Abstract
There is a growing body of evidence establishing exposure to environmental agents as a risk factor for cardiovascular disease. In this review, the interaction between gene and estrogenic environmental chemicals has been described. Since estrogenic environmental compounds such as arsenic, constituents in tobacco smoke, and polychlorinated biphenyls (PCBs) are widespread and persistent environmental contaminants known to induce oxidative stress in human vascular cells, research defining the mechanism of how estrogenic environmental chemicals may promote vascular lesions is highly relevant to cardiovascular public health.
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