Cardiovascular Effects of Secondhand Smoke Nearly as Large as Smoking

Cardiovascular Effects of Secondhand Smoke Nearly as Large as Smoking
Joaquin Barnoya, MD, MPH; Stanton A. Glantz, PhD
Background—Secondhand smoke increases the risk of coronary heart disease by
30%. This effect is larger than one would expect on the basis of the risks associated with active smoking and the relative doses of tobacco smoke delivered to smokers and nonsmokers.
Methods and Results—We conducted a literature review of the research describing the mechanistic effects of secondhand smoke on the cardiovascular system, emphasizing research published since 1995, and compared the effects of secondhand smoke with the effects of active smoking. Evidence is rapidly accumulating that the cardiovascular system—platelet and endothelial function, arterial stiffness, atherosclerosis, oxidative stress, inflammation, heart rate variability, energy metabolism, and increased infarct size—is exquisitely sensitive to the toxins in secondhand smoke. The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking.
Conclusions—The effects of secondhand smoke are substantial and rapid, explaining the relatively large risks that have been reported in epidemiological studies. (Circulation. 2005;111:2684-2698.)
Key Words: smoking; cardiovascular diseases; endothelium; epidemiology; tobacco smoke pollution
Secondhand smoke (SHS) increases the risk of heart disease by
30%,1–7 accounting for at least 35 000 deaths annually in the United States.2,8 Protection of nonsmokers through smoke-free environments leads to a decrease
in heart disease mortality through a combination of reduced exposure to SHS and an environment that makes it
easier for smokers to stop smoking.9 The California Tobacco Control Program that stressed smoke-free policies has been associated with preventing 59 000 deaths resulting from heart disease between 1989 and 1997.10 An evaluation of a geographically isolated community (Helena, Mont) showed that the number of hospital admissions resulting from acute myocardial infarction decreased after the implementation of a law ending smoking in public and workplaces, an effect that partially reversed when enforcement of the law was suspended by a lawsuit.11 The effects observed in epidemiological studies are both larger and faster than one would expect if there were a simple linear dose-response relationship between level of smoke exposure in passive smokers and active smokers.12 Despite the fact that the dose of smoke delivered to active smokers is 100 times or more that delivered to a passive smoker, the relative risk of coronary heart disease for smokers is 1.78,5 compared with 1.31 for passive smokers (Figure 1). Rapidly accumulating evidence, however, indicates that many important responses of the cardiovascular system (Table 1) are exquisitely sensitive to the toxins in SHS. These mechanisms, rather than isolated events, interact with each other to increase the risk of heart disease.
The present article extends earlier reviews of the biological effects of SHS on the cardiovascular system,3–5,14–21 with particular emphasis on literature on the effects of low doses of tobacco smoke exposure and the speed of the effect on the cardiovascular system. In many cases, the effects of even brief (minutes to hours) passive smoking are nearly as large as those from chronic active smoking.