ABSTRACT
The role of a variety of occupational and environmental toxins in the development and progression of cardiovascular disease is of growing public health interest.1,2 Although the importance of tobacco smoke in the pathogenesis of atherosclerosis is well established, the cardiovascular effects of other potentially important toxins, such as ethanol, cocaine, anthracyclines, and heavy metals, are less well understood. What knowledge we do have is largely a product of observational studies in humans and is, therefore, subject to confounding influences such as self-reporting and selection biases. Apparent associations generated by these observations can be confirmed or refuted, and mechanisms defined, by the use of appropriate experimental animal models in which precise measurements of cardiovascular function can be monitored over an extended period of time.
