A study that is scheduled to be presented this week at the annual meeting of the American Physiological Society concludes that very brief exposure to tobacco smoke, wood smoke, and cooking oil fumes all cause potentially damaging cardiovascular changes (see press release; see news article). The study was conducted by researchers at the University of Kentucky and the Oak Ridge National Laboratory and was funded by Philip Morris (Evans JM, Patwardhan AR, Jenkins RA, Ilgner RH, Hartman EC, Jayanthi AK, Knapp CF. Autonomic responses of men and women to particulate exposures. Presented at the 122nd Annual Meeting of the American Physiological Association, New Orleans, LA, April 18-22, 2009).
The study was conducted in experimental environmental chambers at the Oak Ridge National Laboratory. Healthy nonsmoking volunteers were subjected to a 10-minute exposure to either tobacco smoke, cooking oil, wood smoke, or water vapor (the control). Cardiovascular parameters were measured before, during, and after exposure.
The study found that there was "increased sympathetic dominance in control of heart rate during exposure to all particulate exposures" and that "vasomotion increased in response to all particulate exposures."
The press release summarizes the main study findings as follows: "The study found that, particularly among men, exposure to smoke changed breathing patterns, raised blood pressure oscillations in peripheral arteries and shifted control of heart rate toward sympathetic domination. The sympathetic nervous system becomes active during times of stress, but can cause harm to the heart and blood vessels if activated too often or too long."
The news article summarizes the main result as follows: "The study confirmed previous research that has shown that smoke harms cardiovascular function and extended those findings by showing that this harm can occur with lower levels of smoke and shorter exposure times."
The Rest of the Story
This study is important, in part because it demonstrates that a variety of short-term exposures to particulate matter -- including not only tobacco smoke but also wood smoke and cooking oil fumes -- cause cardiovascular effects that could potentially be damaging, and might plausibly be a trigger for an acute cardiovascular event among individuals with severe, pre-existing heart disease.
But importantly, the study demonstrates that secondhand smoke is not unique in triggering such cardiovascular changes after acute exposure. All of the particulate exposures studied had the same effect.
What does this mean in practice? What it means is that the conclusion of many anti-smoking researchers and groups -- that smoking bans will immediately reduce heart attacks because nonsmokers will no longer have heart attacks triggered by brief secondhand smoke exposure -- is not a sound one. If any short-term (even 10 minute) exposure to any type of smoke or even to cooking fumes can cause acute cardiovascular changes that may trigger a coronary event in a susceptible individual, then simply removing one of those exposures may not necessarily decrease the incidence of heart attacks.
The point is this: if someone's cardiovascular health is so "fragile" that a brief exposure to tobacco smoke may precipitate an acute coronary event, then that person may also be "triggered" by almost any other exposure to particulates, as well as to a range of other exposures which may cause adverse cardiovascular effects, including eating a high-fat meal or experiencing stress.
Thus, it is unlikely that these heart attacks could be prevented simply by banning smoking in bars and restaurants. These individuals are almost certainly going to experience other exposures that affect their cardiovascular system in the same way that secondhand smoke would have.
Thus, even if it is the case that brief secondhand smoke exposures are triggering thousands of heart attacks each year (a fact that has not yet been proven), it is not necessarily true that smoking bans will prevent these heart attacks from occurring.
The bottom line is that anti-smoking and health groups (including the CDC itself) have gone beyond solid science in suggesting that smoking bans are resulting in immediate reductions in heart attacks because of the elimination of a major trigger for these heart attacks. The heart attacks will likely occur anyway, and at the same rate, because it is impossible for individuals to avoid exposure to every possible factor that will also induce the same types of changes in cardiovascular function as observed with short-term tobacco smoke exposure.
The study is also important, of course, because it demonstrates a biologically plausible mechanism by which long-term exposure to particulate matter in smoke can cause cardiovascular disease. While short-term activation of the sympathetic autonomic nervous system is not necessarily harmful if it occurs only occasionally, chronic activation of this system could be harmful to the heart and blood vessels and could result in heart disease.
Many of my colleagues will probably respond to this commentary by pointing out that the study was funded by Philip Morris and that the Oak Ridge National Laboratory has a long history of tobacco industry funding. Nevertheless, one must still look at the actual scientific merit of the work that was conducted. The study is methodologically sound and the conclusions are very well supported by the findings that are presented. There is no reason to dismiss the study simply because of its funding source.
If anything, the researchers have provided quotes to the media that are highly unfavorable to the tobacco companies (arguing that even low levels of exposure to secondhand smoke may be hazardous, and even more dangerous than previously thought). This demonstrates that one must not rely on an ad hominem approach in critiquing the scientific literature.