So here is yet another article that leaves the reader with a lot of questions.

#1- With all the actual case histories of heart transplants out there, why was it necessary to do a study on rats?

#2- It is well known that the success of a transplant depends on suppressing the immune system to prevent rejection of the new heart. It is claimed that tobacco use suppresses the immune system, and yet this study claims that tobacco interferes with immunosuppression, thereby rejecting the new heart. That doesn't make a bit of sense. Either tobacco use should aid in immunosuppression or the claims by other anti-tobacco researchers that it suppresses the immune system are all wrong.

#3- If they chose to not use actual human case histories, preferring rats instead, why did they not try their best to simulate real life transplants by including the use of immunosuppressents? Now we'll never know how different the results might have been if they had.

#4- I'm a 64 year old smoker who has been smoking for 49 years and now there's the question of whether or not anyone would want my heart. I've heard that the best indicator of heart health is the resting BPM. Because mine is in the 50's which is far below the 75 BPM average, I've always thought that all but the most discriminating nonsmokers would jump at the chance to have my heart pumping their blood around. Now it appears that these researchers are telling me "Hey Jim, your heart is not as big a prize as was previously thought!"

Sounds like another study that was conducted more in the interest of somebody's agenda rather than actual science.

Jim Blogg<

This study could be important *IF* its results could be trusted. Why would I doubt those results? Simple: throughout the entire study AND its media presentation, the terminology used refers to "exposure to cigarette smoke."

Clearly anyone reading the stories or even anyone skimming through the study would imagine that "exposure to cigarette smoke" meant "exposure to cigarette smoke." But this is *NOT* what it meant: the rats involved had cotinine readings equivalent to those found in actual regular half-pack a day smokers THEMSELVES - 83ng/Ml. It is hard to imagine a scenario in which nonsmokers would reach such a level in even the smokiest environments: we are talking about smoking, not "exposure to smoke."

By playing with the words to make it sound as though simple "exposure" to wisps of smoke in the air might dramatically kill people's hearts the study and the stories generate support for smoking bans... exactly as I believe they were intended to.

Why would I believe that such intention existed? Simple: because I've seen so much twisting and juggling and distortion of other research in this area seemingly aimed toward such goals. A good example can be seen in the recent study claiming that "Smoking bans do not hurt bar and restaurant employment" while using the word "and" to only mean the combination of the two areas despite the fact that the researchers had the data right in front of them showing bar employment being literally decimated in most of their study population. To see the full story Google:

boggles clearway revisited grier

and read the Comments after "Exemptions and employment revisited."

Other examples abound, ranging from the Pell study in Scotland claiming a 17% drop in post-ban heart attacks despite official government figures showing the real figures were roughly half that and quite in line with general yearly reductions and variations to the Helena "bounce-back" claims where the data showing their falsehood was wiped from the internet and brought back only when I tracked them down through an archival engine.

This study *looks* superficially to be soundly done. I have no substantive criticisms of its technique. But the fact that the findings were presented using such patently prejudicial phrasing makes me wonder.


Michael J. McFadden
Author of "Dissecting Antismokers' Brains"