NEW YORK (Reuters Health) - Even a brief bout with secondhand smoke may be enough to temporarily slow down nonsmokers' blood circulation, new study results suggest. The short-lived slowdown may help explain how, over time, exposure to cigarette smoke can

In a study examining the impact of environmental cigarette smoke on heart blood vessels, Japanese researchers found that 30 minutes of exposure to secondhand smoke reduced nonsmokers' coronary flow velocity reserve (CFVR)--a measure of the speed of blood flow. CFVR readings provide a way to non-invasively gauge how well the cells that line blood vessels are working. These cells, called endothelial cells, help vessels dilate in response to blood flow and help prevent blockages from forming. Dysfunction in endothelial cells contributes to the narrowing and hardening of heart arteries. According to Dr. Ryo Otsuka and colleagues at Osaka City University Medical School, their findings provide ``direct evidence that passive smoking may cause endothelial dysfunction of the coronary circulation in nonsmokers.'' They report the results in the July 25th issue of The Journal of the American Medical Association. In an accompanying editorial, doctors from the University of California, San Francisco note that ``the findings...are important not only because they illustrate the importance of preventing nonsmokers from any exposure to secondhand smoke, but also because they help to explain the relatively large risk of death and other cardiac events associated with passive smoking.'' This study ``adds substantially'' to the belief that exposure to secondhand smoke can ``immediately compromise the cardiovascular system,'' according to Drs. Stanton A. Glantz and William W. Parmley. ``If you sit in a smoky bar for 30 minutes, your endothelial function is temporarily compromised to the level of a pack-a-day smoker,'' Glantz said in an interview with Reuters Health. According to Glantz, the findings counter tobacco industry claims that a nonsmoker would have to sit in a smoky environment for ``hours and hours'' to sustain the immediate damaging effects of smoking one cigarette. This study, he said, shows the short-term effects of secondhand smoke are ``way out of proportion to the dose.'' In their study, the Japanese researchers used a type of ultrasound to measure CFVR in 30 healthy men, half of whom were smokers. They took measurements before and after exposing the men to secondhand tobacco smoke. Before exposure, nonsmokers' CFVR was substantially higher than that of smokers. But after exposure, their measurements dropped to match those of the smokers--whose CFVR was largely unaffected by the secondhand smoke. ``The present study,'' Otsuka's team writes, ``is the first to demonstrate that passive smoking may have a stronger impact on CFVR in nonsmokers than in active smokers.'' Passive smoking did not have any effect on nonsmokers' heart rate or blood pressure. However, the researchers conclude that the changes they saw in participants' blood vessel function may be one reason why passive smoking has been linked to heart disease in nonsmokers. According to Glantz and Parmley, the findings also bolster the belief that ``everyone should be protected from even short-term exposure to the toxins in secondhand smoke.'' This, they argue, includes designating more workplaces, restaurants and bars ``smoke-free.'' Glantz said it is unclear how much exposure to secondhand smoke is necessary to raise a nonsmokers' heart disease risk. But he noted that people who live with smokers have been found to have a 30% increase in their risk.

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