Rapid Responses to:
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Rapid Responses: Rapid Responses published:
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passive smoking
- Ernest A Gildersleve (30 June 2004)
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Re: passive smoking
- Jon f pindar (1 July 2004)
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Dietary nicotine confounds Passive Smoking estimates
- David W Kuneman, none (1 July 2004)
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Re: passive smoking
- Adam Jacobs (2 July 2004)
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Obviously vested interests
- Bill Thompson (2 July 2004)
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Re: Dietary nicotine confounds Passive Smoking estimates
- Ginger A. Carver (2 July 2004)
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Re: Re: passive smoking
- George Vinderoot (2 July 2004)
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Re: Re: passive smoking
- Ben Hirsch (2 July 2004)
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Poor Science
- Anthony S Ward (2 July 2004)
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Re: Re: Dietary nicotine confounds Passive Smoking estimates
- Amanda D (2 July 2004)
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Re: Dietary nicotine confounds Passive Smoking estimates
- Shere Shaeffer (3 July 2004)
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Passive smoking is like statins- both are involuntary manslaughter
- Dr. Herbert H. Nehrlich (3 July 2004)
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Drugged unwillingly
- Phillip J. Colquitt (3 July 2004)
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Re: Dietary nicotine confounds Passive Smoking estimates
- David W. Kuneman (4 July 2004)
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Politically correct nicotine
- Archie D Anderson (4 July 2004)
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Cotinine is only a marker for...cotinine
- Walt Cody (4 July 2004)
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Re: Poor Science
- Anthony S Ward (4 July 2004)
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Passive smoking & CHD
- Kenneth William E. Denson, Foundation. Thame, Oxon OX9 3NY. UK (4 July 2004)
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Re: Re: Dietary nicotine confounds Passive Smoking estimates
- Adam Jacobs (5 July 2004)
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Re: Re: Re: Dietary nicotine confounds Passive Smoking estimates
- Mika Svensk (6 July 2004)
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Pasive smoking & CHD
- Dr. K.W.E. Denson, Thame, Oxon OX9 3NY. (6 July 2004)
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Fatal asymmetries
- Gio B. Gori (7 July 2004)
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Defense of cotinine marker
- Sheila M Duffy (14 July 2004)
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Re: Defense of cotinine marker
- Mika Svensk (15 July 2004)
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ETS - Stess as a Confounding Factor
- Jay R. Schrand (16 July 2004)
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'Passive Smoking' - Effects Underestimated?
- Stephen J. Stotesbury, Dr. Wolfram Röper, Biological Issues Manager (19 July 2004)
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No reliable data from researches without considering Biophysical-Semeiotic Constitutions and Single Patient Based Medicine.
- Sergio Stagnaro (23 July 2004)
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Passive smoking and coronary heart disease
- yehani wedatilake, NN16 8UZ (25 July 2004)
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Passive Smoking
- John E Burgess (31 July 2004)
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speculative claims
- Sue Jeffers (10 August 2004)
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Re: Defense of Cotinine Marker
- Walt Cody (11 August 2004)
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Poor Science - Cotinine & Risk Attenuation
- Anthony S. Ward (19 August 2004)
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Passive smoking and coronary heart disease
- Hugh Tunstall-Pedoe, Ruoling Chen (first author), Roger Tavendale (19 August 2004)
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Ernest A Gildersleve, retired London SE22 8ST
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I am an 84 year old male.(Not a doctor.) From 1932 until about 1950 I was subjected to very dense passive smoking as I travelled to and fro to school and work on the top decks of trams and buses. Almost every passenger was smoking.One could not see from one end of the vehicle to the other in winter when all the windows were closed. The stink was nose- burning and eye smarting! Pipes,cigarettes, you name it. After this I worked in smokey workshops and offices. Despite all this my lungs appear to be perfectly healthy. I have never suffered any serious discomfort. How could this be if passive smoking is really so harmful? Competing interests: None declared |
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Jon f pindar, none 11788
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Here is what mark twain had to say to the anti smoking groups of his day You are blind to the fact that most old men in America smoke and drink coffee, although, according to your theory, they ought to have died young; and that hearty old Englishmen drink wine and survive it, and portly old Dutchmen both drink and smoke freely, and yet grow older and fatter all the time. And you never try to find out how much solid comfort, relaxation, and enjoyment a man derives from smoking in the course of a lifetime (which is worth ten times the money he would save by letting it alone), nor the appalling aggregate of happiness lost in a lifetime by your kind of people from not smoking. Of course you can save money by denying yourself all those little vicious enjoyments for fifty years; but then what can you do with it? What use can you put it to? Money can't save your infinitesimal soul. All the use that money can be put to is to purchase comfort and enjoyment in this life; therefore, as you are an enemy to comfort and enjoyment where is the use of accumulating cash? Competing interests: None declared |
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David W Kuneman, none retired, none
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Please refer to New England J. of Medicine, 329, p437, 1993. Medical Researchers need a better understanding of how much nicotine and therefore continine can be accounted for by diet, not passive smoking. Domino, et.al. calculated eating 140 g of potatoes, 93g tomatoes, 10g eggplant, for example would produce a serum nicotine comparable to a nonsmoker spending three hours in a smoking environment. These are ordinary amounts of common vegetables ingested by typical persons during typical days, and would be extended to subjects of passive smoking studies. To assume most serum nicotine and continine concentrations are due to passive smoke exposure produces results such as those in the current study, that a non-linear relationship between estimated smoke exposure and observed disease is found. Competing interests: None declared |
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Adam Jacobs, Director Dianthus Medical Limited, London SW19 3TZ
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Ernest Gildersleve asks how it is possible for passive smoking to be harmful, given that he is a healthy 84-year-old who has been exposed to heavy passive smoking. Perhaps I can answer the question with an analogy. If a large number of people were to play Russian roulette, using a six-chamber revolver and one bullet, then, on average, one player in six would blow their brains out, but the other five would be completely unharmed. Just because five in six players are unharmed does not mean that Russian roulette isn't harmful on average. I am pleased to hear that Mr Gildersleve has enjoyed 84 years of good health, and I wish him many more. But spare a thought for those passive smokers who were unlucky enough to pick the chamber with the bullet in it. Competing interests: Non-smoker who doesn't like breathing in other people's cigarette smoke |
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Bill Thompson, VP Operations, Comp Stores Winston-Salem, NC
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No real surprises in this new report. Those still fighting smoke-free air (to which EVERYONE has a RIGHT)are either the tobacco people or their "mouthpieces", brain-damaged from tobacco smoke and/or just PLAIN STUPID! Tobacco is terrorism, pure and simple. This lethal drug kills 5,000,000 users and hundreds of thousands more INNOCENT people around the world every year. TOBACCO AND TOBACCO SMOKE SHOULD BE BANNED IMMEDIATELY. Competing interests: None declared |
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Ginger A. Carver, N/A Tulsa, OK
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Potatoes, tomatoes and eggplant are not addictive, defective and lethal, when used as intended. For which tobacco company do YOU work? Competing interests: None declared |
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George Vinderoot, (none) St. Louis, MO
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Mark Twain was a tobacco addict. Have you ever read his hateful accusations about Germany and even the German language? "Tom Sawyer" isn't all he wrote. What a poor choice of a person to use as your example! Competing interests: None declared |
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Ben Hirsch, Research Assisstant University of Massachusetts
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Though many contend that passive smoking is analogous to Russian roulette, there is one fundamental difference. With passive smoking, the revolver has millions of chambers, but only one contains a bullet. Combine the passive smoking gun with the equally large pollution, diet, exercise, and pre-disposition guns and it becomes more difficult to prove that the one bullet in the passive smoking gun exists. Additionally, Ginger A. Carver should note that one does not need to work for a tobacco company to reference a New England Journal of Medicine article detailing the nicotine contents of various fruits and vegetables. There is far more contention surrounding the health risks of passive smoking than there is around the nicotine contents of frequently consumed vegetation. Competing interests: None declared |
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Anthony S Ward, none retired
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Sir, re: Passive Smoking report 30/06/04: I am very concerned that a respectable scientific journal could publish such a study. Further, I am shocked that the press have further exaggerated the reports 'findings'. This at a time when a major political decision on the subject is imminent. Very few doctors, politicians and members of the public will examine the report in detail and fewer will understand it and so will rely on press reports. My scientific/statistical objections to the study could fill several pages, but I will just point out two: 1. The risk factors in the conclusion are taken from table 2(part 1). These figures include ex-smokers (potentially ex heavy smokers of 40+ years). CHD risk is known to be increased for this group and has nothing to do with passive smoking. Table 2 (part2) gives the figures excluding ex-smokers and hey presto, 2 of the 3 results are no longer statistically significant. The remaining one still is (just) but only after the third adjustment ,which at +0.45 is huge. Such adjustments are little more than best guesses and a result that only occurs through adjustment is highly suspect. The authors comment that the figures after excluding ex-smokers look similar has no place in a serious paper. In conclusion - the study shows no statistically significant evidence for a link between CHD and passive smoking (let alone a causal one). 2. Page 4 states that ex-smokers had 'no specific incentive to provide inaccurate information' (i.e. that they had taken up smoking again). Except that if their insurer found out they could invalidate their life assurance. (non-smoking discounts were introduced by all major insurers during 1981/2). What happened to peer review and editorial scrutiny ? Competing interests: Smoker but no affiliations to interest groups. |
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Amanda D, Teacher Buffalo schools 14215
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The point was not that "eating tomatoes or potatoes is safe, so why shouldn’t smoking be safe?" The point that was meant to be made was that the study used the amount of serum nicotine and cotinine concentrations to determine how much exposure to secondhand smoke a participant had. The problem with this correlation occurs when you have a participant who eats a plant based diet, with many potatoes, tomatoes, and eggplants, yet has little exposure to second hand smoke. This person would be put in the same group as people who do not eat those foods, but spend all day in a smoke filled bar. This has the potential to skew the data and perhaps invalidate it as a whole. Just because someone has made a statement contrary to your beliefs does not mean they are malicious or paid by a company to say such things. In the world of science we work hard to contradict what others say, so that we can be certain that what is being said is correct. Competing interests: None declared |
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Shere Shaeffer, Legal Assistant Omaha, NE 68116
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I doubt that my oncologist would agree with you that "eggplant" and other vegetables caused me to have a lung removed four years ago! No, it was the 22 years of working in a restaurant which unwisely allowed smoking. If you really are a teacher, I wouldn't want you to teach anything to MY kids! As someone else here has already posted, tobacco should be banned and tobacco smoke should not be allowed anywhere around others. Competing interests: None declared |
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Dr. Herbert H. Nehrlich, Private Practice Bribie Island, Australia 4507
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Sigmund Freud was a tobacco addict. I was, once upon a time. I was exposed to the 60 + cigarettes a day habit of my father in the cold climate of the Fatherland, where windows were kept closed during the colder months (9 months out of 12). I, too did not(seem to) suffer any effects from this passive smoking and my father lived to the age of 92. I liked Adam Jacobs' analogy because it says it all very precisely. There was a husband and wife team who studied volcanoes and they were considered foolish because of their dare-devil journeys to within metres of the lava. Until a certain day, I think it was the 15th of March, they were doing just fine and delivered the most beautiful footage of volcanic details. On the 16th, however, the Lavadevil got them. Competing interests: None declared |
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Phillip J. Colquitt, Breather Place of work: A declining environment
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Not difficult to see why health care industry people defy the growing belief in our society that smoking should be banned. I got my biggest doses of passive smoke while working in Australian public hospitals as an "non-smoker" RN. Especially so during my much not missed ten years in mental health, where smokes were almost currency. But generalist nurses weren’t much better. The charge nurse and the principal nurse were both smokers and so quite chummy. In small closed rooms, we would listen to “handover” as the charge and his mates puffed, winked, and nudged in conspirational bliss. In the day room where patients and nurses passed the time, the familiar blue air could be carved. In the relaxation room attached to the staff dining room, nurses[mainly women] would regress to the oral stage and go into a smoke feeding frenzy - talking and smoking at speed, an art form which seems to have evolved in response to the ten minute tea break – eerily called “smoko”. The complete take over of normal lives by the drugged, is perhaps best seen in the negative words used to describe normal people – eg. “non- smoker” and “non-drinker”. Competing interests: None declared |
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David W. Kuneman, none retired
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I'm responding to my own original response. After considering further, the important role potatoes play in the diet of U.K. residents, it seem obvious nicotine and continine are also biomarkers for over- eating....which, of course is strongly associated with....you guessed it, heart disease!The research may have picked up the role over-eating plays in heart disease, not passive smoking. With increasing nicotine, participants were found to have increased heart disease, which is consistant with more over-eating producing more heart disease. ( A well known fact)The study cannot distinguish between the two possibilities. Of the further responses I viewed, the one that strikes me most is the analogy of Russian roulet' with a revolver with millions of chambers. The analogy is actually playing Russian roulet' with a revolver with millions of chambers while in a room full of hundreds of other revolvers being fired at the same time. If no one ever got heart disease for any other reason than passive smoking, I could see the validity of the claim of the authors, but since everyone agrees many other risk factors for heart disease exist, then we cannot be sure "the bullet" that struck any individual was fired from the Russian Roulet' revolver, or some other revolver. The authors must exclude all other possibilities before making any conclusion that nicotine came from passive smoke and thus caused the heart disease they found. I cited the New Eng. J. Med reference because in Britian, consuming 8oz potatoes/day can explain all the nicotine the authors found. Since the gut protonates nicotine, all dietary nicotine is absorbed, and appears in the bodily fluids. The way this study was designed, a person never exposed to tobacco smoke, but who over-eats can be assumed to have a high passive smoke exposure. Competing interests: None declared |
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Archie D Anderson, Vice chair political party CFO Minnesota Sentinel Coon Rapids Minnespta 55433-5114
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While shopping at a smoke free drug store I noticed Nicotrol, a stop smoking device on sale for $ 50.99. While hospitalized one 14mg 24 hour nicotine patch was "administered" for only $10.90. Now who may I sue for contaminating my healthy body with Nicotine? The owner of the vegetable market? the manufacturer of Nicotrol?. My doctor?. We plebian citizens need to be informed of the difference between politically correct nicotine and the kind that is not Politically Correct grown by Americans then taxed fifteen times the value of a pack of tobacco for excise, sales, gray market increases and increased prices to pay off a litigeous debt,one quarter of a trillion dollars created by the government and four large tobacco companies that now also funds 100% of the anti smoking industry. Ban tobacco? surely you jest,Second hand smoke danger? a great catalyst for behavior control modification of unwilling citizens and business owners. Archie Anderson Competing interests: Smokers rights'advocate |
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Walt Cody, writer NYC 10021
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The only reason cotinine (a harmless metabolite of nicotine and other nightshade vegetables) is used as a marker for exposure to ETS is because... it's the only thing that's possible to measure. For all the hot talk about "4000 chemicals" in secondhand smoke, most of them exist in such miniscule proportions that they can't be detected (even in the air!); rather, their presence can merely be merely deduced or perhaps just supposed. The question then arises: What does the presence of cotinine measure? Answer: it measures the presence of cotinine. Even the California EPA Report (also known as WHO's "Monograph 10") admits that "cotinine does not serve well as a marker for the presence of other tobacco smoke compounds," an assertion one finds in virtually all the literature on secondhand smoke. Then, too, there's this: "There exists between individuals a genetically determined variation (up to 50 fold) in the level of metabolism to cotinine from a given exposure." (Nyberg et al, "Misclassification of Smoking Status," Epidemiology, 5/97) And this: Men metabolize cotinine faster than women, and whites faster than blacks (by 30%). This would also apply to the cotinine metabolized out of potatoes. And would indicate that either-- and/or-- women and blacks would register higher levels than their white/male counterparts to identical exposure. Further, eating a meal (consisting of anything) can also affect the metabolic speed. (Ahjevych et al, "Nicotine Metabolism Variables," Agency for Health Care Policy.) Nevertheless, it's used as a marker (?) Here's another angle that relates to the study that's now under discussion-- in which serum cotinine at levels of ...what?....8-10 ng/ml are fingered as risky (1.6 RR) for eventual Coronary Heart Disease. According to a study sponsored by the American Lung Assn (Ahjevych et al, in Addiction Behaviors, 2/99) the blood cotinine levels that were measured in LESS than pack-a-day smokers ranged from 182 - 249 ng/ml. And the generally- accepted RR for CHD among first-hand smokers is 1.7. So why are we to believe (by what strange logic?) that serum levels of 8-14 produce a risk almost as high? And cotinine (have I mentioned?) is a harmless metabolite that indicates nothing except exposure to nicotine or nightshade vegetables. But, hey, I'll let Nyberg mention it again: "It is not known how levels of cotinine measured relate to the biologically important components of ETS other than nicotine." (Op cit) Competing interests: None declared |
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Anthony S Ward, retired none
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I should perhaps have prefixed my original posting by noting the disproportional number of ex-smokers in the higher cotinine groups (fig 1 & table 1) and the absence of any adjustment for smoking history (table 2). Further to my second point, it seems remarkable to assume that 99% of the ex-smokers remained ex-smokers without any relapses during the 20 years of the study. Competing interests: Smoker but no affiliations to interest groups, |
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Kenneth William E. Denson, Director Thromb. & Haemost. Res, Foundation. Thame, Oxon OX9 3NY. UK
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The paper by Whincup and colleagues is interesting but it is improbable that the increased risk for coronary heart diseas (CHD)with cotinine levels is due to the inhalation of secondary tobacco smoke. It is difficult to accept that a mean cotinine level of 300 ng/ml in an active smoker results in an increased risk of 70% for CHD and a level of 0.8-1,4 ng/ml results in a 45% increased risk. There is lack of linearity in response and no increased risk for stroke. A more likely interpretation of their results,is confounding by shared risk factors of the smoking partner. Smokers are more stressed and take less exercise and their diet includes a higher intake of saturated fat, and lower intakes of vitamins C and E, beta carotene and fibre compared to non-smokers (p<0.00001). These are strong risk factors for CHD and many are shared by a non-smoking partner. These risks would be shared randomly and not according to the degree of smoke exposure or intensity of the smoking partner and could result in non-linearity of cotinine levels and risk of CHD. Competing interests: None declared |
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Adam Jacobs, Director Dianthus Medical Limited, London SW19 3TZ
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David Kuneman appears to quote somewhat selectively from the literature in support of his theory that high cotinine concentrations are a more reliable marker of aubergine consumption than of passive smoking. Anyone interested in reading the other side of the story might want to have a look at http://bmj.bmjjournals.com/cgi/content/full/308/6920/61/c Competing interests: Non-smoker; avid aubergine eater |
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Mika Svensk, cartoonist, B.A. Finland
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Amount of nicotine in nightshade vegetables can be greater than thought. There is pesticides which include nicotine. Nightshade vegetables and of course other vegetables might contain nicotine remains from pesticide. Competing interests: smoker |
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Dr. K.W.E. Denson, Director Thromb. & Haemostasis Researxh Foundation., Thame, Oxon OX9 3NY.
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Further to my earlier response. For those who require additional evidence I refer you to three recent reviews which concluded that passive smoking does not contribute to an increased risk for CHD. Denson K.W.E. Environmental tobacco smoke and ischaemic heat disease: a critical assesment of recent meta-analyses and reviews. Medical Science Research 1999;27:75-82. Lee PN, Roe FJC. Emviromental Tobacco smoke exposure and heart disease. A critique of the claims of Glantz and Parmley. Human and Ecological Risk Assessment 1999;5:171-218. Nilsson R. Environmental tobacco smoke revisited: The reliability of the data used for risk assessment. Risk Analysis 2000;21:737-760. Competing interests: None declared |
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Gio B. Gori, Director The Health Policy Center, 6704 Barr Road, Bethesda, MD 20816, USA
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One hopes the publishing of this forgettable paper is not the Editor’s penance for having published the venial Enstrom & Kabat (BMJ 2003;326:1057-1067) report of a year ago. If our best journals are given to publish opinion pieces, they should be presented as such, and not passed for scientifically validated stuff.
Epidemiologist would agree that epidemiologic studies of passive smoke are not scientific exercises, but observational reports encumbered by biases and confounders impossible to account for. The literature for cardiovascular diseases alone reports over 300 risk factors. Pressed for honesty, epidemiologists would have to agree that the inconsistency of results even among the largest studies of passive smoke is appalling, and that the best one could say is that the measure of a possible risk -if there is one - is beyond epidemiologic means. Why still throw good money after bad one? The discrepancies of this “large” study and the even larger Enstrom & Kabat report are obvious, but still not as flagrant as a comparison with cardiovascular risks in active smokers. Should authors and reviewers not feel the need of an explanation? Some two dozen explanations may be in fact preferable, for active smokers register average cotinine levels in excess of 300 ng/ml, or about 20 times the maximum levels reported in the study. Yet, they display cardiovascular risks of the same or lower magnitude than reported in this study of passive smoke exposure. Mortality ratios derived from the monumental British Doctors study (BMJ 1994; 301:901-911. BMJ 2004; 328: 1519-1520), which may compare with the anthropology and history of the study at hand, read around 1.6 for active cigarette smokers, and 1.15 for active cigar and pipe smokers. It should not be presumptuous to imagine the authors (and reviewers)af this present paper being familiar with other cardiovascular studies that report even lower risks in active smokers. Should a formal clarification be expected? Should we keep reading such unqualified nonsense? Competing interests: The author has been a consultant to the tobacco industry. That should not matter, but if it does, should the authors of the paper report direct and indirect financial support from the commercial antismoking interests of the pharmaceutical industry? |
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Sheila M Duffy, Head of Information and Communications ASH Scotland, 8 Frederick Street, Edinburgh, EH2 2HB
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The New York Smoke-Free Air Act took effect on March 30th 2003. On May 12, 2004 the New York City Department of Health and Mental Hygiene (DOHMH) announced an 11% decline in the number of smokers in New York City over the previous year - the fastest drop in smoking rates ever recorded nationally. Those who continued to smoke were also smoking less. The DOHMH attributed the fall in smoking rates to its program of tobacco control, including the ban on smoking in public places. New Yorkers widely support the ban. Data from the DOHMH one year review showed that air quality in bars and restaurants had improved dramatically and that levels of cotinine had decreased by 85% over the year in non-smoking workers in bars and restaurants. My presumption is that this has nothing to do with a change in their diet. The report can be viewed at: http://www.nyc.gov/html/doh/pdf/smoke/sfaa-2004report.pdf Competing interests: Head of Information and Communications with ASH Scotland, a non profit organisation originally set up by the Royal College of Physicians to publicise the impacts of tobacco smoking on health. |
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Mika Svensk, cartoonist, B.A. Finland
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A purpose of The State of Smoke-Free New York City: A One-Year Review -report is to try to prove that the smoking ban has been a good and widely accepted thing. It is ignored completely in the report a poll conducted by the firm McLaughlin & Association. The firm polled New Yorkers asking ''Did New York politicians go too far in enacting a total smoking ban in restaurants and bars?''. 67.5 percent of New York State residents and 63.1 percent of the New York City residents said yes. New York's authorities brought up polls conducted by Zogby International and Quinnipiac University. Zogby's and Quinnipiac's polls' results were more suitable. It is claimed in the report too that the smoking ban has not hurt bar business. The impression of it is based on a Department of Finance's way to calculate in it's survey the increase of bar and restaurant business. A Department of Finance spokesperson has admitted in The Irish Echo that much of the survey included economic data gathered from establishments that did not have smoking permitted before the ban, such as McDonalds. These examples point out how expediencely anti-smoking lobby acts and give more reasons to doubt also it's honesty when it claims that secondhand smoke is hazardous. Maybe someone has stopped smoking because of the ban justified by claimed dangers of environmental tobacco smoke but to get people stop smoking is not acceptable reason for ban. Smoking is a personal choice like other lifestyle choices. It is not in authorities power. Competing interests: smoker |
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Jay R. Schrand, Independent Researcher Port Hueneme, CA 93041
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Those who smoke have been exposed to high number of stressful Adverse Childhood Experiences (ACE) (2) during childhood. Traumatic and chronic stress has an adverse effect on the neuro-endocrine and cardiovascular systems. Exposure to Environmental Tobacco Smoke (ETS) indicated by cotinine levels may be an marker for assortive mating(3) and associations. Those who smoke and who have been exposed to the stress of ACE's would still be more likely to marry and associate with individuals with ACE's who simply do not smoke. These non-smokers would still be at higher risk for obesity, depression and other risk factors associated with ACE's and heart disease. Indeed, a graded positive association was found between cotinine concentrations and body mass index in the non-smokers of this study(1). If active smoking reduces stress and BMI in smokers, how can ETS increase BMI in their otherwise nonsmoking spouses and associates?
Exposure to stress, assortive mating, smoker mobility, urbanicity, exposure to vegetables are some of the many possible confounders. The genetic basis for human choice has a certain amount of unpredictability as an adaptive mechanism to cope with a changing environment. This underscores the difficulty of attempting to prove causation in relationships with such low correlations. Is there really causality. Or is it just noise? Jay R. Schrand References: 1. Whincup PH, Gilg JA, Emberson JR, Jarvis MJ, Feyerabend C, Bryant A, Walker M, Cook DG. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ, Jun 2004; 10.1136/bmj.38146.427188.55. 2. Anda RF, Croft JB, Felitti VJ, Nordenberg D, Giles WH, et al. Adverse Childhood Experiences and Smoking During Adolescence and Adulthood. JAMA. 1999;282:1652-1658 3. Willemsen G, Vink JM, Boomsma DI. Letter - Assortative mating may explain spouses' risk of same disease. BMJ 2003;326:396 ( 15 February ) Competing interests: The author is a Systems Engineer, Independent Researcher, and Veteran, and has no financial interest in the tobacco, food or pharmaceutical industries other than as a consumer of their products. |
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Stephen J. Stotesbury, Regulatory Science Manager Imperial Tobacco Limited, Upton Road, Southville, Bristol, BS3 1QZ, Dr. Wolfram Röper, Biological Issues Manager
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Editor – The study by Whincup et al (1) concludes that ‘the effects of passive smoking may have been underestimated in earlier studies'. Given the extensive media reporting of this study, we take issue with the following points: 1. This study uses data from a larger study of heart disease in British men, then aged 40 to 59, that began in 1978. When the men gave blood in 1978 they were asked about their smoking habits, but not about their possible exposure to ETS. 2. The premise that a single blood sample is representative of exposure to ETS over the past 25 years exceeds the bounds of credibility. Many life-style factors are likely to change over this time. 3. There is no acknowledgement of the potential for degradation in blood samples stored over 25 years. 4. Whilst acknowledging that cotinine may indicate whether a person has recently been exposed to tobacco smoke or not, patterns of nicotine metabolism are different in different people (2), and for that reason cotinine alone cannot reliably be used to compare relative exposure between different individuals. 5. The classification of non-smokers and active smokers relies on questionnaire responses which the authors acknowledge may not always be accurate. Some very high serum cotinine levels raise questions about the classification of ‘former smokers’ and any conclusions based on this group should be made with great caution. There is no evidence of either a dose response relationship or a significant increase in the risk of CHD for the group who claim to be ‘never smokers’. In conclusion, the results of this study do not provide any definitive answers about the nature of the association, if any, between ETS and heart disease. References 1. Whincup PH, Gilg JA, Emberson JR et al. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ, doi:10.1136/bmj.38146.427188.55 (published 30 June 2004). 2. Benowitz NL, Jacob P 3rd, Fong I, Gupta S. Nicotine metabolic profile in man: comparison of cigarette smoking and transdermal nicotine. J Pharmacol Exp Ther 1994;268:296-303. Competing interests: Both authors are employees of Imperial Tobacco Limited |
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Sergio Stagnaro, Specialist in Blood, Gastrointestinal, and Metabolic Diseases. Researcher in Biophysical Semeiotics. Via Erasmo Piaggio 23/8 16037 Riva Trigoso (Genova)Italy.
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Sirs, In the P.H.Whincup’s et al. article there is a common fundamental bias, now-a-days present unfortunately in all clinical researches: individuals have not been rationally selected and enroled, overlooking doctors their “real risk”, i.e., in such as case, coronary heart disease and stroke genetically inherited risk. One essential problem, facing doctors treating patients affected by whatever disorder, is certainly tobacco smoking, as I have found in "clinical" researches, gathering data from large and diverse populations, rationally selected, during the last 46 years by means of an original physical semeiotics: Biophysical Semeiotics (See: HONCode website 233736, www.semeioticabiofisica.it). Actually, apart from the well-known negative influences of tobacco on health, as regards the importance of whathever risk factor (e.g., passive smoking) we have to consider the genetic predisposition ("CAD real risk", for instance: See in above-cited website: Biophysical-Semeiotic Consitutions). In fact, as far as the onset of a lot of disorders is concerned, I would underline here its pathological powerful influence on tissue oxygen supply to all biological systems (2). This varies in intensity among individuals, of course, in relation to a congenital functional mitochondrial cytopathology, I termed Congenital Acidosic Enzyme-Metabolic Histangiopathy (3), biophysical- semeiotic constitutions are based on. This both "silent" and dangerous action is easy to evaluate at the bed-side with the aid of a stethoscope. I suggest at first (baseline) to investigate, e.g. myocardial oxygenation from the "latency time" of the heart-gastric aspecific reflex (stomach dilation: in healthy, latency time is 8 sec. See Technical Page, N° 1) and then immediately after the patient has smoked "a" cigarette. Latency time appears clearly reduced, however, varying among subjects (4, 5). From the above brief remarks, doctor can recognize easily subjects involved by CAD “real risk”, among those with ATS, DM, arterial hypertension, a.s.o., biophysical-semeiotic constitutions. As a matter of fact, it is clearly a non-sense to assess passive smoking as risk of CAD or strioke…in individuals without congenital “real risk”, according to my theory of Single Patient Based Medicine, now-a-days recognized also by EU Competent Authorities for European Health Planning, for Cancer Primary Prevention, http://europa.eu.int/comm/health/ph_info rmation/documents/ev_20030710_co01_en.pdf , wherein they quote a Rapid Response of mine from BMJ. 1) Whincup P.H., Gilg J.A., Emberson J.R., et al. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement BMJ 2004;329:200-205 (24 July), doi:10.1136/bmj.38146.427188.55 (published 30 June 2004) 2) Stagnaro-Neri M., Stagnaro S. Indagine clinica percusso- ascoltatoria delle unità microvascolotessutali della plica ungueale. Acta Med. Medit. 4, 91 1988. 3) Stagnaro S., Stagnaro-Neri M., Una patologia mitocondriale ignorata: la Istangiopatia Congenita Acidosica Enzimo-Metabolica. Gazz. Med. It. – Arch. Sci. Med. 149, 67 1990. 4)Stagnaro-Neri M., Stagnaro S., Deterministic Chaos, Preconditioning and Myocardial Oxygenation evaluated clinically with the aid of Biophysical Semeiotics in the Diagnosis of ischaemic Heart Disease even silent. Acta Med. Medit. 13, 109 1997 5) Stagnaro Sergio. A clinical efficacious maneouvre, reliable in bed-side diagnosing coronary artery disease, even initial or silent, as well as "heart coronary risk". 3rd Virtual International Congress of Cardiology, FAC, http://www.fac.org.ar/tcvc/marcoesp/marcos.htm Competing interests: None declared |
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yehani wedatilake, Senior House Officer medicine kettering general hospital Kettering, NN16 8UZ
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I think it is quite interesting to note that this study concluded that high overall exposure to passive smoking seems to be associated with a greater excess risk of coronary heart disease than partner smoking. The study highlights the role of passive smoking that many non smokers encounter while outside their homes, be it at work or at the pub. More than 1.4 million of the UK population suffer from Coronary heart Disease in some form and smoking is a well known and preventable or avoidable risk factor. It is evident that more research needs to be done in the area of PASSIVE smoking and its effect not just on the heart but in the aetiology of lung carcinoma etc. However in the meantime it is not fair to expose non smokers to the effects of passive smoking in public places including bars, restaurants, pubs and clubs with the potential risks involved. At a time where we are encouraging people to actively change their lifestyle through exercise and diet in combatting ischaemic heart disease, it is also timely that there are clear cut rules laid down to protect non smokers from the effects of passive smoking in public areas. Competing interests: None declared |
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John E Burgess, Consultant Occupational Physician Hunstanton PE36 6DQ
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23 July 2004 The Editor British Medical Journal BMA House Tavistock Square London WC1H 9JR Sir I was interested to read the paper by Whincup et al in the BMJ dated 24 July 2004, concerning passive smoking and risk of coronary heart disease. I realise the great efforts which the profession has properly made to identify the hazards of smoking since the original work of Sir Richard Doll. The current vogue appears to be devoted mainly to “passive smoking” hazards and this paper attempts to address these. Unfortunately, the paper is full of comments such as “suggests”, “study modest in size”, “limited precision”, “weak measure”, “seems to be”. These terms are almost certainly used because of the lack of real statistical evidence in the report. Indeed the Hazard ratios after Adjustments 2 and 3 indicate a reduced hazard in those with Cotenin concentrations of 2.8-14.0 ng/ml compared with those with Cotenin concentrations between 1.5 and 2.7 ng/ml. Why were the ranges of Cotenin concentrations chosen ? The level 2.8-14.0 ng/ml appeared to be an enormous range compared to the other three groups. Perhaps I am missing some subtle statistical methodology but my original training in statistics at the London School of Hygiene always emphasised the importance of statistical significance and the tests used to measure it. As a profession, we should be offering real and accurate guides to the general public. It is clear that many in the population do not actually “believe” what we say or write. Much of this could be the result of poorly designed and biased studies and the reporting of these by the popular press as “proof” when the conclusions are not that significant. The lobby for eliminating smoking is a powerful one and is vitally important, but we would have much more credence and plausibility if the information which we present is more convincing. Sincerely Competing interests: None declared |
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Sue Jeffers, self employeed 55414
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I have to question your study. To measure cotinine, which can be obtained in many ways besides second hand smoke, and use those levels to find a correlation between passive exposure to tobacco smoke and the risk of coronary heart disease and stroke is interesting. To determine there is no consistant association between cotinine concenetration and the risk of stroke should be highly publicized. Where are the press releases, where is the publicity and just why do we need to keep repeating studies that you already already know the answers to it. Sue Jeffers 227 S.E. Oak Street Minneapolis, Mn 55414 612-384-4374 Competing interests: None declared |
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Walt Cody, writer New York City 10021
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Ms Duffy seems to confound two totally different issues. That removing the source of cotinine resulted in a "dramatic" decline in cotinine (duh) has nothing at all to do with whether cotinine (at all--let alone in minute amounts) is in any way harmful, or with whether its removal is in any way "helpful" in terms of public health. (It isn't, and It isn't.) As for the assertions in her opening paragraph, if Ms Duffy is really buying the DOH's propaganda, they can probably also give her a good price on the Brooklyn Bridge. Competing interests: New Yorker |
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Anthony S. Ward, Retired n/a
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The most intriguing aspect of the Whincup et al report is the data in table 3 and the authors' conclusions. Table 3 shows a RR of 3.73 amongst the higher cotinine groups for the first five years, which declines to 1.04 in the final five. Their report is based on the assumption that a single measurement of cotinine concentration (at ages 40-59) provides clear information about exposure to tobacco smoke over the following twenty years. If so then it must also provide the same for the preceding forty years or more. So the RR must have been around 3.73 for many years prior to measurement. It is absurd to suggest that passive smoking is more than twice as risky as active smoking (RR about 1.7). It is also wildly out of line with other passive smoking studies. Further, table 3 shows a RR of 3.32 for light active smokers in the first five years (and so for many years previously). The study of active smoking risks is much less controversial and the CHD risk is generally considered to be no more than 1.5 for light smokers. Therefore the figures for the early years must be regarded as unreliable. The final period figure for light active smoking (1.34) is in line with expectation, so maybe the final period is reliable in which case the passive RR is 1.04 ( i.e. no risk). The figures for the early years are probably the result of fluke, design or process problems. However, given the small numbers of actual events I suggest the following conjecture: A slightly elevated cotinine level may be symptomatic of some serious CHD related 'illness' that also affects normal elimination of cotinine. Such 'illness' would be evenly spread amongst all cotinine groups (including active smokers) except the lowest. As sufferers died out (or recovered) the initial high mortality would subside. If around 5% of the initial study population were sufferers then the anomalies of table 3 would be accounted for. Competing interests: Smoker, but no affiliation to interest groups |
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Hugh Tunstall-Pedoe, Cardiovascular epidemiologist Dundee DD1 9SY, Ruoling Chen (first author), Roger Tavendale
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EDITOR—Whincup et al show passive inhalation of environmental tobacco smoke to be an unexpectedly strong risk factor for coronary heart disease, when assessed using serum cotinine,(1) in contrast with a recent negative paper in the BMJ, which did not.(2) They stress the need for further prospective studies using biomarkers. We measured serum cotinine and other biomarkers of smoking at baseline in our Scottish Heart Health Study and Scottish MONICA surveys,(3) and recently reported on cardiovascular mortality in never smokers, finding excess risk with passive smoking,(4) preliminary work now being extended to include 16-year morbidity and mortality. Using biomarkers and questionnaire results we found discrepancies between self-reported exposure and serum cotinine in passive smoking.(3) Cotinine results are affected by individual differences in nicotine metabolism and by time delays from exposure. Because of this we have found a combination score of grades of self-reported exposure and of cotinine valuable. (4,5) Campaigners against tobacco tend to talk-up positive results on passive smoking and to discount weak or negative ones as “flawed” for non- scientific reasons. It is important for the future to obtain the best overall estimates of risks of exposure to smoke without bias. It seems implausible that nicotine itself is responsible for the risk of passive smoking, but cotinine is a useful biomarker of a recently common, now disappearing, form of smoke exposure. Banishing the traditional clouds of tobacco smoke forever may be dear to the hearts of many of us for social as well as medical reasons (they stink), but were any exposure to smoke from combustion of vegetable matter, however caused, be labelled ‘very dangerous’ this might have severe long-term occupational and economic consequences. It is important for that reason to get the best estimates of risk that we can. Ruoling Chen, honorary senior lecturer
Hugh Tunstall-Pedoe, professor of cardiovascular epidemiology Roger Tavendale, biochemist Cardiovascular Epidemiology Unit, Institute of Cardiovascular Research, University of Dundee, Ninewells Hospital, Dundee, Scotland, DD1 9SY Competing interests: None declared. References 1. Whincup PH, Gilg JA, Emberson JR, Jarvis MJ, Feyerabend C, Bryant A, et al. Passive smoking and risk of coronary heart disease and stroke: prospective study with cotinine measurement. BMJ 2004;329:200-205 2. Enstrom JE, Kabat GC. Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98. BMJ 2003; 326:1057-67. 3. Tunstall-Pedoe H, Brown CA, Woodward M, Tavendale R. Passive smoking by self-report and serum cotinine and the prevalence of respiratory and coronary heart disease in the Scottish heart health study. J Epidemiol Community Health 1995; 49:139-43. 4. Chen R, Tavendale R, Tunstall-Pedoe H. Passive smoking measured by self report, serum cotinine and their combination and 14-year cardiovascular mortality among never smokers in the Scottish Heart Health Study. Circulation 2003;108: IV 751 (abstract) 5. Chen R, Tavendale R, Tunstall-Pedoe H. Measurement of passive smoking in adults: self-reported questionnaire or serum cotinine? J Cancer Epidemiol & Prev 2002; 7:85-95. Competing interests: None declared |
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