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Downloaded 113 No Lead David C. Bellinger, PhD, MSc ABSTRACT. Children differ from adults in the relative The later use of lead as a gasoline additive, begun in importance of lead sources and pathways, lead metabo- the 1920s and lasting into the 1990s in the United lism, and the toxicities expressed. The central nervous States,3 contributed further to the contamination of system effects of lead on children seem not to be revers- environmental media with which children have inti- ible. Periods of enhanced vulnerability within childhood mate daily commerce, including air, dusts, and soils. have not consistently been identified. The period of greatest vulnerability might be endpoint specific, per- haps accounting for the failure to identify a coherent DIFFERENCES BETWEEN CHILDREN AND ADULTS “behavioral signature” for lead toxicity. The bases for the IN LEAD SOURCES, METABOLISM, AND substantial individual variability in vulnerability to lead TOXICITIES are uncertain, although they might include genetic poly- Children and adults differ somewhat in the rela- morphisms and contextual factors. The current Centers tive importance of different lead exposure sources for Disease Control and Prevention screening guideline ␮ and pathways, in aspects of lead metabolism, and in of 10 g/dL is a risk management tool and should not be the specific ways in which toxicities are expressed. interpreted as a threshold for toxicity. No threshold has To a greater extent than adults, young children nor- been identified, and some data are consistent with effects well below 10. Historically, most studies have concen- mally explore their environment via hand-to-mouth trated on neurocognitive effects of lead, but higher ex- activity, behaviors that are likely to increase the lead posures have recently been associated with morbidities intake of a child who lives in an environment with such as antisocial behavior and delinquency. Studies of hazards such as leaded paint in poor repair or ele- lead toxicity in experimental animal models are critical to vated levels of lead in house dust or yard soils.4,5 The the interpretation of nonexperimental human studies, average fractional gastrointestinal absorption of lead particularly in addressing the likelihood that associa- is much greater in infants and young children than in tions observed in the latter studies can be attributed to adults,6 and absorption is increased in the presence residual confounding. Animal models are also helpful in of nutritional deficiencies that are more common in investigating the behavioral and neurobiological mecha- children than in adults (eg, iron, calcium).7,8 nisms of the functional deficits observed in lead-exposed humans. Studies of adults who have been exposed to In both children and adults, lead toxicity can be lead are of limited use in understanding childhood lead expressed as derangements of function in many or- toxicity because developmental and acquired lead expo- gan systems. Although lead causes central nervous sure differ in terms of the maturity of the organs affected, system abnormalities in adults,9–11 peripheral neu- the presumed mechanisms of toxicity, and the forms in ropathies tend to be more prominent. In the devel- which toxicities are expressed. Pediatrics 2004;113:1016– oping nervous system, in contrast, central effects are 1022; lead toxicity, children, toxicology, epidemiology. more prominent than peripheral effects.12 Moreover, peripheral nervous system effects in adults tend to 13,14 ABBREVIATION. CDC, Centers for Disease Control and Preven- reverse after cessation of exposure, whereas the tion. central effects in children seem not to do so,15–18 perhaps because lead perturbs the complex processes by which synaptic connections are selected and mod- lthough children are viewed as the most vul- ified.19 Even pharmacotherapy, at least succimer ad- nerable segment of the population with re- ministered to young children who present with Agard to lead poisoning, recognition of lead as blood lead levels of 20 to 44 ␮g/dL, does not seem to an adult toxicant preceded by thousands of years the 20 1 reduce or reverse cognitive injury. An important first description of childhood lead poisoning. For exception to these generalizations is that neurobe- millennia, exposure to lead was primarily via occu- havioral deficits associated with modest elevations of pation, but the introduction of leaded paint for resi- prenatal lead levels, if ever present, seem largely to dential use in the 19th century brought large attenuate by the time children reach school age.21 amounts of this metal within easy reach of children.2 CRITICAL WINDOWS OF VULNERABILITY AND INTERINDIVIDUAL DIFFERENCES IN From the Children’s Hospital Boston, Harvard Medical School, Boston, Massachusetts. SUSCEPTIBILITY Received for publication Oct 7, 2003; accepted Oct 20, 2003. It is difficult to identify discrete windows of en- Reprint requests to (D.C.B.) Children’s Hospital, Farley Basement Box 127, hanced developmental vulnerability to lead expo- 300 Longwood Ave, Boston MA 02115. E-mail: david.bellinger@childrens. harvard.edu sure. The intraindividual stability of blood lead level PEDIATRICS (ISSN 0031 4005). Copyright © 2004 by the American Acad- over time is substantial, particularly in lead-rich en- emy of Pediatrics. vironments such as the inner city or areas around 1016 PEDIATRICS Vol.Downloaded 113 No. 4 from April www.aappublications.org/news 2004 by guest on September 25, 2021 lead smelters, where many of the major epidemio- in their responses to lower levels of exposure, as logic studies have been conducted.22,23 In addition, well. An important implication is that children with under many exposure scenarios, the half-life of lead the same blood lead level should not be considered in blood is greater in children than in adults.5,24 to be at equivalent developmental risk. When blood lead levels do vary over time, age at The potential sources of individual variability in exposure and magnitude of exposure are often lead-associated neurodevelopmental risk are legion, highly confounded, with blood lead level peaking in although none has been confirmed with even a mod- the age range of 1 to 3 years.25 This is probably est degree of certainty. One type of explanation fo- because this period encompasses both the onset of cuses on toxicokinetic and toxicodynamic factors. It independent ambulation and the time when a child’s is assumed that blood lead level, the biomarker of oral exploration of the environment is greatest. As a internal dose that is most often used, is a valid index result, if a study were to find that blood lead level of the biologically effective dose at the brain, the measured at age 2 is most predictive of some critical critical target organ for neurotoxicity. The many in- neurocognitive outcome at school age, then it would tervening steps that link the internal dose and the be difficult to ascertain whether this reflects a special response in the brain, however, provide many op- vulnerability of the central nervous sytem at age 2 or portunities for interindividual differences in sensitiv- that blood lead levels tend to be highest during this ity to arise.36 Certain genetic polymorphisms in- period. Some studies support the former hypothe- volved in lead metabolism are thought to affect sis,26 whereas others have found that school-age neu- individual vulnerability, including those for the vi- rocognitive outcomes are most strongly related to tamin D receptor11 and for lead-binding red blood recent or concurrent blood lead levels.22,27 The find- cell proteins such as amino levulinic acid dehy- ings of yet other studies fail to provide evidence for dratase.37,38 Supportive evidence is sparse, howev- the existence of any critical periods of vulnerability.28 er.39 Gender differences have been reported in the Another reason that it is difficult to identify a immunotoxicity of gestational lead exposure in single critical period of heightened vulnerability to rats.40 In humans, gender differences in neurotoxic- lead toxicity is that there might be many such peri- ity have been reported,41–45 although in some stud- ods, depending on the particular endpoint of inter- ies, it is male individuals who seem to be more est. Using primate models, Rice29,30 demonstrated vulnerable, whereas in others it is female individu- that the timing of developmental lead exposure af- als. Co-exposure to other toxicants is another candi- fected the nature and the severity of deficit on a date explanation for individual differences in suscep- variety of tasks (spatial discrimination reversal, non- tibility, although greater attention has been paid to spatial discrimination reversal, and a fixed-interval the potential of co-exposures to be confounders than response operant task). In contrast, performance on a to be effect modifiers. In a rodent model, the effect of spatial delayed alternation task was not affected by lead on mortality, spatial learning, and the N-meth- age at exposure.31 Morgan et al32 observed different yl-D-aspartate receptors differed depending on expressions of attentional dysfunction in rats de- whether pups were exposed to lead alone or in com- pending on the timing of lead exposure. It seems bination with magnesium and zinc.46 Finally, char- eminently plausible that this fundamental principle acteristics of a child’s rearing environment might of toxicology applies to children as well, although influence the toxicity of a given lead dose.47 Lead the evidence is meager. This is likely to be attribut- seems
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