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      Low-Level Environmental Lead Exposure and Children’s Intellectual Function: An International Pooled Analysis

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          Abstract

          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.

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          Most cited references55

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          Intellectual impairment in children with blood lead concentrations below 10 microg per deciliter.

          Despite dramatic declines in children's blood lead concentrations and a lowering of the Centers for Disease Control and Prevention's level of concern to 10 microg per deciliter (0.483 micromol per liter), little is known about children's neurobehavioral functioning at lead concentrations below this level. We measured blood lead concentrations in 172 children at 6, 12, 18, 24, 36, 48, and 60 months of age and administered the Stanford-Binet Intelligence Scale at the ages of 3 and 5 years. The relation between IQ and blood lead concentration was estimated with the use of linear and nonlinear mixed models, with adjustment for maternal IQ, quality of the home environment, and other potential confounders. The blood lead concentration was inversely and significantly associated with IQ. In the linear model, each increase of 10 microg per deciliter in the lifetime average blood lead concentration was associated with a 4.6-point decrease in IQ (P=0.004), whereas for the subsample of 101 children whose maximal lead concentrations remained below 10 microg per deciliter, the change in IQ associated with a given change in lead concentration was greater. When estimated in a nonlinear model with the full sample, IQ declined by 7.4 points as lifetime average blood lead concentrations increased from 1 to 10 microg per deciliter. Blood lead concentrations, even those below 10 microg per deciliter, are inversely associated with children's IQ scores at three and five years of age, and associated declines in IQ are greater at these concentrations than at higher concentrations. These findings suggest that more U.S. children may be adversely affected by environmental lead than previously estimated. Copyright 2003 Massachusetts Medical Society
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            The long-term effects of exposure to low doses of lead in childhood. An 11-year follow-up report.

            To determine whether the effects of low-level lead exposure persist, we reexamined 132 of 270 young adults who had initially been studied as primary school-children in 1975 through 1978. In the earlier study, neurobehavioral functioning was found to be inversely related to dentin lead levels. As compared with those we restudied, the other 138 subjects had had somewhat higher lead levels on earlier analysis, as well as significantly lower IQ scores and poorer teachers' ratings of classroom behavior. When the 132 subjects were reexamined in 1988, impairment in neurobehavioral function was still found to be related to the lead content of teeth shed at the ages of six and seven. The young people with dentin lead levels greater than 20 ppm had a markedly higher risk of dropping out of high school (adjusted odds ratio, 7.4; 95 percent confidence interval, 1.4 to 40.7) and of having a reading disability (odds ratio, 5.8; 95 percent confidence interval, 1.7 to 19.7) as compared with those with dentin lead levels less than 10 ppm. Higher lead levels in childhood were also significantly associated with lower class standing in high school, increased absenteeism, lower vocabulary and grammatical-reasoning scores, poorer hand-eye coordination, longer reaction times, and slower finger tapping. No significant associations were found with the results of 10 other tests of neurobehavioral functioning. Lead levels were inversely related to self-reports of minor delinquent activity. We conclude that exposure to lead in childhood is associated with deficits in central nervous system functioning that persist into young adulthood.
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              Low-level lead exposure and children's IQ: a meta-analysis and search for a threshold.

              To assess the strength of the association between blood lead and children's IQ, a meta-analysis of the studies examining the relationship in school age children was performed. Emphasis was given to the size of the effect, since that allows comparisons that are informative about potential confounding and effect modifiers. Sensitivity analyses were also performed. A highly significant association was found between lead exposure and children's IQ (P < 0.001). An increase in blood lead from 10 to 20 micrograms/dl was associated with a decrease of 2.6 IQ points in the meta-analysis. This result was robust to inclusion or exclusion of the strongest individual studies and to relaxing the age requirements (school age children) of the meta-analysis. Adding eight studies with effect estimates of 0 would still leave a significant association with blood lead (P < 0.01). There was no evidence that the effect was limited to disadvantaged children and there was a suggestion of the opposite. The studies with mean blood lead levels of 15 micrograms/dl or lower in their sample had higher estimated blood lead slopes, suggesting that a threshold at 10 micrograms/dl is implausible. The study with the lowest mean blood lead level was examined using nonparametric smoothing. It showed no evidence of a threshold down to blood lead concentrations of 1 microgram/dl. Lead interferes with GABAergic and dopaminergic neurotransmission. It has been shown to bind to the NMDA receptor and inhibit long-term potentiation in the hippocampal region of the brain. Moreover, experimental studies have demonstrated that blood levels of 10 micrograms/dl interfere with a broad range of cognitive function in primates. Given this support, these associations in humans should be considered causal.
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                Author and article information

                Journal
                Environ Health Perspect
                Environmental Health Perspectives
                National Institue of Environmental Health Sciences
                0091-6765
                July 2005
                18 March 2005
                : 113
                : 7
                : 894-899
                Affiliations
                1Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio, USA
                2Department of Environmental Health, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
                3Institute for Health Policy and Health Services Research, Department of Environmental Health, University of Cincinnati, Cincinnati, Ohio, USA
                4Women and Children’s Hospital, North Adelaide, South Australia
                5Department of Neurology, Children’s Hospital Boston and Harvard Medical School, Boston, Massachusetts, USA
                6Division of Nutritional Sciences, Cornell University, Ithaca, New York, USA
                7Department of Biostatistics and Epidemiology, Cleveland Clinic Foundation, Cleveland, Ohio, USA
                8Center for Research in Population Health, National Institute of Public Health, Cuernavaca, Morelos, Mexico
                9Drew University, Los Angeles, California, USA
                10University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA
                11National Institute of Perinatology, Mexico City, Mexico
                12Department of Child Psychiatry, Columbia University, New York, New York, USA
                13Department of Environmental Health Sciences, Columbia University, New York, New York, USA
                14School of Applied Psychology, Griffith University, Queensland, Australia
                Author notes
                Address correspondence to B.P. Lanphear, Cincinnati Children’s Hospital Medical Center, 3333 Burnet Ave., Mail Location 7035, Cincinnati, OH 45229-3039 USA. Telephone: (513) 636-3778. Fax: (513) 636-4402. E-mail: bruce.lanphear@cchmc.org

                This study was funded, in part, by the National Institute of Environmental Health Sciences, the Centers for Disease Control and Prevention, and the U.S. Environmental Protection Agency.

                The authors declare they have no competing financial interests.

                Article
                ehp0113-000894
                10.1289/ehp.7688
                1257652
                16002379
                a0ff9dd3-2907-40f8-bc47-96bbcf74039d
                This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original DOI.
                History
                : 22 October 2004
                : 17 March 2005
                Categories
                Research
                Children's Health

                Public health
                intelligence,epidemiology,lead toxicity,environment,lead,blood lead concentration,children
                Public health
                intelligence, epidemiology, lead toxicity, environment, lead, blood lead concentration, children

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