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Gene-Environment Interaction and Targeted Intervention

George P. Vogler, PhD; Lynn T. Kozlowski, PhD

JAMA. 2002;287:241-242.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Maternal smoking is a significant risk factor for low-birth-weight (LBW) infants, which, in turn, influences infant mortality and the long-term health outcome of surviving infants. Maternal smoking is an ideal target for intervention and the optimal public health outcome would be prevention of all maternal smoking. But given variability in the response to intervention attempts, a secondary strategy is to target more effectively those individuals at highest risk for adverse outcomes.

In this issue of THE JOURNAL, Wang and colleagues¹ provide evidence that the magnitude of the effect of smoking by pregnant women on birth weight depends on their genotype at 2 genes involved in the metabolism of smoking toxins (CYP1A1 and GSTT1). Those with CYP1A1 Aa and aa (heterozygous and homozygous variant types) and GSTT1 absent genotypes had greater reductions in birth weight than CYP1A1 AA (homozygous wild type) . . . [Full Text of this Article]

Author Affiliations: Department of Biobehavioral Health (Drs Vogler and Kozlowski) and Center for Developmental and Health Genetics (Dr Vogler), Pennsylvania State University, University Park.

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