Professor Konrad Jamrozik and his BMJ paper on his estimate of deaths in the UK from passive smoking.

Editor-in-Chief of Lifestyle Reviews Rollo Tomassi has been mentioning the late Konrad Jamrozik’s paper on “Estimate of deaths attributable to passive smoking among UK adults: database analysis.” Here is the abstract:

Objective To estimate deaths from passive smoking in employees of the hospitality industry as well as in the general workforce and general population of the United Kingdom.

Design Calculation, using the formula for population attributable proportion, of deaths likely to have been caused by passive smoking at home and at work in the UK according to occupation. Sensitivity analyses to examine impact of varying assumptions regarding prevalence and risks of exposure.

Setting National UK databases of causes of death, employment, structure of households, and prevalences of active and passive smoking.

Main outcome measures Estimates of deaths due to passive smoking according to age group (< 65 or ≥ 65) and site of exposure (domestic or workplace).

Results Across the United Kingdom as a whole, passive smoking at work is likely to be responsible for the deaths of more than two employed people per working day (617 deaths per year), including 54 deaths in the hospitality industry each year. Each year passive smoking at home might account for another 2700 deaths in persons aged 20-64 years and 8000 deaths among people aged ≥ 65.

Conclusion Exposure at work might contribute up to one fifth of all deaths from passive smoking in the general population aged 20-64 years, and up to half of such deaths among employees of the hospitality industry. Adoption of smoke free policies in all workplaces and reductions in the general prevalence of active smoking would lead to substantial reductions in these avoidable deaths.”

http://www.bmj.com/content/330/7495/812.abstract

Alas some of the comments in the Rapid Responses do not seem to singing from the same hymn sheet. Best comment is “Overall, the paper must be regarded as speculative and unscientific, adding nothing to the debate on passive smoking.”

“Alastair G Browne, Civil Servant

EH11 3XD

Response to BMJ, doi:10.1136/bmj.38370.496632.8F (published 2 March 2005)

There are several issues with the above report which make it’s results and conclusion meaningless.

To start off with, the report does not examine the null hypothesis. To quote from the abstract of the report:-

“Objective: To estimate deaths from passive smoking in employees of the hospitality industry as well as in the general workforce and general population of the United Kingdom.”

Here, the assumption is being made that deaths are indeed caused by so-called “passive smoking”. By approaching the subject in this manner, it is not possible to conduct an un-biased study.

The whole paper itself seems to be based upon calculations and estimates, not hard facts. Despite this, this paper is supposedly intended to be taken as fact itself. Would the author care to explain how he has managed to turn assumption into so-called fact without having done any scientific tests himself?

During the introduction, the author suggests that with regard to pubs, bars, nightclubs etc. “…the generation of tobacco smoke is not intrinsic to the process of selling food and drink…” There are plenty who will argue against this. For some people, smoking tobacco goes hand in hand with enjoying alcohol in its various forms. Additionally, on completion of a good meal, there are many who may enjoy rounding it off with a good cigar. Therefore, the smoking of tobacco is far from being “not intrinsic” to these kind of establishments. To view things in any other way is biased.

The author then goes on to state that making these kind of establishments smoke-free would protect staff who work there. Is this not a bit premature to suggest this kind of thing in the introduction? Before any research has been carried out? The assumption has been made here that environmental tobacco smoke (ETS) is harmful to non-smokers. This has been made a-priori and is therefore questionable.

The introduction then goes on to attempt to argue about the economics of the leasure industry vis-a-vis smoking bans. Would the author kindly explain the relevance of this argument in the context of the title of the paper? All this does is set the scene for a biased paper.

Moving on the the method of the experiment, the author talks about percentages of people exposed to ETS. This appears to be justified. However, the author then makes the broad, sweeping statement that smoke exposure in the home provides “…a relatively clear picture of the risks for lung cancer and ischaemic heart disease.” Once again, this is pure supposition. Where is the proven link between ETS and the ailments mentioned? Why is the assumption made that lung cancer and ischaemic heart disease can only be caused by tobacco smoke? What stops other factors such as motor vehicle exhausts, airborne benzine from petrol, or anything else for that matter, from causing these diseases? There is no mention of these other substances in the report. Why not?

Of course, the fabled cotinine test is cited. Bearing in mind that cotinine levels may be raised by the subject eating potatoes, what measures were taken to ensure that this was not a confounding factor?

The calculations performed by the author carry on the assumption that ETS is solely responsible for the ailments listed in the results table. To make such an assumption is completely unfounded and produces results that are invalid.

It is basic scientific procedure that to measure cause and effect, one must first establish and isolate the causes that lead to the effects in question. No attempt has been made to do this in this instance. The fact that a percentage of “smoking-related diseases” may in fact be caused by factors other than ETS has not been considered. The author cites previous work as being definitive with regard to ETS. If one reads these reports, one will find that they are far from definitive. Many of them have similar assumptions to those made in this paper. Additionally, many of these papers make suggestions or suppositions within their summaries. Once again, would the author please explain how he managed to turn these into fact without further work?

To summarise, this paper is biased and scientifically invalid. It draws upon material produced from other sources and rather than analysing them, accepts them as hard fact—even though it may not have been the case that the authors of the sources in question intended for their papers to be taken as fact. The act of taking potentially false information, then applying statistical analysis to it, results in a completely meaningless set of figures.

Alastair G Browne MSc BEng(Hons)”

“Michael J. McFadden, Writer/Researcher/Activist

Two points raised in the Rapid Responses immediately prior to this come together with a question I have written about for several years. USDHHS (U.S. Dept. of Health and Human Services) has classified Ethyl Alcohol as a carcinogen. To be true, they have only classified it as such when it is “consumed,” presumably in liquid form, but alcohol is a very volatile liquid. (1)

A cigarette emits roughly a half milligram of active Class A carcinogens with the most significant in terms of weight being benzene at 3/10ths of a milligram. A standard martini releases roughly one full gram of the Class A carcinogen ethyl alcohol into the air in the space of an hour: an amount equal to 2,000 cigarettes. You can see this for yourself most clearly if you pour a large shot (48 grams) of grain alcohol into a martini glass and set it someplace ventilated and safe for two days. When you come back it will be gone. If the cat didn’t drink it the alcohol went into the air and was breathed and ingested by any who wandered through the room during that period.

Some might claim that DHHS specified “consumption” of alcohol in order to rule out any airborne effects, but to say that mucosal cancers from liquid alcohol do not imply mucosal cancers from evaporated alcohol makes an absolute mockery of the old “tar in acetone painted on mouse skin” proofs that medical scientists were so fond of in the 1950s and 60s.

As Dr. Lee, in the Response immediately above this one, points out: “Logic dictates that if cigarette smoke is harmful when inhaled into the lungs of smokers then the same smoke when inhaled into the lungs of non- smokers will also be harmful. To argue otherwise would be foolhardy.” People like myself argue that the dilution of that smoke, particularly in modern venues with far better ventilation than generally reflected in epidemiological studies based on exposures stretching back 30 or 40 years, make a huge difference.

Nonsmokers in well designed and ventilated bars and restaurants would normally inhale no more than a few micrograms of active Class A carcinogenic material from cigarettes. In exceptionally well designed and ventilated venues the total amount would probably be measurable only in nano- and picograms. The alcohol case is clearly far stronger: nondrinkers would be likely to inhale milligrams rather than mere micrograms in drinking allowed venues… particularly if smoking is banned and ventilation levels reduced.

Of course there’s no massively funded Antialcohol lobby to run huge epidemiological studies on passive drinking and such studies would be very difficult to design. Non-drinking bar workers could be compared to non- drinking pool-hall workers (both groups would be exposed to similar amounts of smoke thereby removing that as a variable) but such population pools aren’t very large. However, as Luc Bonneux pointed out above, risk management often involves making decisions “not supported by hard epidemiologic data.”

He also points out that risk management principles dictate that “risks are to be reduced to levels as low as possible. The lowest level possible is easy to identify: apply the law, ban smoking in all public places.” Following those principles, and following the thinking and reasoning of Dr. Lee, one would have to accept the necessity of banning alcoholic drinks in restaurants and perhaps even in bars.

Sure, it might hurt their businesses a bit. Fancy upscale restaurants would lose their profits on $100 bottles of wine and the clientele frequenting bars would probably suffer an initial dip until people got used to enjoying each others’ company over glasses of vegetable juice or soda pop. However, as has been stated consistently by smoking ban proponents, any possible risk to health is first and foremost: nonpartakers should not be forced to partake anything over a zero- tolerance exposure to any potentially harmful chemical, and the removal of drug use from the visual environment of children and teenagers will make them less likely to become addicted themselves.

We should remember that underage drinkers account for nearly 20% of alcohol consumption (2) while underage smokers account for just 3% to 5% of the cigarette market (3). Would removing alcohol from bars, restaurants, TV commercials, movies, and sports events while quintupling its taxes cut underage drinking by 400%? Antismoking advocates feel such measures are effective for tobacco so they should be similarly effective for alcohol, true?

Do I really think alcohol should be banned from bars and restaurants, from movies and TV, from sports events and wedding champagne toasts? Of course not: the risk levels of nondrinkers, if evaluated honestly in studies not funded by pressure groups would be below consideration by any rational person. And anyone who did not want to be exposed to such fantastical wisps of risk could simply avoid establishments where alcohol was allowed.

Exactly the same argument can be made about smoking and smoking bans.

Michael J. McFadden

Author of “Dissecting Antismokers’ Brains”

http://cantiloper.tripod.com

References:

(1) National Toxicology Program. DHHS. 11th Report on Carcinogens http://ntp.niehs.nih.gov/ntp/roc/eleventh/known.pdf

(2) Foster, S.E., R.D. Vaughn, W.H. Foster and J. A. Califano, Jr. 2003. Alcohol consumption and expenditures for underage drinking and adult excessive drinking. JAMA 289 (8): 989-95

(3) Viscusi, W. Kip. “Smoke and Mirrors….” The Brookings Review, Winter 1998 Vol. 16 No. 1, pp. 14-19

I am a member of several Free Choice organizations, and have absolutely no financial interests with Big Tobacco, Big Hospitality, or any other player in this arena other than as a customer and as the author of a book in the field.

Competing interests: I am a member of several Free Choice organizations, and have absolutely no financial interests with Big Tobacco, Big Hospitality, Big Pharma, or any other player in this arena other than as a customer and as the author of a book in the field.”

“Gio B. Gori, Principal Scientists, The Health Policy Center

6704 Barr Road, Bethesda, MD 20816, USA

In the enumeration of UK deaths attributable to ETS, Konrad Jamrozik – professor of evidence based healthcare – makes a number of arguable assumptions. (1) Of these, none is more consequential than stipulating that the claimed epidemiologic risks of ETS exposure are based on valid evidence.

A number of critics favorable and unfavorable to ETS risk claims have voiced concern for some 30 years about the uncertainties attending epidemiologic studies of passive smoking, with special reference to the central role of exposure recall. Likely because not much could be done about the latter, the issue remained dormant and was eclipsed by sideline interests in recall bias, smoker misclassification, matching bias, confounders, publication bias, statistical issues, and meta-analysis. Still, some notion of the potential dimensions of recall uncertainties is crucial and long overdue. Recently, I chanced to examine the questionnaire used to interview participants in the largest multi-country IARC/WHO European ETS study of 1998. (2) The editors of BMJ or anyone interested in evidence based findings ought to analyze this document critically, for it is claimed to be among the best if not the best of ETS questionnaires, and is intended to generate the essential input to risk estimates, namely an integral of ETS exposure over the lifetime of each study subject.

What and how many cigarettes, pipes, or cigarillos did mom or dad smoke daily in my presence during my childhood and youth? What about uncle Joe and granddad? What and how many cigarettes, pipes, or cigarillos did my spouse(s) smoke in my presence during a lifetime? How airtight were my homes? How smoky were different workplaces during my lifetime? Can I recall my precise diet of last week? How much better is it than throwing dice?

Even a cursory perusal of the IARC questionnaire reveals that most questions can be leading, and that answers can only be vague guesses open to multifold error. Moreover, risk calculations utilize indexes of exposure that are extruded from a combination of several answers, whereby the error of composite indexes is the amplified sum of the errors of their components, as defined by standard rules. (3)

It is a common sense notion and the fundamental principle of metrology that a measurement is not a measurement unless coupled to an estimate of its uncertainty. (3) Inexplicably however, individual recalls of exposure are written down as precise digits, and are later used in estimates of risk and statistical significance under the delusory assumption that such digits have no margin of uncertainty. In reality, and although unknown and unknowable, the uncertainties of individual ETS exposure recalls jump in the face as obviously real, and their composite weight can easily exceed the claimed 20-50% risk excesses attributed to ETS exposure.

We are facing the ugly prospect that the entire epidemiologic literature on ETS is in fact a gross delusion. Should the flagrant inconsistency of the various results surprise? As gatekeepers and purveyors of evidence based information, the editors of BMJ have an obligation to clarify this conundrum to their readers. It could not be dismissed with the unworthy retort that I might be an industry spokesman, for these are verifiable facts an not opinion. Wisely, the editors have noted that “passive smoking is accepted as a cause of fatal disorders”. Indeed it may be accepted, but is it so? Is BMJ prepared to make a similar allowance for creationism?

1.Jamrozik K. Estimate of deaths attributable to passive smoking among UK adults: database analysis. BMJ, doi:10.1136/bmj.38370.496632.8F, March 2, 2005.

2.http://www.data-yard.net/who_quest/quest_iarc_98.pdf

3.http://physics.nist.gov/Pubs/guidelines/TN1297/tn1297s.pdf

Competing interests: I have occasionally consulted with the tobacco industry. I have also been deputy director of the Division of Cancer Cause and Prevention and director of the Smoking and Health Program of the US National Cancer Institute. My interest is truth, or its closest possible approximation.”

“Peter N Lee, Consultant Statistician

Hamilton House, 17 Cedar Road, Sutton, Surrey SM2 5DA, UK

EDITOR – Whereas previous estimates of risk from passive smoking have been limited to nonsmokers, Jamrozik produces much higher estimates of deaths by including deaths in smokers. He notes that the joint effect of active and passive smoking has not been examined epidemiologically and argues, not unreasonably, that an additive model is appropriate. However his calculations, which extrapolate relative risk estimates derived from studies of nonsmokers to the whole population – smokers included – actually involve an implausible multiplicative model. The huge difference this makes can be seen by assuming that, compared to unexposed nonsmokers, passively exposed nonsmokers have a relative risk of lung cancer of 1.24 and unexposed smokers have a relative risk of 20. Under the multiplicative model that Jamrozik actually uses, the relative risk of a smoker exposed to passive smoking would be 20 x 1.24 = 24.8, with 4.8/24.8 = 19.4% of deaths in this group attributed to passive smoking. Under the additive model that he argues for, but does not actually use, the relative risk would be 20.24, the percentage of deaths attributed to passive smoking being much lower, at 0.24/20.24 = 1.2%.

There are other technical problems with Jamrozik’s analysis. He assumes that, because 85% of adults aged 20-64 work, 85% of deaths in adults of this age occur in workers, clearly incorrect in view of the well -known “healthy worker effect”. He also assumes without any support that at home and at work exposure are independent, again leading to overestimation of the risk. Failure properly to take age into account is also a potential problem. Among adults of working age, is the average age of workers in the hospitality industry really the same as that of the whole population, as implicitly assumed?

The whole calculation is only relevant if the relative risk estimates used for lung cancer, ischaemic heart disease (IHD) and stroke actually represent causal effects of passive smoke exposure. For lung cancer, my colleagues and I1 recently concluded that most, if not all, of the association is an artefact due to various sources of bias, based on a detailed analysis which recent reviews2,3 have considered, but have not refuted. For IHD, there are also problems of interpretation4, with the largest studies showing little or no association.5,6

For stroke, the relative risk estimate is based on only seven studies, and overlooks evidence from as many other studies,7-13 most of which find little or no relationship. Until a full review of the evidence taking proper account of potential sources of bias and confounding has been published, it remains unclear whether any causal effect exists.

Overall, the paper must be regarded as speculative and unscientific, adding nothing to the debate on passive smoking.

Peter Lee Independent Consultant in Epidemiology and Statistics 17 Cedar Road, Sutton, Surrey SM2 5DA PeterLee@pnlee.demon.co.uk

Competing interests : Long-term consultant to the tobacco industry”

 

 

 

 

 

 

 


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56 Responses to Professor Konrad Jamrozik and his BMJ paper on his estimate of deaths in the UK from passive smoking.

  1. Terr says:

    Professor Konrad Jamrozik

    Is this the bigoted, fascist anti smoking puritan who died aged 54 !!
    The one that died of ‘sarcoma’……..In other words cancer.,

  2. ChrisB says:

    Was any account taken of the slight possibility that employees in the hospitality industry accepted far too many drinks from the clientèle and enjoyed the ambience of their workplace?
    They could accept drinks when behind the bar but the certainly couldn’t smoke there. Was drink the real cause of these supposed deaths?
    The answer is ‘simples’ – ban the tokens of appreciation for good staff or simply ban drinking in pubs. The result would be the closure of all pubs and an end to all risk.
    Job done.

  3. Iro Cyr says:

    Has everyone read Pr. Robert Molimard’s analysis of how they came about the estimates of deaths ”caused” by SHS in the hospitality industry in the The European Report ‘‘Lifting the SmokeScreen’’?
    A must read for anyone who still hasn’t read it.
    http://cagecanada.homestead.com/AnalyseCritiqueMolimard.html

  4. Junican says:

    Where is Rollo the Terrified Master Debater?

    “”Results: Across the United Kingdom as a whole, passive smoking at work is likely to be responsible for the deaths of more than two employed people per working day (617 deaths pe year), including 54 deaths in the hospitality industry each year. Each year passive smoking at home might account for another 2700 deaths in persons aged 20-64 years and 8000 deaths among people aged ≥ 65.””

    And Elvis Presley might still be alive, and Plato might be dead. But, there again, Elvis might be dead, and Plato might be alive.

    But can I say, once again, that in all these studies there seems to be an assumption that there is such a thing as ‘A Standard Human Being’. No account ever seems to be taken of variable genetic propensities. For example, in 2009 in Eng & Wales, 730 people in the age range 35-44 died as a result of Ishcaemic heart failure and 2630 died from Ischaemic heart failure who were in the age range 45 – 54. That is almost 3400 people below the age of 55. How did it come to pass that 3400 people died from Ischaemic heart failure under the age of 55? And how was it that nearly 50,000 did not die from Ichaemic heart failure until after 75 when almost all these people would have been exposed to vast amounts of SHS?

    Thus, we can see this:

    1. The reason for the ‘ifs, buts and maybes’ in Jamrozik’s study was that his evidence was nonsensical.
    2. That he was being well paid to produce the ‘ifs, buts and maybes’.

  5. Frank J says:

    Didn’t he do this during the 4 years he was at Imperial College and not back in Oz? Wonder if this is why he came here? i.e. a nice little earner to produce this bollox! I’d heard he’d just multiplied other peoples figures to arrive at the ‘hospitality Industry’ deaths. Are these deaths even real? Did they genuinely work in the ‘hospitality Industry’? did he include people who’d worked in it, say, 30 years ago? Shot full of holes is an understatement!

    The APPG must have pulled in every favour they had to obtain a ban.

  6. Rollo Tommasi says:

    Hi Dave.

    Sorry to be blunt, but I have to say this blog proves one thing about your work. You are not interested in truth. You are simply interesting in trawling for anything, no matter how dodgy, which you can use as an argument to claim that passive smoking is not harmful.

    Why do I say that about this post? You’re trying to suggest that the Jamrozik report was fatally flawed. But what you offer is a ragbag of comments, most of which don’t even deal with how Jamrozik made his calculations! Did you even stop to think about what these comments were saying?!!

    Browne and McFadden’s comments both focus largely on the policy arguments about smoking laws. Browne also argues that Jamrozik should have considered other possible causes of lung cancer. But his claims just betray his ignorance about the purpose of the Jamrozik study. Those considerations have been undertaken as part of other studies and meta-analyses previously. Jamrozik didn’t need to cover that ground again. What he did was convert well recognised relative risks for passive smoking into actual numbers of deaths. Similarly there was no need for Jamrozik to deal with McFadden’s claims about toxicology (which, by the way, are addressed well in the 2006 US Surgeon General’s report). Crucially, neither Browne nor McFadden criticise Jamrozik’s calculations of fatalities.

    Gori doesn’t criticise Jamrozik’s calculations of fatalities either. All he does is return to his oft-repeated comments about how case control study surveys are conducted. Funnily enough, Gori only ever seems to complain about the results of these surveys when passive smoking is involved (but then he has been handsomely paid by Big Tobacco). I’ve not seen him try to deny links between radon gas or air pollution and lung cancer, even though these links are based on the same kind of epidemiological evidence. And Gori also conveniently ignores the fact that his criticisms don’t wash for cohort studies – and the results of these cohort studies show very similar levels of risk from passive smoking as case-control studies do.

    In fact, the only person to criticise Jamrozik’s actual methodology was Lee. But even if you accept the claims he makes, they only reduce Jamrozik’s calculation of fatalities (or at least the figure I quote) by a small amount. The 6,600 figure I quote only covers deaths from lung cancer and heart disease. There is good reason to believe that passive smoking contributes to strokes as well, but I’ve always excluded that anyway. And the 6,600 figure only relates to deaths from exposure in the home – deaths resulting from workplace exposure are on top of this.

    So there you have it. Four sets of quotes. Three of these don’t criticise Jamrozik’s calculations at all. The fourth, even if correct, would only make a modest reduction to Jamrozik’s totals. We’re still talking about thousands of premature deaths in the UK each year caused by passive smoking.

  7. Klaus K says:

    Mr. Tommasi: There is no reason to critizise details of Jamrozik’s calculations at all, since it is a wild speculation in itself to calculate death rates from a risk that has not been proven to exist. Even though it is true that a few (poorly structured) epi-studies have shown a weak association between a fatal disease and passive smoking you still have to consider that 85% of all studies on passive smoking did not show any significant association.

    This means that it is not possible to draw any causal conclusion regarding passive smoking and fatal diseases. In other words: Passive smoking has not been proven to be fatal. At least not yet. So how could it be possible to calculate death rates from it? It is not.

  8. Junican says:

    Nothing that Rollo says makes any sense whatsoever UNLESS he can produce at least one certain death from SHS – just one. He cannot produce just one.

    I wish to accuse Rollo Tommasi of corruptly accusing me of surepticiously killing my children by smoking in their presence. All of them are healthy, but Rollo claims that they are ill and about to die. What percentage of my children’s bodies is dying? And to which particular bit of their bodies does Rollo’s death threat apply? And I have four grandchildren. I have smoked as much as I wish in their presence. I have amused them as best I can and talked to them about the past. I have never, and never will, condemn myself for smoking in their presence. Such a thought is inhuman.

    But that inhumanity is precisely what ASH ET AL are trying to propagandise, isn’t it? They want to set grandchildren against their grandparents, don’t they? Even if that is not the actual intent, that is the what they are doing. When my 5 year old grandson said to me, “Grandad, why do you smoke when it is bad for you?” , I found it difficult to say, “Who was the unutterably stupid arsehole who told you these lies?”

    The above little sentence explains a lot. Our children’s minds are being corrupted. Where will it end?

    It comes down to what schools should be doing.. It is not the purpose of schools to spread propaganda.

    Enough for tonight.

  9. Rollo Tommasi says:

    Well well. Two responses to my comment. Needless to say, neither of them deal with either the points I made nor Jamrozik’s own calculations.

    Klaus K repeats the tired old comment that most studies “did not show any significant association” in themselves. That comment is meaningless – professional scientists do not draw conclusions from separately listing the results of individual studies. And, contrary to Klaus K’s claims, meta-analyses DO draw “causal conclusion regarding passive smoking and fatal diseases” in a reasonable and strong way. Jamrozik’s estimates of fatalities are based on the best and most justifiable calculations available about the added risk from passive smoking.

    Junican’s remarks are simply bizarre. His approach is to retreat to that old chestnut about naming a person who has died from passive smoking. Once again, that is an argument that only pro-smoking zealots use – respected scientists do not take that kind of argument seriously. And funnily enough, the few people who ask for names of people who die of lung cancer caused by passive smoking never ask for names of people whose lung cancer was caused by radon gas or vehicle pollution. They seem quite willing to accept these as hazards, even though they are based on the same epidemiological methods as for passive smoking.

    And Junican’s accusations are not worthy of reply by me. It is up to him to justify his actions in smoking in front to his children and grandchildren to them, not to me. But for Junican to dismiss the fact that smoking is bad for you as “lies” sums up his mentality perfectly.

    • Klaus K says:

      I regret that you find my comments tiring, Mr. Tomassi. You are quite right, that authorities have drawn causal conclusions regarding SHS and fatal diseases. Or else it would not have been possible to impose smoking bans all over Europe.

      This conclusion however was a mistake, since 85% of the studies carried out did not even show an association between lung cancer and SHS. Authorities have in fact drawn a causal conclusion based on only 15% of the studies that did show an association. As you can see at Peter Lee’s site these 15% were the lowest quality studies, most of then did not even adjust for age: http://www.pnlee.co.uk/documents/refs/lee2010B.pdf

      High quality studies do not show any association between SHS and lung cancer. This is also very clear in the IARC 1998 study where an (insignificant) association could only be shown in two countries with missing or imperfect data. The five countries with perfect data (GB among them) showed no association, remember?
      https://daveatherton.wordpress.com/2011/06/11/more-on-the-whoboffetta-paper-hat-tip-klaus-k/

      The truth is that in every statistical study of two populations – one exposed to SHS, the other not exposed – the crude rates will show associations with many diseases. Why? Because people exposed to SHS are different kind of people. They take more risks, they are poorer, they live in smaller & cheaper apartments in bad areas, they have more unhealthy habits – and as a result they get many diseases earlier than the unexposed group. However that does not mean that the risk factor under study is the cause of the association.

      There are 30 different risk factors for lung cancer. They must to some extent be controlled for if you want to find the real association in these studies. As you can check for yourself in another one of Lee’s papers, controlling for just a handful confounding factors will remove any association between SHS and lung cancer:
      http://www.pnlee.co.uk/documents/refs/lee2006n.pdf

      I regret to inform you I find it meaningless to conclude that SHS causes lung cancer – and since that association is by far the strongest compared with the other claimed “causes” of SHS – that SHS could be a cause of any fatal disease. Thus – it is a real stretch to calculate death rates from SHS, like Jamrozik did.

    • Rollo if the overall risk assessments are not significant and cannot be repeated over and over again then the theory fails!

      To use something thats contrived to begin with and try and build a concensus where 85% of the studies dont show the theory to be true then you have no case!

      The lowering of a causal effect is whats going on. It cant be demonstrated as harmful nor can it be shown to cause death biologically! The entire ETS myth is just that a MYTH!

      But then we all know if you can repeat a lie often enuf and to the right audience somebodys gonna believe it,until the claims keep building and building until even the most brainwashed anti-smoker wont buy it any longer.

      Thats where this SHS/ETS trash science is now! In THE TWILIGHT ZONE!

      • Rollo Tommasi says:

        Harley Rider – All you are doing is inventing your own scientific principles, so you can claim that passive smoking is a “myth”.

        Like other pro-smoking zealots, you simply conclude that a statistically insignificant finding means “no risk” when in fact that claim is wholly wrong. As Egger and Davey Smith say:

        “A single study often cannot detect or exclude with certainty a modest, albeit clinically relevant, difference in the effects of two treatments. A trial may thus show no significant treatment effect when in reality such an effect exists—that is, it may produce a false negative result.” (bmj.com/content/315/7119/1371.full)

        As the article then goes on to show, meta-analyses are valid and effective ways of testing whether there is actually an effect in these studies. Meta-analyses of passive smoking studies show there is an effect, even among the studies you dismiss as statistically insignificant.

        If you’ve got proper evidence which says I’m wrong, then I’m interested to read it. If not, don’t bother trying to invent your own nonsensical and flaky scientific principles.

      • Rollo I understand why you have to defend your REAL SCIENTISTS err cough!

        But when 85% of the studies go against your sides claims the totality is what is considered to make a conclusion.Not the 15% that support your position and thats where bias is resulting the most.

        The bar for a causal effect was lowered so low for the SG to make a claim as to make milk and tap water prohibitited too,as Dr Kabat stated!

        Even this came out from the ACS:

      • [[“We are being bombarded” with messages about the dangers posed by common things in our lives, yet most exposures “are not at a level that are going to cause cancer,” said Dr. Len Lichtenfeld, the American Cancer Society’s deputy chief medical officer.
        Linda Birnbaum agrees. She is a toxicologist who heads the government agency that just declared styrene, an ingredient in fiberglass boats and Styrofoam, a likely cancer risk.
        “Let me put your mind at ease right away about Styrofoam,” she said. Levels of styrene that leach from food containers “are hundreds if not thousands of times lower than have occurred in the occupational setting,” where the chemical in vapor form poses a possible risk to workers.
        Carcinogens are things that can cause cancer, but that label doesn’t mean that they will or that they pose a risk to anyone exposed to them in any amount at any time.]]

      • Now,Im glad to see the ACS admitting to the dose response relationship finally!

        So now we understand why the following is factual:

        [[are hundreds if not thousands of times lower than have occurred in the occupational setting,” where the chemical in vapor form poses a possible risk to workers.]]

        Regulatory Toxicology and Pharmacology, Vol. 14, No. 1. (August 1991), pp. 88-105.

      • [[ETS between 10,000- and 100,000-fold less than estimated average MSS-RSP doses for active smokers]]

    • Klaus K says:

      I regret that you find my comments tiring, Mr. Tomassi. You are quite right though, authorities have drawn causal conclusions regarding SHS and fatal diseases. Without these it would not have been possible to impose smoking bans all over Europe.

      This conclusion however was a mistake, since 85% of the studies carried out did not even show an association between lung cancer and SHS. Authorities have in fact drawn a causal conclusion based on only 15% of the studies that did show an association. As you can see at Peter Lee’s site these 15% were the lowest quality studies, most of then didn’t even adjust for age: http://www.pnlee.co.uk/documents/refs/lee2010B.pdf

      High quality studies do not show any association between SHS and lung cancer. This is also very clear in the IARC 1998 study where an (insignificant) association could only be shown in two countries with missing or imperfect data. The five countries with perfect data (GB among them) showed no association, as I’m sure you remember.

      The truth is that in every statistical study of two populations – one exposed to SHS, the other unexposed – the crude rates will show associations with many diseases. Why? Because people exposed to SHS are different kind of people. They take more risks, they are poorer, less educated, they live in smaller & cheaper apartments in bad areas, they have more unhealthy habits – and as a result they get many diseases earlier than the unexposed group. However that does not mean that the risk factor under study is the cause of the association.

      There are 30 different risk factors for lung cancer. They must to some extent be controlled for if one wants to find a real association in these studies. As you can check for yourself in another one of Lee’s papers, controlling for just a handful confounding factors will remove any association between SHS and lung cancer:
      http://www.pnlee.co.uk/documents/refs/lee2006n.pdf

      I regret to inform you I find it meaningless to conclude that SHS causes lung cancer, and – since that association is by far the strongest compared with the other claimed “causes” of SHS – that SHS could be a cause of any fatal disease. Thus – it is a real stretch to calculate death rates from SHS, like Jamrozik did.

  10. Fredrik Eich says:

    “Once again, that [name one peron killed by passive smoking] is an argument that only pro-smoking zealots use – respected scientists do not take that kind of argument seriously.” – Rollo.
    Rollo, I don’t see why an anti-smoking zealot would use that argument unless the anti-smoking zealot was unbeliveably stupid in addition to being zealous. Anyway, Rollo, I have a question for you, I have developed a drug that I believe will cut risk of a bunch of largley cryptogenic diseases . Don’t ask me how this drug works but it just does.
    I am 95% sure it will save up to 3,000,000 lives over 40 years or it will kill up to 1,000,000 people over 40 years. I am 5% sure it will have an effect outside of that range. How many lives should I say my drug will save as a resonable estimate?

    • Rollo Tommasi says:

      “Rollo, I don’t see why an anti-smoking zealot would use that argument unless the anti-smoking zealot was unbeliveably stupid in addition to being zealous”.
      Fredrik – I don’t understand what point you are trying to make.

      As for your question, my reply is that you need to set proper and sufficient scientific testing to assess how beneficial or harmful this new Eich Industries product is.

      • Fredrik Eich says:

        Eich Industries has spent ~30 years asking millions of people about their exposure to our product. Eich Industries is 95% sure that our product will save up to 3,000,000 lives over 40 years or it will kill up to 1,000,000 over 40 years. Eich Industries is 5% sure our new miracle drug will have an effect outside of that range. Eich Industries is unsure as to how many live we should claim our drug will save.

  11. Rollo Tommasi says:

    Good morning Mr Atherton, our happy host!

    I see you’ve moved onto a new subject. You’ve had plenty of opportunity to defend your claims in this thread and the preceding ones. So why haven’t you?

    Is it safe to assume that, having failed to defend these claims here, you’re not going to try to reinvent them somewhere else as Zombie Arguments????

  12. Frank J says:

    I don’t know why you bother. Rollo’s case is quite simple, His 15% are better, more reliable than the other 85% and he keeps repeating it. There’s no debate to be had.

    • Rollo Tommasi says:

      No. If you bother to read what I say (as well as proper science, instead of the pro-smokers’ lies), you will find that even the “85%” (or whatever the figure is) do NOT conclude that passive smoking is harmless.

      If you could find justifications for your claims from proper scientific principles, then there would be plenty of debate to be had.

      The question is, can you?

      • Frank J says:

        Statistically insignificant and for very good reasons. No statistical survey can EVER rule out a small effect for reasons of error, misclassification, etc. Standard practice and procedure, particularly in statistics wholly reliant on memory recall. In Jamrozik’s case he even used the memory recall of other people’s studies, taking them as read. An Oxford statistician recently stated that it was 13% of 80 studies. The RR of this 13% was quoted as 1.13. In either case, hypochondria springs to mind. To be fair, probably more to do with fear of litigation.

        It may come as a surprise to you but you don’t actually have to be a scientist to see if a conclusion is logically based on the facts. Your repetition is tedious.

  13. Since 1981 there have been 148 reported studies on ETS, involving spouses, children and workplace exposure. 124 of these studies showed no significant causal relationship between second hand smoke and lung cancer. Of the 24 which showed some risk, only two had a Relative Risk Factor over 3.0 and none higher. What does this mean. To put it in perspective, Robert Temple, director of drug evaluation at the Food and Drug Administration said “My basic rule is if the relative risk isn’t at least 3 or 4, forget it.” The National Cancer Institute states “Relative risks of less than 2 are considered small and are usually difficult to interpret. Such increases may be due to mere chance, statistical bias, or the effect of confounding factors that are sometimes not evident.” Dr. Kabat, IAQC epidemiologist states “An association is generally considered weak if the relative risk is under 3.0 and particularly when it is under 2.0, as is the case in the relationship of ETS and lung cancer. Therefore, you can see any concern of second hand smoke causing lung cancer is highly questionable.” Note that the Relative Risk (RR) of lung cancer for persons drinking whole milk is 2.14 and all cancers from chlorinated water ranked at 1.25. These are higher risks than the average ETS risk. If we believe second hand smoke to be a danger for lung cancer then we should also never drink milk or chlorinated water.

  14. So rollo,if we take TAP WATER and apply the same death rate statistics as your folks use for shs/ets then we find the same numbers and roughly more die of water induced cancer a year!

    What about that milk RR of 2.14 care to do the numbers there…….

    What other irrational subjects can we think of to use to create fake death rates from!

    Oh the cell phone study……..err how about coffee,oh ya they keep bouncing back and forth on that one…….UH,how about tanning beds……ya thats another HYPED up risk factor too!

  15. Rollo Tommasi says:

    Fredrik – Then Eich Industries had better improve the research conducted on its product. If its purpose is to save lives yet in practice it possibly may harm lives, then that’s potentially undermining its purpose. I suggest Eich Industries invest in some major independently conducted research studies to find out more. If the results of these further studies remain inconclusive, then a properly conducted meta-analysis may provide clarity. Results should also be checked against Bradford Hill’s other criteria.

    Hope my free consultancy is helpful.

  16. Rollo Tommasi says:

    FrankB’s comments raise the generic possibility of error, misclassification, etc. Yet he cannot show how studies into passive smoking have supposedly been affected by these to the extent that there is actually no added risk. It is argument by innuendo and smearing.

    If you want to claim that the added risk of studies into passive smoking is the result of these other factors, then you need to show evidence of how they have actually done so.

    • Frank J says:

      Dear me! How desperate.

      No more, there’s no point.

      • Rollo Tommasi says:

        So in other words Frank, you can’t show evidence about how passive smoking studies have supposedly been completely blighted by these other factors.

        Why am I not surprised?

      • Frank J says:

        I said no more, there’s no point, you go round in circles. You’re like a stuck record.

  17. Rollo Tommasi says:

    HarleyRider’s comments are his usual combination of copy-and-pasted nonsense and outright lies.

    Let’s look at your chlorine example.

    It’s based on ONE study. Compare that with our understanding about harm from passive smoking, which is based on dozens of studies.

    The study took place in Iowa. There is nothing to suggest the water chlorination levels in the UK are as they are there. Indeed, the Drinking Water Inspectorate says “The level of chlorine in tap water is very low in England and Wales which contrasts very favourably with practices in other countries where much higher levels are common” (dwi.defra.gov.uk/consumers/advice-leaflets/chlorine.pdf).

    The 1.25 figure relates to highest levels of exposure only, not typical levels.

    There is a purpose to having chlorine in water – to reduce risks of other infections. Whereas there is absolutely no purpose to having to inhale other people’s tobacco smoke.

    Oh, and there is no suggestion of secondhand harm to other people from drinking chlorinated water.

    No let’s look at your whole milk example.

    Again, it is based on ONE study (unlike the dozens of studies on which our knowledge that passive smoking is harmful is based).

    The 2.14 figure relates to drinking large amounts of whole milk – at least 3 glasses per day.

    There is plenty of information and advice to people about taking care not to consume too much animal fat, for instance from whole milk.

    And, once again, if you drink whole milk you are not harming the health of anyone else.

    And the outright lies are HarleyRider’s insistence of misquoting people about relative risk. These quotes relate to conclusions drawn from the results of SINGLE studies, not large bodies of evidence. This is a point I often have to repeat. Nobody has justified their use of these quotes. They just run away and then quote the same lies again on another occasion.

    • The point was the relative risk factors rollo a point you completely miss and on purpose no doubt…..Your junk studies on shs/ets are based upon questionaires not actual measured risk……The point still remains insignificant is INSIGNIFICANT and does not justify criminal laws being enacted…..sooner or later the bans will be repealed. Its only a matter of time!

      Where did I misquote anything rollo care to point that out! The RR’s show the rediculousness of shs risk factors based upon lifetime questionaires its absolutley absurd to even consider such trash as science!

      • Rollo Tommasi says:

        No HR. The point is that you should not just rely on RRs. You’ve got to take account of other factors as well, including how potential risks play against all of Bradford Hill’s criteria. The risks about passive smoking are built on the collective findings of scores of studies, whereas you’re trying to compare them with whole milk and chlorinated water, which were based on the results of a SINGLE study. Plus neither whole milk or chlorinated water studies suggest harm to anyone other than the person actually consuming these – there is no secondhand harm argument for these.

        I don’t know how often I’ve had to repeat this point about the misquotes you use. Here we go again….

        The Robert Temple quote relates to a discussion about the relative risk required before a “single epidemiologic study is persuasive by itself” (http://www.nasw.org/awards/1996/96Taubesarticle.htm ). So he’s not suggesting that studies reporting smaller relative risks aren’t relevant – he’s simply stating that a SINGLE study needs to show a large relative risk to be conclusive on its own, without the need for further supporting evidence.

        The National Cancer Institute quote comes from a press release about a study into the links between abortion and breast cancer. The release does say “relative risks of less than 2 are considered small and are usually difficult to interpret.” But the quote is made in the context of a single study which lacked supporting evidence. Far from stating the results of the study were irrelevant, the National Cancer Institute states “…the findings are not conclusive. Further research is needed to interpret the results”. In other words, the research was valid, but not conclusive in itself without further evidence. Here’s the release: tobaccodocuments.org/pm/2072055014-5016.html.

        I don’t know where the Kabat quote came from. But if Kabat had really thought that such a high RR was required in all cases, the Enstrom and Kabat would have said that upfront – and it absolutely did not do that.

      • But the quote is made in the context of a single study which lacked supporting evidence.

        Rollo 148 studies plus a few others over 30 years, when you scream the need for more study is just a cop out that you need more time to create junk studies to build a perception of causal effect!

        Everywhere we go,we see the mountain of evidence claims……mountains of junk science do not make a case,its more akin to shouting down in an argument than a sane discussion! I will tell you this,Im the type unless you can prove it from the end points your just blowing smoke. I was a jurist once and the prosecution was trying to convict on circumstantial evidence alone,with no eye witnesses and no video or pictures not even a finger print,no DNA no nothing! Just the fact the crime fit the mans MO and he happened to live in the local area where the crimes, occurred a rash of car break-ins. Burglary tools were found in a garage along with stolen itmes from those cars near his residence.

        I refused to convict along with one other jurist, The man was released and within 2 months 3 kids were arrested for the break-ins. The garage where the items were found was an unlived in home. However, it belonged to the grandfather of one of the 3 kids who were arrested. Shoddy police work but the public was yelling for it to be stopped so this man was arrested for the crime and he was on probation at the time.

        ASH and tobacco control are like these prosecuters trying to convict on trumped up created evidence with the money and power of the state to back them. Yet NO PROOF!

        To me epidemiology is mere heresay evidence and even that evidence is of such low value as in RR’S its not worthy of making a conviction/criminal laws!

        Its a sad state of affairs when 10s of billions of dollars has been wasted creating junk science against tobacco when the money should have been used discovering cures!

        Instead ot increased the profits of big pharma and financed a prohibition movement!

        of which you support!

    • And the outright lies are HarleyRider’s insistence of misquoting people about relative risk. These quotes relate to conclusions drawn from the results of SINGLE studies, not large bodies of evidence. This is a point I often have to repeat. Nobody has justified their use of these quotes. They just run away and then quote the same lies again on another occasion.

      I believe they say exactly what the body of evidence is Rollo:

      Since 1981 there have been 148 reported studies on ETS, involving spouses, children and workplace exposure. 124 of these studies showed no significant causal relationship between second hand smoke and lung cancer. Of the 24 which showed some risk, only two had a Relative Risk Factor over 3.0 and none higher.

      Now rollo how does small insignificant RR’S equate to death…..show me the biological pathway that shs/ets causes death from the first breath…..make the end points meet Rollo…..They cant even do that for direct smoking now can they……there is no proof except junk science by questionaire surveys…….Rollo if shs ever caused death or disease it would have been seen centuries ago! The only thing that we know for sure thru the centuries is that there have always been tobacco haters like yourself!

      • Rollo Tommasi says:

        Wrong HR – 124 of these studies DID NOT SHOW “no significant causal relationship between second hand smoke and lung cancer”.

        Like most pro-smokers, you confuse statistical significance with clinical significance. The two are not the same. Statistical significance is not proof of clinical significance. But factors can be clinically significant even though results from epidemiological studies are non statistically significant. That is why statisticians refer to Type II errors – false negative results. And meta-analyses are respected means of overcoming these potential errors. In the cases of heart disease and lung cancer from passive smoking, meta-analyses show that, where individual studies show statistically insignificant results, these are the result of Type II errors.

      • false negative results…..SO you are insinuating that 124 studies were false negative results…….LMAO! Rollo when were you born……..

        Meta-analysis is just another way to corrupt the outcomes rollo! The EPA study did this lowering CI to get a higher RR! It was tossed as junk science,we all know this.

    • Klaus K says:

      Mr. Tomassi – I think you made a little mistake when citing Egger & Davey Smith for endorsing meta-analysis of SHS studies in your earlier post to Harley Rider. You wrote:

      Quote: — “Like other pro-smoking zealots, you simply conclude that a statistically insignificant finding means “no risk” when in fact that claim is wholly wrong. As Egger and Davey Smith say:

      “A single study often cannot detect or exclude with certainty a modest, albeit clinically relevant, difference in the effects of two treatments. A trial may thus show no significant treatment effect when in reality such an effect exists—that is, it may produce a false negative result.” (bmj.com/content/315/7119/1371.full).”

      “As the article then goes on to show, meta-analyses are valid and effective ways of testing whether there is actually an effect in these studies. Meta-analyses of passive smoking studies show there is an effect, even among the studies you dismiss as statistically insignificant. If you’ve got proper evidence which says I’m wrong, then I’m interested to read it. If not, don’t bother trying to invent your own nonsensical and flaky scientific principles.” — unquote.

      ————————————————-

      However the Egger-Smith quote – and the linked article – deals with the use of meta-analysis in random controlled trials – which, as you may know, among scientists are regarded as the gold standard of epi-studies. These trials are done with random selection and double blinding of participant groups with placebo control in order to avoid bias. Because of their controlled structure results from random trials are considered much more reliable than results from observational studies. FYI: All SHS studies are observational studies.

      So what does Egger and Davey Smith have to say about the use of meta-analysis of observational studies? In another article in the same series: “Spurious precision? Meta-analysis of observational studies”, where the SHS-studies are mentioned – http://www.bmj.com/content/316/7125/140.long – the authors sum up their conclusions in the article’s “summary points”:

      * Meta-analysis of observational studies is as common as meta-analysis of controlled trials

      * Confounding and selection bias often distort the findings from observational studies

      * There is a danger that meta-analyses of observational data produce very precise but equally spurious results

      * The statistical combination of data should therefore not be a prominent component of reviews of observational studies

      * More is gained by carefully examining possible sources of heterogeneity between the results from observational studies

      Mr. Tomassi, this is not compatible with your claim: “meta-analyses are valid and effective ways of testing whether there is actually an effect in these studies”.

      In fact Egger & Davey Smith are warning against meta-analysis of SHS-studies.

      This is a very understandable warning, since anti-smoking authorites have used meta-analysis to lump together 85% negative observational studies of SHS & lung cancer and ended up with a positive overall result.

      • Rollo Tommasi says:

        KlausK: Thanks for coming back, but I don’t accept your critique.

        In particular, nowhere “In fact Egger & Davey Smith are warning against meta-analysis of SHS-studies”.

        Your argument seems to be that Egger and Davey Smith prefer randomised controlled trials to observation studies; therefore Egger and Davey Smith reject all observation studies; therefore Egger and Davey Smith argue that SHS studies should not be subject to meta-analysis.

        Actually I agree with the first part of that argument. They quite clearly state that randomised controlled trials are preferable, where they can be undertaken.

        BUT the rest of your logic chain is nonsense. They do NOT reject the use of observational trials. In fact – COMPLETELY CONTRARY TO YOUR CLAIM – they explicitly REJECT any suggestion that meta-analysis of observational studies should be abandoned altogether. They simply state they have to be undertaken with care.

        And – surprise surprise – there is absolutely nothing in the articles to support pro-tobacco’s bogus claim that the risk of passive smoking should be calculated by adding up how many individual studies are statistically significant.

      • Klaus K says:

        Mr. Tommasi – I don’t think you should change the subject of the discussion, which is the use of meta-analysis. The subject is not the use of observational studies ctr. random controlled trials.

        You quoted Egger & Davey Smith for saying that meta-analysis was a useful tool when dealing with observational studies like the SHS-studies. Well, that was not true. They were talking about the use of meta-analysis of random controlled trials in the article cited by you.

        In their following article – about meta-analysis of observational studies, like the SHS-studies ( http://www.bmj.com/content/316/7125/140.long ) Egger & Davey Smith are quite clear in their warning against the use of meta-analysis. They state that:

        “There is a danger that meta-analyses of observational data produce very precise but equally spurious results” – and:

        “The statistical combination of data (i.e. meta-analysis) should therefore not be a prominent component of reviews of observational studies”

        I call that a warning. And what they warned against is exactly what happened: The meta-analysis of the SHS studies have produced “very precise but equally spurious results”.

        Think about it: You have 85% negative results and just 15% positive results. You pool them together and end up with a positive result.

        That makes the meta-analysis of the SHS-studies an analogy of the old saying that if you repeat a lie often enough, it will in the end become the truth.

  18. Junican says:

    RT’s comments make no sense. They sound like a commentator on the a tennis match at Wimbledon – “I say! What a wonderful smash! Golly!” “Oh! And look! There is a lesser spotted smoker, walking across the court! Ho! Ho! Ho!” “Oh! It has flown away! Ha! Ha!Ha!”

    The reality is that there is no REAL, ACTUAL evidence whatsoever that anyone, of any age, at any time and in any circumstances has ever suffered in any way from SHS. That is FACT.

    • Rollo Tommasi says:

      No Junican. That is RUBBISH.

      Only in the deluded world of pro-smoking zealots, who convince each other that their home-spun inventions somehow are more truthful than rigorous application by professional scientists, is passive smoking harmless.

  19. What really blows my mind is we find for direct smoking and lung cancer we get rr’s of 2000 and 4000% yet tobacco control claims an rr of 20-30% is proof positive of LC and heart disease in non-smokers…….its rediculous,total insanity! To this day with smoking they still cant prove it biologically causes any of the claimed diseases! Heres another fact Rollo no disease aetiology has yet to be assigned to tobacco alone,none nada!

    The fact remains non-smokers die of the same things smokers die of and suffer the exact same things while alive. Your groups spin its just tobacco while refusing to identify all other potential causes!

    With cigarette smoking Benzene is probably the biggest factor for lung cancer,but then we see what 92% of smokers never ever developing any cancers in their lifetime. The Insanity of TC is beyond belief……

    If SHS/ETS caused disease we would have seen all the studies showing RR’s way up there but thats not what happened! You guys use meta studies to try and spin a new life into studies that find no risk or insignificant risk levels…..Tobacco control is guilty of flagrant scientific lies,spin and propaganda by the scientific method!

    The government should put these spin meisters in jail and make them financially responsible for financial losses and social lives destroyed because of the bans…….

    Freedom shall be returned to the people!

  20. Rollo Tommasi says:

    Really HR? Let’s see id SHS is treated any differently from other possibe risk factors…..

    Radon gas and diesel emissions are also regarded as recognised causes of lung cancer. Yet their relative risk is pretty much identical to the RR of passive smoking.

    Kind of blows your argument away, doesn’t it?

    Unless, that is, you want to argue that radon and diesel emissions are also harmless.

    • Frank J says:

      If radon gas and diesel emissions are the same level of RR as so called SHS, I, for one, would have few problems with either!

    • Rollo radon and diesel emissions are a non-entity for risk!

      In the 1980s the radon scare began and ended only being brought back by the Obama administration.Nobody had bothered to do any testing in 25 years even though it was on the books to be done.The reason nobody bothered was because its risk factor was NEIL!

      Thanks for comparing those to shs/ets as its no risk to people either,we are biologically stronger than that or we would have never evolved from being around campfires in the stoneage!

  21. Rollo Tommasi says:

    I see you’ve also given up on your arguments about the Temple and Kabat quotes which supposedly prove your case……

    • Klaus K says:

      Tha Kabat quote is from his book, Hying Health Risks, from 2008. Here Kabat also writes about the SHS-reports of The Surgeon General and other government reports – page 175:

      “What is objectionable is that these voluminous and authoritative-appearing documents convey the message that passive smoking is a major cause of fatal disease, which few scientists believe to be the case.”

    • Rollo your arguments are moot when looking at the overall studies and thats what everyone is stating. How you can defend insignificant risk as deadly dangerous is beyond belief! As I said the bar for whats causal has been lowered so much to claim shs a danger boggles the mind….The cancer society has warned about such daily bombardments of such claims…..Let me ask you why is it tobacco smoke has billions spent trying to prove shs a risk when TAP water and the milk risk are as high and higher,yet no worldwide group spends billions to go after those 2 things and theres others too, as in tanning beds and emissions……Rollo what I am pointing at is their is a worldwide agenda against tobacco and its users and that is the most MAJOR BIAS FACTOR of proof their is! And it is apparent in the studies of that carry over……You take that type of major bias and apply it to findings of low RR’s and the neil result kicks in!

      The best example of BIAS is the EPA junk study!

  22. Rollo Tommasi says:

    KlausK: Creative use of selecting (mis-)quoting, but not an accurate reflection of Egger and Davey Smith.

    It is true that they focus on randomised controlled trials more than observational studies. But their basic statement about the potential value of meta-analyses, and the need to overcome the risk of Type II errors is common to both. When you raised the difference between the two types of study, it is quite reasonable for me to respond – that is not changing the subject.

    Indeed, your latest post continues to try to distinguish between the 2 types of study (so how can I possibly be changing the subject?). And this is where your mis-quoting really gets going. You quote warnings about how observational studies are conducted as statements that these studies are not reliable – which is patently wrong. And they most certainly did NOT criticise studies into SHS.

    In fact, they highlight the value of well-conducted observational studies:

    “Studies of such “menaces of daily life”6 use observational designs or examine the presumed biological mechanisms in the laboratory. In these situations the risks involved are generally small, but once a large proportion of the population is exposed, the potential public health implications of these associations—if they are causal—can be striking.”

    “Analyses of observational data also have a role in medical effectiveness research.”

    As you say, Egger and Davey Smith say “we think that the statistical combination of studies should not generally be a prominent component of reviews of observational studies”. If you look at overview reports like the US Surgeon General’s 2006 report or the 2004 IARC monograph, you will find that they are designed in the very way that Egger and Davey Smith suggest. Statistical findings are tested in detail to assess potential heterogeneity. Potential confounders are considered. Other causation criteria are also tested – including dose-responsiveness and toxicology.

    I laughed when I read your remark “that if you repeat a lie often enough, it will in the end become the truth”. That is exactly what I thought when I read your reference to “85% negative results”. That is a dodgy claim. The truth is that +80% of study results are positive (either statistically significant or non-significant). The meta-analysis findings showing a statistically significant positive finding is exactly what you would expect to find from that collection of findings.

  23. Rollo questionaire studies are useless,recall bias and outright lying by participants is what you get! Why would people lie,because as soon as you go to a hospital the first thing your bombarded with is ”DO YOU SMOKE” and they wont stop until you tell them something. The ACS in america uses that information to create even more trash claims!

    The truth is that +80% of study results are positive (either statistically significant or non-significant).

    The truth is only 2 are what would be called significant!

    Of the 24 which showed some risk, only two had a Relative Risk Factor over 3.0 and none higher.

    The fact is overall risk of shs/ets is INSIGNIFICANT!

  24. Cyrenia says:

    My God, if these are typical of anti smokers arguments where one person thinks that they are right and half a dozen intelligent people are wrong, then I am baffled.
    Every normal sensible person knows for a fact that so called ‘second hand smoke’ is totally harmless and only a complete idiot could believe that it was.
    Rollo must be a very deluded lady indeed.

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