Biomedical subjects
D Bellinger
Publications and source records attributed to D Bellinger.
Pre-natal blood lead levels and learning difficulties in children: an analysis of non-randomly missing categorical data.
This paper presents an analysis of categorical variables subject to non-response. We incorporate the incomplete data into the analysis by modelling the distribution of the variables of interest and the non-response mechanism. We discuss issues of model selection and interpretation and the effect of discarding incomplete observations. In addition, we describe how to perform all of the computations with standard statistical software. We discuss the problem of incomplete categorical data within the context of a study of the effect of lead exposure on learning difficulties in children. In this study, many of the children are not observed on some of the variables of interest. It is particularly important in this study to incorporate the incomplete data, since there is evidence that non-response is related to the variables of interest. We reach different conclusions when we incorporate the incomplete data into the analysis than we reach when we discard the incomplete data. We also examine the sensitivity of our conclusions to the choice of a model for the non-response mechanism.
Lead correction.
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Lead levels among various deciduous tooth types.
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Weight gain and maturity in fetuses exposed to low levels of lead.
The relationship between prenatal low-level lead exposure and fetal growth was evaluated in a sample of 4354 pregnancies in which the mean umbilical cord blood lead level was 7.0 micrograms/dl (SD = 3.3; 10th percentile, 3.4 micrograms/dl, 90th percentile, 10.9 micrograms/dl). Higher cord blood lead levels were significantly associated with gestations of slightly longer duration. Comparing infants with cord blood lead levels greater than or equal to 15 micrograms/dl to those with levels less than 5 micrograms/dl, adjusted risk ratios of 1.5 to 2.5 were observed for low birth weight (less than 2500 g) and for fetal growth indices that express birth weight as a function of length of gestation (e.g., small-for-gestational age, intrauterine growth retardation). The 95% confidence intervals of these risk ratios included 1, however, precluding rejection of the null hypothesis of no association. We conclude that the risk of adverse fetal growth is not increased at cord blood lead levels less than 15 micrograms/dl but that modest increases in risk may be associated with levels greater than or equal to 15 micrograms/dl.
The health effects of low level exposure to lead.
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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.
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.
Antecedents and correlates of improved cognitive performance in children exposed in utero to low levels of lead.
Up to 2 years of age, children with umbilical cord blood lead levels of 10 to 25 micrograms/dL achieve significantly lower scores on tests of cognitive development than do children with lower prenatal exposures. By age 5 years, however, they appear to have recovered from, or at least compensated for, this early insult. Change in performance between 24 and 57 months of age was examined in relation to level of postnatal lead exposure and various sociodemographic factors. Among children with high prenatal lead exposure, greater recovery of function was associated with lower blood level at 57 months, higher socioeconomic status, higher Home Observation for Measurement of the Environment scores, higher maternal IQ, and female gender. The difference between the scores at 57 months of children with optimal and less optimal values on these variables generally exceed 1/2 standard deviation. Higher prenatal lead exposure is associated with an increased risk of early cognitive deficit. Furthermore, the risk that a deficit will persist through the preschool years is increased among children with high prenatal exposure and either high postnatal exposure or less optimal sociodemographic characteristics.
Prenatal/early postnatal exposure to lead and risk of developmental impairment.
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Consequences of unremitting middle-ear infection in early life.
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Changes in the explicitness of mothers' directives as children age.
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Coronary atherosclerosis in the pig. Induced plaque injury and platelet response.
The thrombogenic potential of atherosclerotic diet-induced coronary atherosclerotic plaques was investigated in normal swine and in bleeder swine with homozygous von Willebrand disease. Fourteen paired normal and bleeder swine were placed on a 1% cholesterol diet for 1 to 16 weeks. Serum cholesterol was elevated in all animals at sacrifice. Foam cell deposits developed in all major epicardial coronary arteries, and lesions progressed over time from small subendothelial foam cell deposits to fibrous cap lesions that contained foam cells, elastic fibers, collagen, degenerative material, and smooth muscle cells. Balloon catheter injury resulted in platelet deposition, largely in a monolayer or as small platelet clumps devoid of fibrin. Lipid debris was present in injured areas of the subendothelium but did not induce thrombus formation. When the injury involved the media, platelet-fibrin thrombi were formed. Lipid was not present in these thrombi. Morphometric analysis of platelet deposition on ballooned atherosclerotic vessels showed similar numbers of platelets in both phenotypes. However, the attached platelets in bleeder pigs showed significantly less spreading than did those in the normal animals. The results show that injury to intimal foam cell and mixed cellular lesions in coronary arteries of cholesterol-fed swine does not promote the development of platelet-fibrin thrombus formation. In contrast, when the injury extended to the media, mixed thrombi were formed.
Antecedents and correlates of hypoplastic enamel defects of primary incisors.
Four hundred and fifty-five exfoliated primary incisors were obtained from children whose mothers provided information about a wide range of pre-, peri-, and postnatal characteristics of both the mother and child. These teeth then were examined for the presence of hypoplastic enamel defects (HED). The basic form of the null hypothesis tested was that children who had HED of a primary incisor did not differ from those who did not have such a defect. Of the primary incisors examined, 18.5% had HED (25.0% maxillary and 10.1% mandibular). The following items were found to be associated most strongly (P less than 0.003) with an increase in a child's risk of developing HED; 1) maternal antenatal history of smoking, higher prepregnancy weight, and failure to obtain prenatal care during the first trimester; 2) prematurity, low birth-weight and their associated correlates; and 3) postnatal measles infection. Left-handedness, maternal tea and Tylenol (McNeil Consumer Products Co., Fort Washington, PA) consumption, and failure to screen for undue lead burden were associated less prominently (P less than 0.05) with HED prevalence. Season of birth and serum and dentin lead levels were not related to the prevalence of HED. Many of these risk factors are also covariates of low socioeconomic status such as suboptimal nutrition and increased risk of infection. Additional investigation is needed to delineate the associations between specific pre- and perinatal nutritional and infectious factors, socioeconomic status, and HED development.
In utero lead exposure.
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Low-level lead exposure and infant development in the first year.
The developmental impact of prenatal and early postnatal low-level lead exposure was assessed in a prospective study of 249 middle and upper-middle class infants with umbilical cord blood lead levels in the range currently considered "normal." Infants were classified into three exposure groups: "low" (less than 3 micrograms/dl), "mid" (6 to 7 micrograms/dl), and "high" (greater than or equal to 10 micrograms/dl). At 6 and 12 months, the lead concentration of capillary blood was measured, and the Bayley Scales of Infant Development administered. At both ages, Mental Development Index scores, adjusted for confounding, were inversely related to infants' umbilical cord blood lead levels. The difference between the mean adjusted scores of the infants in the low and high cord blood lead groups was 5.8 points at 6 months and 7.3 points at 12 months. At neither age were scores significantly related to postnatal blood lead levels. Prenatal exposure to lead levels relatively common among urban populations appear to be associated with less favorable development through the first year of life.