Lead neurotoxicity in children: basic mechanisms and clinical correlates

被引:741
作者
Lidsky, TI [1 ]
Schneider, JS
机构
[1] New York State Inst Basic Res Dev Disabil, Ctr Trace Element Studies & Environm Neurotoxicol, Staten Isl, NY 10314 USA
[2] Thomas Jefferson Univ, Sch Med, Dept Pathol Anat & Cell Biol, Philadelphia, PA 19107 USA
[3] Thomas Jefferson Univ, Sch Med, Dept Neurol, Philadelphia, PA 19107 USA
关键词
lead poisoning; neurotoxicity; children; toxic mechanisms; toxic threshold;
D O I
10.1093/brain/awg014
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Lead has been recognized as a poison for millennia and has been the focus of public health regulation in much of the developed world for the better part of the past century. The nature of regulation has evolved in response to increasing information provided by vigorous scientific investigation of lead's effects. In recognition of the particular sensitivity of the developing brain to lead's pernicious effects, much of this legislation has been addressed to the prevention of childhood lead poisoning. The present review discusses the current state of knowledge concerning the effects of lead on the cognitive development of children. Addressed are the reasons for the child's exquisite sensitivity, the behavioural effects of lead, how these effects are best measured, and the long-term outlook for the poisoned child. Of particular importance are the accumulating data suggesting that there are toxicological effects with behavioural concomitants at exceedingly low levels of exposure. In addition, there is also evidence that certain genetic and environmental factors can increase the detrimental effects of lead on neural development, thereby rendering certain children more vulnerable to lead neurotoxicity. The public health implications of these findings are discussed.
引用
收藏
页码:5 / 19
页数:15
相关论文
共 121 条
[11]  
BELLINGER DC, 1992, PEDIATRICS, V90, P855
[12]   Effect modification in epidemiologic studies of low-level neurotoxicant exposures and health outcomes [J].
Bellinger, DC .
NEUROTOXICOLOGY AND TERATOLOGY, 2000, 22 (01) :133-140
[13]   In vitro effect of lead on Ca2+-ATPase in synaptic plasma membranes and microsomes of rat cerebral cortex and cerebellum [J].
Bettaiya, R ;
Yallapragada, PR ;
Hall, E ;
Rajanna, S .
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY, 1996, 33 (02) :157-162
[14]   Synaptotagmin I is a molecular target for lead [J].
Bouton, CMLS ;
Frelin, LP ;
Forde, CE ;
Godwin, HA ;
Pevsner, J .
JOURNAL OF NEUROCHEMISTRY, 2001, 76 (06) :1724-1735
[15]  
BRADBURY MWB, 1993, NEUROTOXICOLOGY, V14, P131
[16]   Molecular mechanisms of lead neurotoxicity [J].
Bressler, J ;
Kim, K ;
Chakraborti, T ;
Goldstein, G .
NEUROCHEMICAL RESEARCH, 1999, 24 (04) :595-600
[17]   MECHANISMS OF LEAD NEUROTOXICITY [J].
BRESSLER, JP ;
GOLDSTEIN, GW .
BIOCHEMICAL PHARMACOLOGY, 1991, 41 (04) :479-484
[18]   BLOOD LEAD LEVELS IN THE US POPULATION - PHASE-1 OF THE 3RD NATIONAL-HEALTH AND NUTRITION EXAMINATION SURVEY (NHANES-III, 1988 TO 1991) [J].
BRODY, DJ ;
PIRKLE, JL ;
KRAMER, RA ;
FLEGAL, KM ;
MATTE, TD ;
GUNTER, EW ;
PASCHAL, DC .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1994, 272 (04) :277-283
[19]   Sensory and cognitive functions of the basal ganglia [J].
Brown, LL ;
Schneider, JS ;
Lidsky, TI .
CURRENT OPINION IN NEUROBIOLOGY, 1997, 7 (02) :157-163
[20]   Randomised study of cognitive effects of iron supplementation in non-anaemic iron-deficient adolescent girls [J].
Bruner, AB ;
Joffe, A ;
Duggan, AK ;
Casella, JF ;
Brandt, J .
LANCET, 1996, 348 (9033) :992-996