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Mechanisms and Risk

Stanton A. Glantz, PhD; William W. Parmley, MD

JAMA. 1995;273(13):1047-1053.

Abstract
Objective.
—Recent clinical, laboratory, and epidemiological evidence that passive smoking causes heart disease was reviewed, with particular emphasis on understanding the underlying physiological and biochemical mechanisms.

Data Sources.
—Publications in the peer-reviewed literature were located via MEDLINE, citation in other relevant articles, and appropriate reports by scientific agencies. Greatest emphasis was given to work published since 1990.

Conclusions.
—Passive smoking reduces the blood's ability to deliver oxygen to the heart and compromises the myocardium's ability to use oxygen to create adenosine triphosphate. These effects are manifest as reduced exercise capability in people breathing secondhand smoke. Secondhand smoke increases platelet activity, accelerates atherosclerotic lesions, and increases tissue damage following ischemia or myocardial infarction. The effects of secondhand tobacco smoke on the cardiovascular system are not caused by a single component of the smoke, but rather are caused by the effects of many elements, including carbon monoxide, nicotine, polycyclic aromatic hydrocarbons, and other, not fully specified elements in the smoke. Nonsmokers exposed to secondhand smoke in everyday life exhibit an increased risk of both fatal and nonfatal cardiac events.

(JAMA. 1995;273:1047-1053)

Author Affiliations
From the Division of Cardiology, Department of Medicine, Cardiovascular Research Institute, University of California, San Francisco.

Footnotes
Reprint requests to Division of Cardiology, University of California, San Francisco, CA 94143 (Dr Glantz).

Clinical Cardiology section editors: William A. Gaasch, MD, University of Massachusetts Medical School, Worcester; Margaret A. Winker, MD, Senior Editor, JAMA.

This article is one of a series sponsored by the American Heart Association.

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