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(Pediatrics in Review. 2005;26:191-198. doi:10.1542/10.1542/pir.26-6-191)
© 2005 American Academy of Pediatrics

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(Pediatrics in Review. 2005;26:191-198.)
© 2005 American Academy of Pediatrics

Environmental Neurotoxins


Bruce P. Lanphear, MD, MPH*
Robert O. Wright, MD, MPH{dagger}
Kim N. Dietrich, PhD*
* The Departments of Pediatrics and of Environmental Health, Cincinnati Children’s Environmental Health Center, Cincinnati Children’s Hospital, Medical Center University of Cincinnati, Cincinnati, Ohio
{dagger} Departments of Pediatrics and Environmental Health, Children’s Hospital, Boston, and the Channing Laboratory Harvard Medical School, Harvard School of Public Health Boston, Mass

The first 300 words of the full text of this article appear below.


    Objectives
 
After completing this article, readers should be able to:

  1. Describe the toxic substances that may affect the environment and the health of children.
  2. Discuss how to elicit a history of exposure to toxic substances in the environment.
  3. Explain why infants are at greater risk than are others from toxic substances in the environment.


    Introduction
 
Environmental neurotoxins, such as lead, methyl mercury, polychlorinated biphenyls (PCBs), and environmental tobacco smoke (ETS), are widely disseminated in a child’s environment. Exposures to environmental neurotoxins, during both fetal development and early childhood, have been associated with substantial morbidity and mortality. Many recognized environmental neurotoxins were discovered only after environmental contamination led to local outbreaks of newly identified diseases. Emerging evidence links even lower-level exposures to environmental neurotoxins with behavioral problems, prematurity, and intellectual deficits.

Epidemics following environmental contamination heralded the discovery of children’s vulnerability to lead, methyl mercury, and PCBs. In 1904, an epidemic of overt lead poisoning was described among children who ingested leaded house paint. (1) The children, who were weakened and pale from anemia, were afflicted with encephalopathy, peripheral neuropathies, and ocular neuritis. In the 1950s, in a small Japanese fishing village on methyl mercury-tainted Minamata Bay, children exposed in utero to methyl mercury were afflicted with cerebral palsy, limb defects, hearing loss, visual defects, and mental retardation. (2) Ingestion of PCB-contaminated rice bran oil by pregnant women in Taiwan and Japan led to low birthweights and cola-colored children who tended to be dull and apathetic. (3) These early epidemics of overt poisoning were due to extremely heavy exposures to environmental toxins. Evidence is increasing that even low-level chronic exposure to such toxins produces subtle, but substantial morbidity in children. (4)(5)(6)(7) The consequences of low-level chronic exposure to many . . . [Full Text of this Article]


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