Exposure to "aged" secondhand smoke – even to a small amount and even for a brief time – impairs endothelial function, according to a report in the May 22 issue of the Journal of the American College of Cardiology.
"Aged" secondhand smoke refers to smoke that lingers in an indoor area 30 minutes or more after a smoker has finished a cigarette, and it is known to be more toxic to the respiratory epithelium than is fresh secondhand smoke, said Dr. Paul F. Frey of the division of cardiology, San Francisco General Hospital, and his associates.
The investigators performed a study to determine whether stale secondhand smoke also impairs endothelial function at the relatively low exposure levels that people are likely to encounter in the community setting. Endothelial dysfunction is a key mechanism in all stages of cardiovascular disease, they noted.
painless/Fotolia.com
Just because the smoker is gone doesn’t mean it’s safe: Stale, lingering cigarette smoke can be more toxic than fresh secondhand smoke.
The typical level of aged secondhand smoke found in smokers’ homes or in restaurants or other public venues that allow smoking is 100 mcg/m3 respirable suspended particles (RSPs), and the typical level found in bars or casinos in which smoke is more concentrated is 400 mcg/m3 RSPs. Dr. Frey and his colleagues assessed the response to 30 minutes of exposure at both of these levels, as well as to filtered smoke-free air, in 33 healthy nonsmoking adults aged 18-40 years.
All the study participants reported no exposure to secondhand smoke during the month preceding the study. None of them had conditions that could adversely affect endothelial function such as diabetes, hypertension, respiratory disease, kidney disease, coronary artery disease, or heart failure.
Endothelial function was assessed using high-resolution ultrasound to measure maximal percent flow-mediated dilation of the brachial artery before and after exposure.
The study participants were exposed to smoke-free air (11 participants), 100 mcg/m3 RSPs (11 participants), or 400 mcg/m3 RSPs (11 participants) in a hooded device attached to a smoking machine. The secondhand smoke was aged for 60 minutes, then routed to the hood for a single 30-minute exposure time. The RSP level was monitored continuously.
Endothelial function was impaired in a dose-dependent fashion at both levels of exposure to aged secondhand smoke. For every 100 mcg/m3 increase in RSP level, maximal percent flow-mediated dilation of the brachial artery decreased by 0.67%, Dr. Frey and his associates said (J. Am. Coll. Cardiol. 2012;59:1908-13).
"Our research strengthens the evidence that secondhand smoke is detrimental to cardiovascular health even at very short exposures and low particulate concentrations," they noted.
The findings highlight the importance of policies that limit the public’s exposure to secondhand smoke, the researchers said.
The study conditions may underestimate the effect of aged secondhand smoke in real-world settings, they added.
The subjects remained at rest throughout their exposure to secondhand smoke and were exposed for only half an hour. In real-world experience, people are exposed for much longer durations and may be physically active during their exposure, which increases minute ventilation. Moreover, "our subjects were healthy and may have been less susceptible to decrements in endothelial function than patients with vascular disease who are at greater risk for secondhand smoke–induced acute cardiovascular events."
This study was supported in part by the Tobacco-Related Disease Research Program and the Flight Attendants Medical Research Institute Bland Lane Center of Excellence on Secondhand Smoke at the University of California, San Francisco. One coauthor reported ties to pharmaceutical companies that develop or market smoking-cessation medications and being a paid expert witness in litigation against tobacco companies.