Date: Thursday, October 25, 2012
Time: 3:30pm - 5:00pm
Session: Session #10
Learning Objectives:
- To review results pertaining to immune regulation in both the mother and the child on neurodevelopment and its origins.
- The central role of gene-environment interactions will be discussed,
- Review the challenges in determining critical windows during which the fetus or infant is most susceptible.
- To identify modifiable risk factors that represents the primary strategy and hope for a future reduction in the risk for autism
Outline of Presentation:
Dr. Irva Hertz-Picciotto, Ph.D., is an internationally renowned environmental epidemiologist who has published widely on environmental exposures, including metals, pesticides, air contaminants and persistent pollutants like PCBs, their interactions with nutrition, and their effects on pregnancy, the newborn, and early child development. Dr. Irva Hertz-Picciotto, Ph.D., is an internationally renowned environmental epidemiologist who has published widely on environmental exposures, including metals, pesticides, air contaminants and persistent pollutants like PCBs, their interactions with nutrition, and their effects on pregnancy, the newborn, and early child development. For the last ten years she has focused her efforts on understanding the environmental causes of autism. In this presentation, she will begin by reviewing evidence regarding time trends in the occurrence of autism, describe the state of knowledge, as of ten years ago, about factors that alter risk for autism spectrum disorders, and provide up-to-date information on what has been learned in the last decade.
Her research program began with the CHARGE (CHildhood Autism Risk from Genetics and Environment) Study, which was launched in 2002 and is the first large-scale comprehensive investigation of environmental contributions to autism. Findings from the CHARGE Study will be presented, covering: maternal nutritional status, pregnancy complications, infections, air pollution exposure, and use of pesticides. Additional results pertaining to immune regulation in both the mother and the child highlight a new perspective on neurodevelopment and its origins, and the mechanisms by which exogenous exposures might produce brain aberrations that lead to autism. The central role of gene-environment interactions will be discussed, as well as the challenges in determining critical windows during which the fetus or infant is most susceptible.
To date, this body of research has contributed most of the new advances in understanding of autism’s non-genetic etiology. Newer studies that can provide prospective data collection, such as MARBLES (Markers of Autism Risk in Babies—Learning Early Signs) and EARLI (Early Autism Risk Longitudinal Investigation) will help to replicate, complement, and refine these results. Ultimately, it is the identification of modifiable risk factors that represents the primary strategy and hope for a future reduction in the risk for autism.