Lead neurotoxicity in children: basic mechanisms and clinical correlates

• Published in: Brain (London, England : 1878) England : 1878), 2003-01, Vol.126 (1), p.5-19
• Main Authors: Lidsky, Theodore I., Schneider, Jay S.
• Format: Article
• Language: English
• Subjects: ALA = δ‐aminolevulinic acid; Apoptosis; BBB = blood–brain barrier; Biological and medical sciences; Bone and Bones - metabolism; Brain - metabolism; Brain - pathology; Calcium Signaling - drug effects; Chemical and industrial products toxicology. Toxic occupational diseases; Child; Child, Preschool; children; Cognition Disorders - chemically induced; Cognition Disorders - metabolism; Environmental Exposure; Female; Genetic Predisposition to Disease; Heme - biosynthesis; Humans; Infant; Lead - blood; lead poisoning; Lead Poisoning, Nervous System, Childhood - complications; Lead Poisoning, Nervous System, Childhood - etiology; Lead Poisoning, Nervous System, Childhood - metabolism; Maternal Exposure; Maximum Allowable Concentration; Medical sciences; Metals and various inorganic compounds; Neuroglia - drug effects; Neuroglia - metabolism; neurotoxicity; Neurotransmitter Agents - metabolism; PKC = protein kinase C; Pregnancy; Prenatal Exposure Delayed Effects; SES = socioeconomic status; Social Class; toxic mechanisms; toxic threshold; Toxicology; VDR = vitamin D receptor
• ISSN: 0006-8950; 1460-2156
• DOI: 10.1093/brain/awg014

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.