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(Circulation. 1996;94:599.)
© 1996 American Heart Association, Inc.

Articles

Cardiovascular Effects of Environmental Tobacco Smoke

Scott T. Weiss, MD, MS

Harvard Medical School, Channing Laboratory, Brigham and Women's Hospital, Boston, MA.

Correspondence to Scott T. Weiss, MD, MS, Professor of Medicine, Harvard Medical School, Channing Laboratory, Brigham and Women's Hospital, 180 Longwood Ave, Boston, MA 02115. (Circulation. 1996;94:599.)

Key Words: Editorials • smoking

	Introduction

 
Active cigarette smoking represents the single most important preventable cause of death in the United States, accounting for over 400 000 deaths from cancer, cardiovascular disease, and chronic lung disease. Until the mid 1980s, cigarette smoking was considered a matter of personal choice and individual rights. However, publication of the 1986 Surgeon General's Report on the Health Effects of Involuntary Smoking,¹¹ which clearly documented that exposure to environmental tobacco smoke (ETS) causes lung cancer in nonsmokers, spawned a rapid public health response. Today, the ban on smoking in offices, airplanes, public buildings, and restaurants is seen by many as an appropriate response to preservation of public health. This represents an evolution in the attitudes of the American public since the television advertising ban was instated after the landmark 1964 Surgeon General's Report on active smoking.

The 1986 Surgeon General's Report devoted only 2 of its 359 pages to adverse cardiovascular health outcomes related to environmental tobacco smoke. Since 1984, there have been at least 15 publications (including Steenland et al² in this issue of Circulation) that have demonstrated that ETS affects lipid levels, angina, and myocardial infarction. These adverse health effects may be due to a myriad of biochemical mechanisms of tobacco smoke exposure, including greater platelet aggregation, endothelial cell damage, reduced oxygen supply, greater oxygen demand, and the direct effects of nicotine and carbon monoxide. Meta-analyses of these data and the current report by Steenland et al indicate a 20% increase in coronary disease mortality secondary to ETS . . . [Full Text of this Article]