title: Lead neurotoxicity in children: is prenatal exposure more important than postnatal exposure?
abstract: Numerous studies indicate that low-level lead poisoning causes mild mental retardation and low IQ scores in children. The general mean lead intake in the adult European population corresponds to a reassuring 14% (0.5-56%) of the tolerable daily intake: at this low level of exposure only few children (less than 10%) have blood lead levels (PbB) higher than 10 microg/dl, previously considered the PbB of concern. In more recent years data now suggest that even when 'the lifetime average blood lead concentration' is below 10 microg/dl an inverse association exists with intelligence quotient (IQ) scores. Two-thirds (45-75%) of lead in blood, however, comes from long-term tissue stores and this is especially true for newborn infants and pregnant women. Several data suggest that for lead the main toxic event is prenatal exposure: therefore we should focus our attention on maternal lead stores and whenever possible avoid their mobilization during pregnancy. In this regard we should design appropriate studies to confirm whether dietary supplementations can reduce bone resorption and lead mobilization during pregnancy. The hypothesis that the amount of maternal bone lead stores is the relevant parameter for predicting the level of neurotoxicity of this metal gives some optimism for the future: if we study children whose mothers never underwent high environmental pollution (born after the withdrawal of lead from gasoline) and hence have relatively low bone lead stores we could find that, at the population level, lead has little influence on children IQ scores.
authors.affiliation: Department of Paediatrics, Second School of Medicine, University 'La Sapienza', Rome, Italy. roberto.ronchetti@ospedalesantandrea.it
authors.forename: Roberto
authors.initials: R
authors.lastname: Ronchetti
authors.forename: Peter
authors.initials: P
authors.lastname: van den Hazel
authors.forename: Greet
authors.initials: G
authors.lastname: Schoeters
authors.forename: Wojtek
authors.initials: W
authors.lastname: Hanke
authors.forename: Zusana
authors.initials: Z
authors.lastname: Rennezova
authors.forename: Mario
authors.initials: M
authors.lastname: Barreto
authors.forename: Maria Pia
authors.initials: MP
authors.lastname: Villa
mesh_terms: D015415:Biomarkers / Q000032:analysis; D001842:Bone and Bones / Q000737:chemistry / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002648:Child; D004781:Environmental Exposure; D005060:Europe; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007854:Lead / Q000097:blood / Q000378:metabolism / Q000633:toxicity; D020264:Lead Poisoning, Nervous System, Childhood / Q000453:epidemiology* / Q000503:physiopathology; D018811:Maternal Exposure; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000453:epidemiology / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D007854:Lead; D002118:Calcium