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Biomedical subjects

H L Needleman

Publications and source records attributed to H L Needleman.

At least 19 recordsLinked to original sources
PubMed1992

Low-level lead exposure, intelligence and academic achievement: a long-term follow-up study.

The implications of low-level lead exposure for children's intellectual and academic performance at school age are uncertain. This issue was investigated in a prospective study of middle-class and upper-middle-class children with low lifetime exposures to lead. A battery of neuropsychological tests was administered at age 10 years to 148 children whose lead exposure and cognitive function had been previously assessed at ages 6, 12, 18, 24, and 57 months. Primary endpoints were Wechsler Intelligence Scale for Children-Revised (WISC-R) and the Kaufman Test of Educational Achievement (K-TEA). Higher levels of blood lead at age 24 months, but not at other ages, were significantly associated with lower global scores on both the WISC-R and the K-TEA after adjustment for potential confounders. Over the range of approximately 0 to 25 micrograms/dL, a 0.48-mumol/L (10 micrograms/dL) increase in blood lead at 24 months was associated with a 5.8-point decline in WISC-R Full-Scale IQ (95% confidence interval: 1.7 to 9.9, P = .007) and an 8.9-point decline in K-TEA Battery Composite score (95% confidence interval: 4.2 to 13.6, P = .0003). Mean blood lead level at age 24 months was 0.31 mumol/L (6.5 micrograms/dL; SD: 4.9, 90% percentile: 12.5). Slightly elevated blood lead levels around the age of 24 months are associated with intellectual and academic performance deficits at age 10 years.

Child↗
PubMed1991

Low-level lead exposure and children's cognitive function in the preschool years.

In a cohort of 170 middle and upper-middle class children participating in a prospective study of child development and low-level lead exposure, higher blood lead levels at age 24 months were associated with lower scores at age 57 months on the McCarthy Scales of Children's Abilities. The mean blood lead level at age 24 months was 6.8 micrograms/dL (SD = 6.3; 75th, 90th, and 99th percentiles: 8.8, 13.7, 23.6, respectively) and for all but 1 child was less than 25 micrograms/dL, the current definition of an "elevated" level. After adjustment for confounding, scores on the General Cognitive Index decreased approximately 3 points (SE = 1.4) for each natural log unit increase in 24-month blood lead level. The inverse association between lead level and performance was especially prominent for visual-spatial and visual-motor integration skills. Higher prenatal exposures were not associated with lower scores at 57 months except in the subgroup of children with "high" concurrent blood lead levels (ie, greater than or equal to 10 micrograms/dL). The concentration of lead in the dentine of shed deciduous teeth was not significantly associated with children's performance after adjustment for confounding.

Age Factors↗
PubMed1990

Low-level lead exposure and the IQ of children. A meta-analysis of modern studies.

We identified 24 modern studies of childhood exposures to lead in relation to IQ. From this population, 12 that employed multiple regression analysis with IQ as the dependent variable and lead as the main effect and that controlled for nonlead covariates were selected for a quantitative, integrated review or meta-analysis. The studies were grouped according to type of tissue analyzed for lead. There were 7 blood and 5 tooth lead studies. Within each group, we obtained joint P values by two different methods and average effect sizes as measured by the partial correlation coefficients. We also investigated the sensitivity of the results to any single study. The sample sizes ranged from 75 to 724. The sign of the regression coefficient for lead was negative in 11 of 12 studies. The negative partial r's for lead ranged from -.27 to -.003. The power to find an effect was limited, below 0.6 in 7 of 12 studies. The joint P values for the blood lead studies were less than .0001 for both methods of analysis (95% confidence interval for group partial r, -.15 +/- .05), while for the tooth lead studies they were .0005 and .004, respectively (95% confidence interval for group partial r, -.08 +/- .05). The hypothesis that lead impairs children's IQ at low dose is strongly supported by this quantitative review. The effect is robust to the impact of any single study.

Child↗
PubMed1990

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.

Adolescent↗
PubMed1990

What can the study of lead teach us about other toxicants?

The history of knowledge about lead toxicity may serve as a useful template to judge and predict progress in understanding other toxicants. A paradigm shift has occurred in which toxicity has been recognized at levels long held to be harmless. This shift has been accelerated by the use of newer tools for measuring outcome. Lead effects have been identified in children at blood lead levels as low as 15 micrograms/dL. They include impaired psychometric intelligence, language function, attention, and classroom behavior. Lead exposure during pregnancy results in increased risk for minor malformations and lowered infant IQ scores until at least 2 years of age. Understanding of this toxicant has been blurred by seven unrecognized Type II errors frequently encountered in the lead literature. These errors are discussed. A meta-analysis of thirteen informative lead studies in children is presented. The joint probability of the findings occurring by chance under the null hypothesis is less than 3 x 10(-12).

Child↗
PubMed1990

The future challenge of lead toxicity.

Five decades ago, lead toxicity in childhood was thought in nonlethal cases to be without residual effect. This misconception was corrected in 1943 by Randolph Byers, who began the modern era of lead neurotoxicology by asserting that lead not only killed cells, but interfered with the normal development of central nervous system neurons. The human data from Byers forward is reviewed, with particular attention on methodological issues that have emerged. The papers on human neurotoxicology presented at the NIEHS lead conference held in Research Triangle Park, NC, in 1974 are examined to demonstrate the progress made over the last 15 years. Seven methodological solecisms have clouded judgment over the question of lead toxicity at low dose: worship of the sacrament of p = 0.05; inaccurate causal modeling; drawing conclusions from studies with inadequate power; positing phantom covariates; underestimating the importance of "small" effects; demanding proof of causality; and evaluating studies in isolation. The principles behind these errors are discussed. Lead exposure is associated with hyperactivity, and hyperactivity is a risk factor for antisocial behavior. The relationship between lead exposure and antisocial behavior is estimated. A plan for the effective removal of one major lead source, housing stock, is presented.

Child↗
PubMed1989

The persistent threat of lead: a singular opportunity.

Recent data have demonstrated health effects of lead in children at doses previously believed to be harmless. Data from epidemiological studies in many countries, and from experimental studies of animals given lead, demonstrate psychological impairment at blood lead concentrations of 0.5-0.7 mumol/L. Current estimates are that 17 per cent of American children (3-4 million) exceed the level of 0.7 mumol/L. Lead exposure is not a problem for urban poor children alone, but inner-city minorities have a higher rate of exposure. The overabundance of lead coexists in the same area with two serious shortages: affordable housing and jobs. It is argued that a program to train unemployed inner-city residents in safe de-leading, while expensive, makes hygienic, economic, and common sense.

Child↗