A new study published in the current issue of the Journal of the American College of Cardiology reports that a 30-minute exposure to secondhand smoke causes sustained vascular injury, consisting both of a damaged endothelium and an impaired ability to repair the endothelium (see: Heiss C, Amabile N, Lee AC, et al. Brief secondhand smoke exposure depresses endothelial progenitor cells activity and endothelial function: sustained vascular injury and blunted nitric oxide production. Journal of the American College of Cardiology 2008; 51(18): 1760-71).
Ten volunteers were exposed for 30 minutes to secondhand smoke at levels that one might encounter in a smoky bar, or to smoke-free air. The investigators found that acute tobacco smoke exposure was associated with decreased flow-mediated dilation that persisted for 2.5 hours and with impaired endothelial progenitor cell function that persisted for at least 24 hours.
The article concludes: "These results show that brief exposure to real-world levels of SHS [secondhand smoke] leads to a mobilization of dysfunctional EPCs [endothelial progenitor cells] in response to acute vascular injury that persists for more than 24 h [hours]. Mechanistically, these effects are linked to an impairment of NO [nitric oxide] production in EPCs. Taken together, these findings provide further evidence that even a very short period of passive smoke exposure has strong, persistent vascular consequences. The SHS may harm the vasculature not only by directly injuring the vascular endothelium but also by interfering with the vascular repair system, which may lead to chronic damage with recurrent exposures. These results provide further scientific evidence that involuntary SHS exposure constitutes a significant public health risk even at low levels."
One of the study authors - Dr. Stan Glantz - told the press that these results support the conclusion that individuals who are exposed briefly to secondhand smoke are at an increased risk of suffering a heart attack. According to an article in the Washington Post: "Secondhand smoke not only damages the delicate cells that line blood vessels but also disrupts the body's natural repair mechanism for those cells, a new study shows. The research was done because there still are skeptics who doubt the health value of public smoking bans, said study co-author Stanton A. Glantz, professor of medicine at the University of California, San Francisco, Center for Tobacco Control Research and Education. 'There still are some people out there saying these effects [from smoking bans], seen in terms of reduced heart attacks and an immediate drop in heart attacks, are just not feasible,' Glantz said."
The Rest of the Story
Although I was not mentioned by name, it is quite clear that Dr. Glantz is referring to me when he points to "some people out there" saying that a large immediate decline in heart attacks from smoking bans is not plausible (see example of one of my commentaries arguing that a 40% decline in heart attacks from the smoking ban in Helena is not scientifically plausible). It is reassuring to see, however, that Dr. Glantz takes my skepticism seriously enough that it is apparently a motivation for him to conduct research to try to discredit my commentary.
The research itself is not the story. The research itself is quite sound and the conclusions drawn in the paper are reasonable. There is clearly evidence of sustained (for at least 24 hours) vascular injury caused by a brief exposure to secondhand smoke. If sustained over time, this endothelial injury could initiate and sustain the process of atherosclerosis, which could eventually lead to heart disease. Thus, the paper provides compelling mechanistic support for the conclusion that chronic secondhand smoke exposure is a cause of heart disease among nonsmokers.
The story here is the conclusion that is being disseminated to the media by Dr. Glantz. That conclusion is far removed from the actual conclusion of the study. Instead of reporting to the media that this research has detected a mechanism by which sustained tobacco smoke exposure leads to atherosclerosis and heart disease, Dr. Glantz has informed the media that this study supports the assertion that smoking bans lead to the kinds of dramatic and immediate declines in heart attack incidence that were observed in places like Helena and Pueblo.
In other words, Dr. Glantz is telling the media and the public that the way to interpret these study findings is to believe that they show that a brief secondhand smoke exposure increases the immediate risk of suffering a heart attack.
The problem is that the study provides no such evidence. It is not clear that the effects documented in this study lead to the precipitation of heart attacks. In fact, the study provides some evidence that the opposite might be the case.
Specifically, the study finds that while a decrease in flow-mediated dilation is present for the first two hours after exposure, the remaining post-exposure period (from 2 hours to 24 hours) is characterized by an increase in flow-mediated dilation, which the authors describe as "increased vasodilation in the absence of further SHS exposure."
Now I am not prepared to conclude that this increase in flow-mediated dilation decreases acute heart attack risk. However, Dr. Glantz and many anti-smoking groups have taken evidence of a transient decrease in flow-mediated dilation following tobacco smoke exposure to indicate that there is an increase in immediate heart disease risk. So using the same logic employed by these groups, the results from this study would indicate that there is a prolonged period of time where acute heart attack risk might actually decline following a single, 30-minute secondhand smoke exposure among nonsmokers.
The truth is that this study does not have anything to do with the acute heart attack risk posed by 30 minutes of secondhand smoke exposure. What it has to do with is identifying a plausible mechanism by which chronic and sustained tobacco smoke exposure can and does lead to atherosclerosis and consequently, heart disease.
I don't understand why some anti-smoking advocates see the need to distort the findings of the study when communicating these results to the public. It almost seems that the intention is to try to scare nonsmokers into thinking that if they are exposed briefly to secondhand smoke, they might suffer a heart attack (even if they do not have severe existing coronary artery disease).
This story serves to confirm what I have been arguing for several years now: that anti-smoking groups are exaggerating and distorting the results of scientific studies to try to scare the public into believing that brief exposure to secondhand smoke is causing heart attacks among otherwise healthy nonsmokers.
In fact, this study has no relevance whatsoever to the scientific claim with which I have actually taken issue: that a 30-minute tobacco smoke exposure causes heart disease or increases heart attack risk among healthy nonsmokers. However, the early indication is that anti-smoking advocates and groups are going to try to use these data to convince the public of exactly that.
Without distortion or misrepresentation, these data would constitute powerful evidence that chronic exposure to secondhand smoke has severe cardiovascular disease implications for nonsmokers, and that public smoking bans in workplaces are therefore justified in order to protect workers from these serious health effects. However, instead of sticking to the facts, anti-smoking advocates are already distorting the evidence and using it to try to convince people that a 30-minute exposure to secondhand smoke puts you at risk of suffering an immediate heart attack.
Unfortunately, the absurdity of this distortion of the evidence is going to not only kill the claim that the advocates are trying to make, but it is also going to kill the true claim that the advocates could make from the very same evidence. The baby is going to be thrown out with the bath water.