New data show that exposure to levels of lingering secondhand smoke, at increasingly lower concentrations than in prior studies, for a short period results in marked signs of cardiovascular dysfunction among nonsmoking adults.
According to a study published in the May 22 issue of the Journal of the American College of Cardiology, researchers found that the brachial artery failed to dilate optimally among those exposed to lingering secondhand smoke, suggesting the endothelium was not functioning as it should. Endothelial dysfunction has been linked to all phases of atherosclerosis, from its inception to cardiac events, such as stroke or heart attack.
"Breathing in very low levels of secondhand smoke—the same amount many people and children would encounter out and about in the community—appears to impair one’s vascular function after just 30 minutes of exposure," said Paul F. Frey, MD, MPH, FACC, Division of Cardiology, San Francisco General Hospital and the study’s lead investigator. "These findings have significant public health implications. We saw a steep decline in vascular function even after a very short exposure to low levels of secondhand smoke, and that’s very concerning."
According to the study's authors, the findings add to the growing body of evidence connecting environmental tobacco with heart problems and at increasingly lower concentration levels, as well as further underscore the value of and need for broader policies to ban public smoking. In addition, the study serves as a reminder to clinicians to not only focus on asking individual patients if they are smokers, but also to find out whether they live with or occassionally spend time around smokers, even if they are not in the same room when smoking occurs, says Frey.
The impetus for this study came from the 2009 Institute of Medicine report, "Secondhand Smoke Exposure and Cardiovascular Effects: Making Sense of the Evidence," and a call for more science to uncover the mechanisms by which secondhand smoke exposure can damage the heart, particularly among nonsmokers.
Unlike previous studies that have relied on self-reporting or metabolites of nicotine in the bloodstream as a proxy for secondhand smoke exposure, the present study used a smoking machine to produce specific particulate concentrations. "We were able to faithfully characterize the concentration of secondhand smoke people were exposed to and produce very low levels that have not often been studied," explained Frey.
The study involved 33 healthy nonsmokers ranging in age from 18 to 40 years old with no known history of diabetes, heart or kidney disease. Researchers checked participants' salivary cotinine level—a biomarker of recent smoking—to confirm they had no evidence of smoke exposure leading up to the one-day study. The participants were then assigned to one of three exposure levels:
- Filtered clean air,
- Levels of smoke typically found in the homes of smokers or lingering in a restaurant, and
- Levels expected in a smoky bar or casino.
In a laboratory-type environment, filtered non-menthol cigarettes were smoked using a smoking machine, and the aged smoke was routed to participants in a measured way, allowing researchers to control the smoke concentration.
Vascular studies including testing brachial artery reactivity with ultrasound measurements were performed before and after exposure to secondhand smoke. A host of other measures, including urine and blood tests, to look for changes in specific metabolites were performed but did not yield significant differences. Risk factors for impaired vascular function including age, sex, body mass index, total cholesterol, baseline cotinine values, and baseline arterial diameter were not significantly related to absolute changes in endothelial in this healthy population.
Frey noted that the study has several limitations, including the small sample size and the fact that exposure was only at a one-time interval. Biomarkers and the magnitude of the effect on cardiovascular function may be greater with repeated short exposure that more closely imitates everyday life. He suggests that further studies should investigate the mechanism by which secondhand smoke affects endothelial function at the cellular level.