whether lower exposures are, for a given change in exposure, associated with greater deficits. The objective of this study was to examine the association of intelligence test scores and blood lead concentration, especially for children who had maximal measured blood lead levels < 10 µg/dL. We examined data collected from 1,333 children who participated in seven international population-based longitudinal cohort studies, followed from birth or infancy until 5-10 years of age. The full-scale IQ score was the primary outcome measure. The geometric mean blood lead concentration of the children peaked at 17.8 µg/dL and declined to 9.4 µg/dL by 5-7 years of age; 244 (18%) children had a maximal blood lead concentration < 10 µg/dL, and 103 (8%) had a maximal blood lead concentration < 7.5 µg/dL. After adjustment for covariates, we found an inverse relationship between blood lead concentration and IQ score. Using a log-linear model, we found a 6.9 IQ point decrement [95% confidence interval (CI), 4.2-9.4] associated with an increase in concurrent blood lead levels from 2.4 to 30 µg/dL. The estimated IQ point decrements associated with an increase in blood lead from 2.4 to 10 µg/dL, 10 to 20 µg/dL, and 20 to 30 µg/dL were 3.9 (95% CI, 2.4-5.3), 1.9 (95% CI, 1.2-2.6), and 1.1 (95% CI, 0.7-1.5), respectively. For a given increase in blood lead, the lead-associated intellectual decrement for children with a maximal blood lead level < 7.5 µg/dL was significantly greater than that observed for those with a maximal blood lead level ≥ 7.5 µg/dL (p = 0.015). We conclude that environmental lead exposure in children who have maximal blood lead levels < 7.5 µg/dL is associated with intellectual deficits.
The preponderance of experimental and human data indicates that there are persistent and deleterious effects of blood lead levels > 10 µg/dL on brain function, including lowered intelligence, behavioral problems, and diminished school performance (Baghurst et al. 1992; Bellinger et al. 1992; Cory-Slechta 1997; Dietrich et al. 1993; Ernhart et al. 1989; National Research Council 1993; Needleman and Gatsonis 1990; Pocock et al. 1994; Rice 1993; Wasserman et al. 1997; Yule et al. 1981). Lead toxicity, defined as whole blood lead ≥ 10 µg/dL, was based on numerous cross-sectional and prospective studies [Bellinger et al. 1987; Centers for Disease Control and Prevention (CDC) 1991; World Health Organization (WHO) 1995]. These studies generally, but not always, found adverse consequences of childhood lead exposure (CDC 1991; WHO 1995). Still, most of the children in those studies had blood lead levels > 10 µg/dL. The WHO and the CDC recognized that there was no discernable threshold for the adverse effects of lead exposure, but too few studies had examined children with blood lead levels < 10 µg/dL to support any firm conclusions (CDC 1991; WHO 1995).
There is emerging evidence that lead-associated intellectual deficits occur at blood lead levels < 10 µg/dL. In the Rochester Longitudinal Study, there was an estimated reduction of 7.4 IQ points associated with an increase in lifetime mean blood lead from 1 to 10 µg/dL (Canfield et al. 2003). In a reanalysis of a Boston, Massachusetts, cohort, a similar finding was observed among children whose maximal blood lead level was < 10 µg/dL (Bellinger and Needleman 2003). Questions about an effect of lead at blood lead levels < 10 µg/dL persist, however, because of the relatively small numbers of children with maximal blood lead levels < 10 µg/dL in the Rochester Longitudinal Study (Rogan and Ware 2003). Other studies were limited because they involved children whose blood lead levels may have exceeded 10 µg/dL at some point in their lifetime or because important covariates, such as maternal IQ scores, were not always available (Fulton et al. 1987; Lanphear et al. 2000; Schwartz 1994; Schwartz and Otto 1991; Walkowiak et al. 1998). Because of the policy implications of this research, it is critical to estimate with greater precision the exposure-response relationship at blood lead levels < 10 µg/dL.
The primary objective of this pooled analysis was to estimate the quantitative relationship between children's performance on IQ tests and selected measures of blood lead concentration among children followed prospectively, from infancy through 5-10 years of age in seven prospective cohort studies. We also sought to test whether the lead-associated IQ deficit was greater for a given change in exposure among children who had maximal blood lead levels < 10 µg/dL compared with children who had higher blood lead concentrations.
Lead is a confirmed neurotoxin, but questions remain about lead-associated intellectual deficits at blood lead levels < 10 µg/dL and whether lower exposures are, for a given change in exposure, associated with greater deficits. The objective of this study was to examine the association of intelligence test scores and blood lead concentration, especially for children who had maximal measured blood lead levels < 10 µg/dL. We examined data collected from 1,333 children who participated in seven international population-based longitudinal cohort studies, followed from birth or infancy until 5-10 years of age. The full-scale IQ score was the primary outcome measure. The geometric mean blood lead concentration of the children peaked at 17.8 µg/dL and declined to 9.4 µg/dL by 5-7 years of age; 244 (18%) children had a maximal blood lead concentration < 10 µg/dL, and 103 (8%) had a maximal blood lead concentration < 7.5 µg/dL. After adjustment for covariates, we found an inverse relationship between blood lead concentration and IQ score. Using a log-linear model, we found a 6.9 IQ point decrement [95% confidence interval (CI), 4.2-9.4] associated with an increase in concurrent blood lead levels from 2.4 to 30 µg/dL. The estimated IQ point decrements associated with an increase in blood lead from 2.4 to 10 µg/dL, 10 to 20 µg/dL, and 20 to 30 µg/dL were 3.9 (95% CI, 2.4-5.3), 1.9 (95% CI, 1.2-2.6), and 1.1 (95% CI, 0.7-1.5), respectively. For a given increase in blood lead, the lead-associated intellectual decrement for children with a maximal blood lead level < 7.5 µg/dL was significantly greater than that observed for those with a maximal blood lead level ≥ 7.5 µg/dL (p = 0.015). We conclude that environmental lead exposure in children who have maximal blood lead levels < 7.5 µg/dL is associated with intellectual deficits.
The preponderance of experimental and human data indicates that there are persistent and deleterious effects of blood lead levels > 10 µg/dL on brain function, including lowered intelligence, behavioral problems, and diminished school performance (Baghurst et al. 1992; Bellinger et al. 1992; Cory-Slechta 1997; Dietrich et al. 1993; Ernhart et al. 1989; National Research Council 1993; Needleman and Gatsonis 1990; Pocock et al. 1994; Rice 1993; Wasserman et al. 1997; Yule et al. 1981). Lead toxicity, defined as whole blood lead ≥ 10 µg/dL, was based on numerous cross-sectional and prospective studies [Bellinger et al. 1987; Centers for Disease Control and Prevention (CDC) 1991; World Health Organization (WHO) 1995]. These studies generally, but not always, found adverse consequences of childhood lead exposure (CDC 1991; WHO 1995). Still, most of the children in those studies had blood lead levels > 10 µg/dL. The WHO and the CDC recognized that there was no discernable threshold for the adverse effects of lead exposure, but too few studies had examined children with blood lead levels < 10 µg/dL to support any firm conclusions (CDC 1991; WHO 1995).
There is emerging evidence that lead-associated intellectual deficits occur at blood lead levels < 10 µg/dL. In the Rochester Longitudinal Study, there was an estimated reduction of 7.4 IQ points associated with an increase in lifetime mean blood lead from 1 to 10 µg/dL (Canfield et al. 2003). In a reanalysis of a Boston, Massachusetts, cohort, a similar finding was observed among children whose maximal blood lead level was < 10 µg/dL (Bellinger and Needleman 2003). Questions about an effect of lead at blood lead levels < 10 µg/dL persist, however, because of the relatively small numbers of children with maximal blood lead levels < 10 µg/dL in the Rochester Longitudinal Study (Rogan and Ware 2003). Other studies were limited because they involved children whose blood lead levels may have exceeded 10 µg/dL at some point in their lifetime or because important covariates, such as maternal IQ scores, were not always available (Fulton et al. 1987; Lanphear et al. 2000; Schwartz 1994; Schwartz and Otto 1991; Walkowiak et al. 1998). Because of the policy implications of this research, it is critical to estimate with greater precision the exposure-response relationship at blood lead levels < 10 µg/dL.
The primary objective of this pooled analysis was to estimate the quantitative relationship between children's performance on IQ tests and selected measures of blood lead concentration among children followed prospectively, from infancy through 5-10 years of age in seven prospective cohort studies. We also sought to test whether the lead-associated IQ deficit was greater for a given change in exposure among children who had maximal blood lead levels < 10 µg/dL compared with children who had higher blood lead concentrations.
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