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Nutr Metab Cardiovasc Dis. 2007 Feb;17(2):162-9. Epub 2006 Mar 31.

Environmental toxicity, nutrition, and gene interactions in the development of atherosclerosis.

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Molecular and Cell Nutrition Laboratory, College of Agriculture, University of Kentucky, Room 591, Wethington Health Sciences Bldg., 900 S. Limestone, Lexington, KY 40536-0200, USA. <>


There is substantial evidence from epidemiological studies that the pathology of cardiovascular diseases is linked in part to environmental pollution. Many environmental contaminants, and especially persistent organic pollutants, are risk factors for atherosclerosis because they may exacerbate an underlying disease by altering gene expression patterns. Many mechanisms and signaling pathways associated with the pathology of "modern" diseases are similarly modulated by poor dietary habits and environmental pollutants. Many genes induced in diseases associated with vascular dysfunction such as atherosclerosis are oxidative stress-sensitive, suggesting that an imbalance in cellular oxidative stress and antioxidant status is a critical underlying factor. One of the emerging issues in modern toxicological sciences is the modification of environmental toxicity by nutrients. Evidence is emerging which suggests that antioxidant nutrients and related bioactive compounds common in fruits and vegetables protect against environmental toxic insult to the vascular endothelium by down-regulation of signaling pathways involved in inflammatory responses associated with vascular diseases such as atherosclerosis. Thus, the concept that nutrition may modify or ameliorate the toxicity of environmental chemicals may have implications for understanding the complex interaction of environmental toxicity and disease development.

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