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Neurotoxicol Teratol. 2014 Jul-Aug;44:30-45. doi: 10.1016/ Epub 2014 May 17.

Exposure to neurotoxicants and the development of attention deficit hyperactivity disorder and its related behaviors in childhood.

Author information

Cincinnati Children's Hospital Medical Center, 3333 Burnet Avenue, ML 7035, Cincinnati, OH 45229-3039, United States. Electronic address:
University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, United States.
Hebrew University Hadassah Medical School, Jerusalem, Israel.
Semel Institute for Neuroscience & Human Behavior, 300 UCLA Medical Plaza, Suite 1524C, Los Angeles, CA 90095, United States; David Geffen School of Medicine at the University of California, Los Angeles, 300 UCLA Medical Plaza, Suite 1524C, 300 UCLA Medical Plaza, Suite 1524C, Los Angeles, CA 90095, United States.
United States Environmental Protection Agency, National Center for Environmental Assessment, 1200 Pennsylvania Avenue, NW, Mailcode 8623P, Washington, DC 20460, United States.
College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana, IL 61802, United States.


The purpose of this manuscript is to review the literature to determine evidence of associations between exposure to prenatal and postnatal environmental agents and the development of attention deficit hyperactivity disorder (ADHD) and related behaviors. A review of published research literature was conducted on associations between exposures to prenatal and postnatal cigarette smoke, prenatal exposure to alcohol, cocaine, and heroin, childhood exposure to lead, and prenatal exposure to organophosphate pesticides and outcomes of ADHD or behaviors related to ADHD. Review of the literature in these areas provides some evidence of associations between each of the exposures and ADHD-related behaviors, with the strongest evidence from prenatal cigarette and alcohol exposure and postnatal lead exposure. However, research on each exposure also produced evidence of weaknesses in these hypothesized links due to imprecise research methodologies and issues of confounding and inaccurate covariate adjustment. More rigorous studies are needed to provide definitive evidence of associations between each of these prenatal or postnatal exposures and the development of ADHD or symptoms of ADHD. Future studies need to clarify the underlying mechanisms between these exposures and the increased risk for ADHD and associated behaviors. More research is also needed utilizing study designs that include genetic information, as ADHD is highly heritable and there appear to be some protective mechanisms offered by certain genetic characteristics as evidenced in gene by environmental studies. Finally, while studies focusing on individual drugs and chemicals are an important first step, we cannot ignore the fact that children are exposed to combinations of drugs and chemicals, which can interact in complex ways with each other, as well as with the child's genetic makeup and psychosocial environment to influence ADHD risk.


ADHD; Childhood; Environmental exposure; Postpartum; Pregnancy; Toxicants

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