The CATCH Debate Recalled

A year ago today, I left Devon. The day also marked the end of the CATCH (Colloquium About The Cigarette Hypothesis) debates on my old blog, which had been running for about a month after Chris Snowdon, who is firmly of the belief that smoking causes lung cancer, had challenged me to a debate about it.

At the time, with the move from Devon imminent, I wasn’t able to devote as much as my time to the debate as I would have liked, and furthermore as the debate developed I found myself more in the role of editor than debater. But Rich White took up the baton, and very forcibly argued the case against smoking as a cause for lung cancer.

At the end of the debate, however, I felt that it had been a 2-2 draw. Chris Snowdon refused to change his mind, and so also did the sceptical Rich White. Much of the debate centred around the Doll and Hill studies of the 1950s, and while Chris (perhaps) retreated somewhat on the value of these studies, he pointed out – quite rightly – that there were several further studies which had drawn the same conclusion on tobacco causation which had yet to be discussed. And so, in many ways, the debate was incomplete in that it failed to look at all the evidence.

Over the past year, I’ve continued thinking about the matter, and have found my scepticism deepening. And if I were to engage in the argument again, I think that I would adopt a far more radical position than I did a year ago: I would now argue that the research conducted by Doll and Hill, and numerous other researchers, wasn’t science at all.

For in my view true science rests upon accurate measurement. For example, the gas law that states that the pressure of a gas varies linearly with its temperature (over a wide range of temperatures and pressures) is one that was empirically derived from making accurate measurements of both the temperature and pressure of gases. Scientists – real ones – take very great pains to measure quantities like pressure, temperature, time, length, mass, electrical potential, etc, as accurately as they possibly can. And indeed it is only because such quantities were accurately measured that it became possible to discover physical laws like the gas laws. Science, in many ways, is accurate measurement.

And in addition, real scientists make estimates of the accuracy of their measurements, and give the length of something as, say, 1.3 cm +/- 0.1 cm. That is to say that the length fell in the range of 1.2 cm to 1.4 cm. Scientists quantify inexactitude, because they are aware that all measurements are inexact, even the most accurate ones.

And furthermore, real science rests upon a set of well-defined units – the kilogram, the metre, the second, etc. -. There are (or for a long time, there were) actual lumps of metal kept in controlled conditions which were the standard against which all other measures of mass and length were ultimately to be compared. The same applied to clocks, such as those kept at Greenwich in England.

It is an aspect of science which is seldom emphasised: the tremendous care that scientists take in defining the units, and measuring the numbers of those units in the experiments they conduct.

But when we consider the epidemiological studies of researchers like Doll and Hill, we find ourselves in a world in which nothing is measured accurately, and in which even the units being used are ill-defined.

Take for example the unit of the ‘cigarette’, according to which some people smoke 10 or 20 of them a day. What is the standard cigarette, kept in controlled conditions in the vaults of some government laboratory in France or Switzerland? The answer is that there isn’t one. A cigarette is whatever looks like a cigarette. It may be king-sized or filter-tipped, hand-rolled or manufactured, and made of a variety of different tobaccos, and of a variety of strengths. By an estimate of mine a while back, I think that it would require two or three of my thin hand-rolled cigarettes to fill a king-sized manufactured cigarette. So we are immediately dealing with a unit – the cigarette – which may vary in size back a factor of 3 at least, and quite possibly more. That’s like having a set of rulers on which the inches on some are 3 times longer than the inches on others.

And then what does it mean to ‘smoke’ a cigarette? This can range all the way from sitting with the burning cigarette sitting on an ashtray, or between one’s fingers (like my current cigarette), to something that is greedily inhaled deep into one’s lungs, with hardly a microgramme of any of the smoke going anywhere else. And in between there are all sorts of different ways of smoking cigarettes which range from not inhaling the smoke at all, to inhaling it mixed with air, or inhaling directly from the cigarette. So ‘smoking’ a cigarette can range from inhaling much the same amounts of smoke as a ‘passive smoker’, or inhaling ten or a hundred times as much.

Another ill-defined unit is the ‘smoker’, whereby studies refer to ‘smokers’ and ‘non-smokers’ (and perhaps ‘ex-smokers’). One might think that a non-smoker was someone who has never smoked any cigarettes. But in reality, in many studies, a smoker is defined as someone who has smoked 100 cigarettes or more in their lifetime, and a non-smoker is defined as anyone who has smoked less. All of which raises a number of questions. Why 100? Is it because it’s a nice round number? Why not 34 cigarettes? Or 276? And anyway, can anybody actually recollect precisely how many cigarettes they have smoked in their lifetime.

This latter problem is sometimes called ‘recall bias’. But it’s more than a matter of bias. There can only be bias if estimates of cigarette consumption could be compared with accurate measurements of actual cigarette consumption. And since there are no accurate measurements of anyone’s actual cigarette consumption, how can it ever be possible to decide how biased recollections may or not be? The truth of the matter is that most people simply don’t know how many cigarettes they have smoked, much like they have no idea whatsoever how many cups of coffee they have drunk, or books they have read, because they weren’t keeping a record.

And here’s another proclivity of real scientists: they keep accurate records. When they measure the length of some object, or find its weight, they carefully record it, usually in words and numbers written on paper. And they do this because they know that if they don’t, they’ll rapidly forget the numbers they’ve measured. They don’t rely on their memories for the results of their experiments, even of the previous day. They record the results they get as and when they get them. And yet tobacco research regularly relies on the recollections of smokers from 10 or 20 or even 50 years earlier. And there is no way of knowing whether such recollections are biased in one direction or the other, underestimating or overestimating.

And then, when these ‘smokers’ have ‘smoked’ some ill-remembered number of ‘cigarettes’ over their lifetime, and they die of lung cancer, nobody is actually sure whether they a) really died of lung cancer, and b) whether the cancer originated in their lungs in the first place or spread from elsewhere.

But in tobacco research, all these various numbers are then treated as if they had been as accurately measured as any lump of plutonium in a nuclear laboratory, and then subjected to statistical manipulations which end up showing that smokers are 13 times more likely to get lung cancer than non-smokers. Or maybe 20 times more likely. Or 3 times more likely. The mathematical techniques used to produce such numbers cannot, however, improve in the least upon the quality of the data on which they are based.

And so to my charge against all these studies: they are not science. They may look like science, with all their charts and tables, and all their relative risks and confidence intervals, but the raw data on which their results all rest is made up of numbers which are guesses and vague recollections using ill-defined and arbitrary units, without any way of knowing how accurate any of these might be. In such circumstances, there is no need to even bother to read any of the studies based on such methods in order to know that their conclusions are devoid of value.

One might even say that even astrology is more scientific than this. At least astrologers base their calculations on accurate measurements of the movements of the planets in the solar system.

I imagine that, faced with such an attack on their science, tobacco epidemiologists might well concede that many (and indeed perhaps all) of the raw data they use is highly suspect, but would say: “That’s the best we can manage. Can you do any better?” To which my answer would be that, in the absence of accurate data, it is quite simply impossible to carry out genuine scientific research of any sort at all, even with the best will in the world, and that if theirs was the best that can be managed, then it wasn’t worth doing in the first place.

The most that I would concede of such ‘research’ is that it vaguely suggests that smoking may have some connection with lung cancer, much in the way that visiting West Africa may have a connection with contracting malaria. Certainly no intrusive advice to anyone to stop smoking (or stop visiting West Africa) is called for, and certainly not divisive and socially and economically destructive laws like smoking (or travel) bans. Such interventions can only be justified to the extent that they are based on near-certainties. And in the case of tobacco research, there is nothing nothing that even begins to approach any certainty.

And yet, it’s a strange thing that from out of this most inexact science (so inexact as to not even merit the title of Science) there has sprung what is perhaps one of the deepest convictions of the age – believed by almost everybody (including Chris Snowdon) – that smoking causes lung cancer. This belief is, it might be said, regarded as a fact of life, more certain than the fact that the earth goes round the sun.

How is it that such an uncertain hypothesis came to be widely regarded as absolutely certain? Perhaps simply by being asserted over and over again for 50 years or more. Or perhaps because the principal sceptics of this dogma died out before its advocates. Sir Ronald Fisher, the ‘father of statistics’, who contested the cigarette hypothesis throughout the 1950s, died in 1962. By contrast, the advocates of the hypothesis, Bradford Hill and Richard Doll, lived respectively until 1991 and 2005. It might have been a different story if Doll and Hill had died in 1962, and Fisher had lived until 2005, and had 40 years to lay his opponents’ arguments to rest.

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56 Responses to The CATCH Debate Recalled

  1. Frank right on again. I find it very odd that to this day they still havent proven smoking causes anything at all much less cancer,I think maybe the new debate should be all the claims that smoking causes not just going back to the SG report of 1964 that really started all this hype. Yes Ive known folks that died of LC.

    But my great grandama lived to the ripe old age of 96 and was smoking at age 4 on the old family homestead in Seebree ky. We had 3 tobacco farms at the time in 1918 and granny added 3 more over the next decade besides running tobacco and booze during prohibition to her speak easy in Booneville Ind and Henderson ky. Even as a kid in my grandpas church in Evansville ind at parkplace mission gramps never said a word about his mother inlaws smoking during services on sunday much less her dipping some snuff and on more than one occassion he went and bought her tobacco products. This was in 1972. This all happened over the period of the first tobacco prohibition movement,before dolls studies back when coal was burned everywhere for heat especially kentucky. We burned our trash in the city to save space in the landfield,it was legal until about 1994. Grandpa lived to 92 he didnt smoke at all,grandma at 87. They were around shs/ets all there lives and myself included as my dad smoked but not mom and she was the only one to ever get a cancer in the whole family,colon cancer. But she has had over 23 abdominal surgeries thru the years for various things mostly female related. She is now 77 and been free for over 15 years. Yes indeed lets rip into all the claims the nazis have made over the years about all of it.If its as shitty as the second hand smoke studies,it will be fun!

  2. Frank my post didnt show up!

  3. junican says:

    It seems to me that the whole idea of using epidemiology in respect of smoking and lung cancer is a fraud. The reason is that real epidemiology starts from ABSOLUTE FACTS. The original epi..study was by Snow (?) about disease produced by bad water supply in London, wasn’t it? His study was based upon the fact that specific Londoners in specific places were dying from this disease. He isolated the source of the disease by the equivalent of ‘triangulation’ – a specific water pump.

    It seems to me that modern epi… starts with the water pump (smoking) and then arrives at the disease.

    • alanxxx says:

      It’s strikes me as disturbing that at least one of the high up professional Ants sees himself as following in the footsteps of John Snow.

      From my novice point of view, I’d say that Cholera was in the water, and that was it.

      Cancer isn’t in the cigarette as cholera is in the water, but many people react as if cancer is in cigarettes waiting to seep out at them.

      Blue asbestos inspires similar dread, when all you’ve got to do to be safe is leave it alone.

      Some say that Hydrofluoric Acid Conc. is a proper man’s toxic substance, and that it’s worth going a long way to avoid that stuff.

      I see charlatan modern Healthists as the equivalent of money lenders in the temple. If we are so concerned with particles in the air, where’s the health warning and pictures of corpses on the barbeques that are sold, why aren’t diesel engined vehicle drivers subjected to moral witch hunts for gassing the cheeldren? – and I hope you anti smokers are satisfied with your carcinogenic ridden smoke free pub. It’s in the fabrics because of the cleaning materials, didn’t you know?

      Anybody up for a chorus of Silent Night on the lead harmonica and a nice hot electric Mercury footbath?

  4. beobrigitte says:

    For in my view true science rests upon accurate measurement.

    Back in the 90s one of my many questions was:
    How can you arrive at the conclusion that smoking causes cancer on the basis of isolating and growing a cell line by just providing the factors these cells require to grow? What about the rest of factors (processes occurring in living bodies), including the ones we encounter in day to day life? What about the subtle, yet much influencing, variation in normal processes in individual people?

    With respect to tests on living animals – e.g. lab rats. Their lives hardly replicate ours. They do not cross busy roads to go to (wonderfully smoke-filled) pubs; they do not eat a curry after a few pints on the way home and so on.

    For TRUE measurements we require TRUE conditions to begin with.

  5. gimper30 says:

    I look forward to your continuing posts on the CATCH debate. Part of my training included the testing of experimental hypotheses using the scientific method. I agree with you in that the ANTIS arguments are not based on these classical methods. As I’ve previously stated in my comments, I really believe that at some future date it will be shown that smoking is NOT the cause of cancer. However the fact that so much money is involved is likely to push the serious pursuit of the real causes well into the future. The one real scientific fact that unfortunately can be agreed on is FOLLOW THE MONEY.

  6. James Burkes says:

    But Frank, it’s not even as exact as your malaria analogy. You can look at cases of malaria and see that most of them are in Africa and none are in Chipping Norton, therefore it’s best to avoid Africa if you want to avoid malaria.

    But with smoking there are still so many issues that need to be answered to my satisfaction. Such as:

    1) If smoking “causes” so many cancers, why do 25% of cancers occur in smokers (who make up 25% of the population (CRUK figures)? Doesn’t this actually show that there is no difference between smokers and non-smokers? Or, if smokers are more likely to get, say, lung cancer, don’t these figures prove that smoking is actually preventative for some cancers? (In order .to get these figures the same, some cancers must be less likely in order to balance out the lung cancer figures).

    2) Why do high smoking developed nations have lower rates of cancer than lower-smoking developed nations? Either smoking is a minor factor that can be counteracted by a good diet or less stress or similar, or smoking is not a factor at all, surely?

    3) Why is cancer and various other lung diseases continuing to rise when smoking is at an all-time low and exposure to SHS for the average non-smoker is non-existent? This is the biggy to me and is the basis of science. If you suspect a factor of causing something and the removal of that factor does nothing, then you need to reconsider your hypothesis. Again, the fact that its removal ties in with a RISE actually suggests, again, a protective effect.

    Put on top of that the fact that we all know the antis are a bunch of liars and then also add in the (purely anecdotal) evidence of all my elderly smoking relatives living well into their 80s (and only dying in car accidents, falls and the like) and I remain to be convinced. Indeed, even my parents, who know nothing of Tobacco Control, recently remarked, completely unprompted, that they had noticed that now that they are in their 70s they spend far too much time going to funerals, many from friends who had died from cancer. And not a smoker among them. The only smoker they know who has died died 20 years ago and had a congenital heart defect which her Dr said could have killed her at any time, smoker or not….

    Until the first three questions can be answered, I remain unconvinced.

    • Frank Davis says:

      You can look at cases of malaria and see that most of them are in Africa and none are in Chipping Norton, therefore it’s best to avoid Africa if you want to avoid malaria.

      This may be true now, but it was not always true. As best I understand it, malaria is likely to appear wherever mosquitoes are able to breed in standing (still) water, such as is found in swamps. Historically, malaria was prevalent in Italy, Spain, and the south of France. And I believe that I’ve heard of it in Britain occasionally. And Siberia, I’ve read many times, is infested with mosquitoes. If we no longer have malaria, it’s because most swamplands have been drained and put to other uses, and mosquitoes have few places to breed.

      I think that there are numerous questions surrounding the tobacco hypothesis (and actually always have been). I think that, for me, the now-established fact (it would appear) that cervical cancer is caused by Human Papilloma Virus, and that the same virus has been found in a number of other cancers (including lung cancer), suggests to me that medical science may at last be on the trail of the real culprit. HPV, as a viral infection, falls in with a whole family of other viral diseases. On the other hand, the idea that “smoke” can cause cancer seems to entail a cause of disease which is radically different from other virally or bacterially caused diseases. It’s one reason why I’ve never been persuaded that exhaust fumes are a cause of lung cancer (although I don’t doubt that they can asphyxiate people, and cause bronchitis, etc.).

      The other thing is that there are always people who hate tobacco, alcohol, drugs, etc, for reasons which have nothing to do with medicine, and everything to do with morality (or their notion of it), and I very much suspect that when lung cancer began to multiply in the 1920s and 30s, these people felt they had a golden opportunity to pin the blame for it on smoking, and did so. Which would be much like fingering someone you don’t like for some crime which he may not have committed.

      • Exactly Frank,they created and manufactured evidence to convict tobacco for a crime their was no eyewitness to. Without conclusive proof thru a cause detailed by chemical reaction in one LC death how can a defendant be convicted of a crime except by a kangaroo court in which James Repace and a few others were the primary witnesses. Judges that tossed out tobacco company witnesses and studies merely because they were from tobacco companies. Then a judge with all the facts that the EPA study was junk,answers up that The dangers of shs come from many places and that mountain of evidence etc etc.Im talking about judge kessler who is still turning a knife in big tobaccos backs! Its a political movement with public health nazis in charge of the inquisition and the judges are just as corrupt and partisan as the witch hunters!

      • http://topnews360.tmcnet.com/topics/a

        WASHINGTON (AP) — The Justice Department was in a new dispute Friday with the tobacco industry over the government’s landmark lawsuit against the companies.

        The government has prepared corrective statements it wants the companies to be forced to make about the health hazards from smoking. But the tobacco companies don’t want those proposed statements put in the public record before they get a chance to review them.

        FORCED TO MAKE…….SOUNDS like somebodys not playing fair doesnt it.So if the tobacco companies make statements then the nazi anti-smokers get to say see even the tobacco companies admit this!!!!! force isnt that what hitler did at bayonet point!

  7. Rose says:

    On this subject

    Medical persons, please can you run your professional eyes over this?

    After a series of conversations, news items and general bits and pieces, is it my imagination or is a pattern beginning to form?

    Genetic link found between breast cancer and heart disease

    “The same mutated genes that put women at greater risk for breast cancer are now being linked with a higher risk of heart disease.

    Mice with the mutated gene had a three to five times higher rate of death following a heart attack, Toronto researchers have found.”

    Reporting in the journals Nature Communications and the Journal of Biological Chemistry, the researchers say they believe BRCA1, as well as BRCA2, act much the same way in the heart as they do in the breast and ovaries, by repairing DNA damage.

    BRCA1 is mutated in as many as half of all inherited breast cancers. Women who carry a defective copy of the gene have a 50 to 85 per cent cumulative lifetime risk of developing breast cancer, and a 12 to 60 per cent chance of developing ovarian cancer, the authors write in Nature Communications.”

    The gene acts as a “caretaker,” allowing cells to repair DNA damage.”
    http://news.nationalpost.com/2011/12/20/genetic-link-found-between-breast-cancer-and-heart-disease/

    BRCA1 Interaction with Human Papillomavirus Oncoproteins

    “The two major HPV oncoproteins, E7 and E6, function in part by inactivating host cell tumor suppressor proteins, retinoblastoma 1 (RB1) (and other retinoblastoma family proteins) and p53 (17). Taken together, these findings raised the possibility that HPV proteins may functionally inactivate BRCA1 in cervical cancer cells.

    The purpose of this study was to evaluate the hypothesis that the HPV oncoproteins E6 and E7 can interact with and inactivate the function of BRCA1.”
    http://www.jbc.org/content/280/39/33165.full

    Human Papillomavirus and Cardiovascular Disease Among U.S. Women in the National Health and Nutrition Examination Survey, 2003 to 2006

    “Background: Oncogenic proteins derived from tumor-associated HPV induce the degradation of tumor suppressor protein p53.

    Inactivation of p53 is associated with accelerated atherosclerotic process. However, the association between HPV infection with CVD remains unclear.”
    http://content.onlinejacc.org/cgi/content/abstract/58/19/2001

    Mapping the role of NAD metabolism in prevention and treatment of carcinogenesis

    “We show that nicotinamide and the resulting cellular NAD concentration modulate expression of the tumor suppressor protein, p53, in human breast, skin, and lung cells.

    Studies to determine the optimal NAD concentrations for responding to DNA damage in breast epithelial cells reveal that DNA damage appears to stimulate NAD biosynthesis and that recovery from DNA damage occurs several hours earlier in the presence of higher NAD or in cells undergoing active NAD biosynthesis.

    Finally, analyses of normal human skin tissue from individuals diagnosed with actinic keratoses or squamous cell carcinomas show that NAD content of the skin is inversely correlated with the malignant phenotype.

    Since NAD is important in modulating ADP-ribose polymer metabolism, cyclic ADP-ribose synthesis, and stress response proteins, such as p53, following DNA damage, understanding how NAD metabolism is regulated in the human has important implications in developing both prevention and treatment strategies in carcinogenesis.”

    “The association of lower NAD with malignancy in skin supports
    the hypothesis that niacin maybe an important preventive
    factor in cancer.”

    Click to access MappingroleofNADmetabolism.pdf

  8. “The association of lower NAD with malignancy in skin supports
    the hypothesis that niacin maybe an important preventive
    factor in cancer.”

    nicotinic acid

    Niacin – Wikipedia, the free encyclopediaen.wikipedia.org/wiki/NiacinCached – Similar
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    Niacin (also known as vitamin B3, nicotinic acid and vitamin PP) is an organic compound with the formula C6H5NO2 and, depending on the definition used, one …

    Pellagra – Niacin (band) – Niacin/simvastatin – Niacin/lovastatinNiacin to boost your HDL, ‘good,’ cholesterol – MayoClinic.comwww.mayoclinic.com/health/niacin/CL00036Cached – Similar
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    Jun 3, 2011 – Niacin is an important B vitamin that may raise your HDL, “good,” cholesterol. Find out if you should talk to your doctor about taking niacin alone …
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    Apr 12, 2009 – Niacin (nicotinic acid) is used to to lower cholesterol and triglycerides. Includes Niacin side effects, interactions and indications.
    Vitamin B3 (Niacin)www.umm.edu › Medical Reference › Complementary MedicineCached – Similar
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    Niacin also helps the body make various sex and stress-related hormones in the adrenal glands and other parts of the body. Niacin helps improve circulation. …

  9. I take “smoking causes lung cancer” to mean that a person who lives his life the same apart from his smoking, increases his probability of getting LC. This is impossible to verify. If I were prevented from smoking, my whole lifestyle would have been different. c.f. Seventh-Day Adventist population. I think what comes closest, is that those with a tendency to getting a nicotine habit are able to satisfy it easily, without inconvenience or high cost, and legally without smoking. Through snus use, this has been possible for decades, in Sweden, which has both the lowest male smoking prevalence and the lowest male LC incidence in the developed world. To me, this is the most compelling evidence that smoking “causes” LC. It also demonstrates that, by opposing the legal sale of snus throughout the EU, anti-tobacco campaigners must take responsibility for a large number of deaths each year. I keep repeating this and they haven’t yet sued me. I guess they don’t want to draw attention to this uncomfortable truth.

  10. kinfree1 says:

    I’m with James Burke on this and fully agree with his 3 points – but there are more, like for instance why are there more cancers in towns/cities than in rural areas; Why has ‘hard’ science never been able to prove that smoking causes cancer etc. This is argument based on ‘common sense’ versus ‘science’ and the ‘science’ has been shown to be unreliable (as you comment above, and I fully agree with Frank).

    ALL the so called anti-smoker scientific ‘evidence’ is statistically based and anyone who has looked at how statistics are/can be used, knows that they can be used to support ANY argument. What’s more, I believe that most anti-tobacco ‘scientists’ and anti-tobacco activists KNOW that their ‘science’ is flawed. They KNOW that all their predictions in relation to prevention of ill health have proved incorrect and it is this that has spurred them into the coercive, de-normalisation techniques we have seen over the last few years, designed to ‘spoil’ the smoker image. They needed to strike a fatal blow in the anti-smoker agenda to reduce the amount of smokers before it became common knowledge that smoking is only a tiny (if any) risk to health. Rather than being a health risk, smoking becomes an undesirable activity practiced by very few people, hence the emphasis on ‘filthy’, ‘smelly’ etc. – the ‘health risks’ become irrelevant. ie. We see this in any smoking debate: – “I don’t care if its not bad for my health, it/you stink”

    Re. James’ point 3; it is true that Lung cancer continues to increase in most countries and Lung cancer is seen to be mainly a smoker disease, but there is a problem. In USA, Lung Cancers increased by over 30% between 2000 and 2008 (while ‘all cancers’ increased by less than 18% over same period) and increases can be seen in such as Australia and Canada. Allegedly however, some US States have seen a decline in LC, as is also claimed in UK. Why are these out of kilter? The answer, I suggest, is in the classification of diseases and how these can be recorded inaccurately or even manipulated. We know that doctors are more likely to wrongly record a smoke related death as the cause of a smoker’s death and the opposite for a non-smoker, but I think the problem of mis-diagnosis is even deeper.

    There has allegedly been a decline in Lung cancer over some years in the UK – BUT – between 1991 and 2006 ‘all cancers’ increased by a whopping 45%; (new cases 1991 – 212647: 2006 – 309700) in England & Wales. (I noted these gov. stats some time ago but unfortunately did not screen print them. They have been removed and replaced with less drastic figures; (new cases 1971 – 143743 : 2006 – 243144) – still indicating a substantial increase, but much less than the original figures)

    If we look at Lung cancer diagnoses we find, for example, that only 5% of small cell LC (allegedly smokers cancer), is first diagnosed ‘before it has metastasized to other parts of the body’. This means that there is a 95% chance or more that the cancer could have originated from some other part of the body and spread TO the lung rather than FROM the lung? As I understand it, the original site is identified by how advanced the cancer in each location has developed. Cancer relies on a rich supply of oxygenated blood to develop so it should be no surprise that Lung cancer is the most aggressive and most unlikely to be cured – where oxygen levels are at a maximum, at source. An analogy could be made with a plant in the desert growing in an area where there is some, but little water. It grows slowly and stunted but can still produce seed. If the seed is blown to an oasis with a plentiful supply of water, the new plant will grow to is full potential, well outgrowing the parent plant. So, for instance, skin melanoma, being farthest from the oxygen source, fed by tiny capillaries, will have access to a limited supply of oxygenated blood and will develop very slowly. If identified early enough skin melanoma is easily treated but could still have released cancer cells to other parts of the body via the blood system and the lungs are an oxygen oasis.

    I have long suspected that the lies surrounding SHS ‘science’ is not exclusive to SHS ‘science’ and anti-tobacco is quite happy that the debate remains focused on SHS, rather than primary smoking. Very few are unaware of the misinformation relating to SHS but many are prepared to turn a blind eye believing that the lies are justified to prevent primary smoking. Their greatest fear is that the debate on primary smoking re-emerges and the public become aware of the true foundations of anti-tobacco; Time to question the anti-smoker cry; ‘the debate is over’!

  11. When cornered , the debate is over is a one liner we here quite often!

  12. garyk30 says:

    In order for any theory to be valid, that theory must work everytime.

    ‘Smoking causes lung cancer’ is not valid; because, not all, or even a majority of, smokers get lung cancer.

    ‘Smoking is the sole cause’ of a smoker’s lung cancer is not valid; because, not smoking does not mean you have zero chance of lung cancer.

    ‘Smoking causes lung cancer’ is not valid; because, given equal numbers of adults, smokers do not have a substantially lower number of adults that do not get lung cancer.

    American CDC data says that the current smokers’ lung cancer death rate is 7/10,000 per year and the never-smokers lung cancer death rate is 2/10,000 per year.

    That is a difference of only 5/10,000 or 5/100ths of 1%.

    In any given year, a current smoker has 99.95% of a never-smoker’s chance of not dying from lung cancer.

    Anti propaganda uses Relative Risk increases to show ‘causation’; because, a 5/10,000 greater death rate isn’t scary enough.

    Actually, lung cancer death is a rather rare event, in any given year, only 7/100ths of 1% of adults will die from lung cancer.

  13. garyk30 says:

    “American CDC data says that the current smokers’ lung cancer death rate is 7/10,000 per year and the never-smokers lung cancer death rate is 2/10,000 per year.”

    Since 2 is about 30% of 7, that data shows us that at least 30% of smokers lung cancers are ’caused’ by factors other than smoking.

  14. garyk30 says:

    Now, let’s look at the ex-smokers.
    Antis would have you believe that all of the lung cancers that occur to ex-smokers are ’caused’ by their having smoked.

    You get statements like this:
    “Since 21% of lung cancer deaths happen to current smokers and 61% of lung cancer deaths happen to ex-smokers, this means that 82% of the lung cancer deaths are ’caused’ by smoking!!”

    However, about 92% pf the ex-smokers have the same risk of lung cancer as never-smokers.

    Since 92% of 61% = 56% , we see that 56% of the yearly lung cancer deaths occur to ex-smokers that have the same risk for lung cancer as never-smokers.

    Since 56% is 68% of 82%, we see that 68% of the lung cancer deaths ’caused’ by smoking happen to ex-smokers that have the same risk for lung cancer as never-smokers!!!!

    ASH-UK

    Click to access ASH_94.pdf

    “Benefits of Stopping Smoking”
    Within 10-15 years of quitting smoking, an ex-smoker’s risk of developing lung cancer is only slightly greater than that of a never-smoker.

    http://www.healthination.com/Videos/Smoking-Quit-Now/The-Quitting-Timeline

    Ten years after quitting, the risk of dying from lung cancer is no longer higher than that of a non-smoker.

    In 1990 there were 44 million(USA) ex-smokers and in 2006 there were 48 million ex-smokers.
    44 is 92% of 48

  15. garyk30 says:

    You get statements like this:
    “Since 21% of lung cancer deaths happen to current smokers and 61% of lung cancer deaths happen to ex-smokers, this means that 82% of the lung cancer deaths are ’caused’ by smoking!!”

    However, about 92% pf the ex-smokers have the same risk of lung cancer as never-smokers.

    Since 92% of 61% = 56% , we see that 56% of the yearly lung cancer deaths occur to ex-smokers that have the same risk for lung cancer as never-smokers.
    ……………………………….

    If a smoker dies from lung cancer, there is an 80% probability that cancer was ’caused’ by factors other than smoking!!!!

    56% plus the 18% lung cancer deaths that occur to never-smokers gives us the fact that 74% of the lung cancer deaths occur to never-smokers and ex-smokers that have the same risk for lung cancer as never-smokers.

    This gives lung cancer death rates like this:

    smokers(current+ex) = 8.1/10,000

    non-smokers(never+ex) = 6.5/10,000

    Since 6.5 is 80% of 8,1, we see that; if a smoker dies from lung cancer, there is an 80% probability that cancer was ’caused’ by factors other than smoking!!!!

  16. Great points gary,it leaves mother natures genetic code as the probale link in each of us!

    WTF is it that goes awry to let it happen,is it age and normal breakdown of the immune system or a catastrophic breakdown in the micro percentage of young that get it!

    Something somewhere is letting it happen in the genetic code,this is where we should be spending those wasted trillions on anti-tobacco research over the last century!

  17. gdf1 says:

    Great comments all…

    I suspect that there is a common factor that makes people tend to smoke and also tend to get lung cancer. This would be consistent with the research publications in Nature in April of 2010 (?) – where 2 of the 3 research teams found a “lung cancer gene” that was associated with a nicotinic receptor gene (but acted independently). That is, folks who are genetically susceptible to lung cancer are also (and independently) more likely to respond favorably to nicotine. (perhaps nature provided some medicine along with the disease). This would be entirely consistent with the epidemiological evidence – and cannot be ruled out by epi evidence alone. The third research team, btw, concluded that the increased risk of LC was directly due to the increased smoking (on weak evidence, I believe however). I don’t know if this is THE answer (perhaps there are environmental exposure factors, or other behavioral factors (physical or emotional stress) that both increase desire to smoke, and independently increase LC risk), but I think the answer will be found to be something like this. (because I don’t doubt that there is some sort of statistical association between smoking and lung cancer). In any case, smoking, I believe, is falsely accused, and likely to be medicinal for some people.

    This is also consistent with the fact that randomizing people who smoke to anti-smoking interventions has spectacularly failed to reduce incidence of lung cancer in the :”treatment groups”. (MRFIT, for example). Unfortunately, it means that people who enjoy tobacco are at higher LC risk – whatever we do.

    I also believe that the reason that stopping smoking used to “reduce risk” of lung cancer more sharply – and now the “risk” continues for 30 years or more (essentially there is less ”risk reduction”) , is because the first wave of “quitters” (self-selected) were those who found it easy to stop (essentially, they either didn’t need to smoke or didn’t enjoy smoking as much as others). Thus the first wave was already “low risk”. They weren’t really tobacco smokers – probably more like dabblers. They weren’t high risk to begin with. As anti pressure increases, they reach closer and closer to those who enjoy smoking, and/or need to smoke – and subsequently, there is less and less “risk reduction” for each wave of quitters. As I mentioned above, eventually they reach those of us for whom smoking may be truly medicinal…. and necessary. And we see the sorts of things we are now beginning to see with LC risk *increasing* for those who quit. (Interestingly the anti’s interpret this new data as “smoking at all is much more dangerous than we thought! – The risk never ends”) . What it really means, I think, is that people who need to smoke, need to smoke.

    Rodents don’t smoke naturally, of course, but the rodent experiments tend to show that the smoking rodents live longer – and they only way to cause increased LC is to make them stop smoking. Researchers call this the “recovery period” which is necessary to induce LC. Even then, if researchers feed them inositol and anti-inflammatory agents (steroids, I believe), the rodents don’t get LC. (Consistent with recent myo-inositol phase I trial in human bronchial pre-cancerous lesions. (Also consistent with epidemiology showing lower LC rates associated with consumption of grapefruit. )

    Clearly there is much more to this question than “smoking causes lung cancer”. I find those four words in that order almost laughable.

    Just a few of my thoughts. (From off the top of my head – so please forgive the lack of precision and links – but you can find this info pretty easily)

    Frank, — glad to get a chance to finally say all of this — because I came late to the last discussion.

  18. garyk30 says:

    Antis say that smoking ’causes’ lung cancer deaths; but, have you ever wondered how many cigarettes smoked it might take to ’cause’ a 50% probability that ONE smoker has died from lung cancer.

    As a ‘Rule of Thumb’, we can say that it takes well over 1/2 billion cigarettes smoked to ’cause’ one smoker’s lung cancer death!!!!
    Then too, there is the 80% probability that cancer was caused by something other than smoking.

    Here: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5644a2.htm
    the USA CDC says that 20.9% of the lung cancers per year happen to current smokers.
    20.9% of the 157,000 lung cancer deaths is 32,814 lung cancer deaths happening to 46 million(USA) current smokers, that is a rate of 1/1,400.

    CDC says there are no smoking related deaths below the age of 35 and the average of smoking ’caused’ death is 73.
    that is, v50% of the deaths occur over the age of 73.

    Let’s take 1,400, pack a day, 18 year old smokers.

    They will smoke 10,220,000 cigarettes per year and,by age 35, have smoked about 174 million cigarettes with out having suffered a single smoking ’caused’ death!!!!

    At the age of 73, they will have smoked about 560 million cigarettes and there is only a 50% chance that one of them has died from a lung cancer ’caused’ by their smoking.

    As a ‘Rule of Thumb’, we can say that it takes well over 1/2 billion cigarettes smoked to ’cause’ one smoker’s lung cancer death!!!!
    Then too, there is the 80% probability that cancer was caused by something other than smoking.

  19. gdf1 says:

    If I may say just a bit more…

    Regarding the failure of randomized trials of smoking cessation. Very often, researchers determine that people with higher levels of some vitamin X have lowers levels of disease Y. Note, this is a self-selected population (free to vary on their Vitamin X level). To test the hypothesis that vitamin X is protective (because correlation aone isn’t enough), they then turn to a randomized trial (as they should) to determine if giving Vitamin X is, in fact, protective. Very often it turns out not to be. The researchers then conclude that some other lifestyle factor — probably associated with higher Vitamin X (but not Vitamin X itself) is the true protective agent – and they run off in search of it.

    In anti-smoking research, they just make sure not to do any more trials.

    Also, I said that if people whi smoke are at higher risk for LC due to some non-causative association, there’s nothing we can do. I should amend that and suggest that we can keep smoking.

  20. garyk30 says:

    At the age of 73, they will have smoked about 560 million cigarettes and there is only a 50% chance that one of them has died from a lung cancer ’caused’ by their smoking.

    Welll,everyone KNOWS that SHS/ETS exposure ’causes’ lung cancer; so, maybe inhaling the SHS from their cigarettes ’caused’ that 50% chance of one lung cancer death.

    The average adult takes 15 breaths per minute and let’s say it takes 5 minutes to smoke a cigarette.

    That is 75 inhalations of SHS/ETS per cigarette.

    75 inhalations of SHS X 560 million cigarettes gives us 42,000,000,000(42 billion) inhalations of SHS to have a 50% chance that ONE lung cancer death ’caused’ by smoking has occurred!!!!

    But remember; the experts have said: “There is NO SAFE LEVEL of exposure to SHS/ETS!!!

    I just laughed so hard that I choked on the red wine I am drinking!!!!

  21. gdf1 says:

    Frank said:
    “Then if 21% of LC deaths occur in the 46 million smokers,
    And 61% of LC deaths occur in the 48 million ex-smokers,
    Then ex-smokers would appear to die of LC at roughly 3 times the rate of smokers –
    So it may not be a good idea for anyone to give up smoking.”

    Although I agree with the conclusion – although for different reasons — I don’t think that Gary has controlled for age (I would think that ex-smokers would be older on average than current smokers). (That is, over-represented among the older population vs the younger).. .

    • Frank Davis says:

      It did occur to me that the ex-smokers would be older than the smokers, and so might be expected to die anyway.
      But by the same token, non-smokers will tend to be younger than either (after all I was a non-smoker for 20 years or so before I became a smoker), and ought to survive better than either smokers or ex-smokers.

  22. garyk30 says:

    “And if 18% of LC deaths occur in the 41 million or so non-smokers,
    Then non-smokers die of LC at the same sort of rate as smokers (18/41 as against 21/46).
    (although I think you’ve maybe said this)”

    Ahhhh no.
    There are about 136 million never-smokers.
    230 million adults minus 46 million current smokers, minus 48 million ex-smokers, leaves 136 million never-smokers.
    ………………………….
    “Then ex-smokers would appear to die of LC at roughly 3 times the rate of smokers -”

    Yes indeed!
    But; remember, 92% of them have the same risk of lung cancer as do never-smokers.

    Also, 33% of ex-smokers are over the age of 65 and only about 8% of current smokers are over the age of 65.

    70% of lung cancer deaths occur over the age of 65.

  23. gdf1 says:

    I think the question is — what are the percentages of never, ex and current smokers among those over 65. (Although you pointed out in your post, Frank, how difficult that is to really measure. – How many cigarettes makes an ex-smoker? How long ago? What do we do with pipe and cigar folks? What about historical effects (changes in cigarettes, changes in social values (nocebo effects) What about social class effects? It’s a very messy question really).

    It’s a question that, as you argue, will only ever be settled by real science – not by statistics.

  24. Frank heads up:

    Dont choke ok,its poetic justice

    Schuman to Pay for the Fight Against His Secondhand Smoke Case
    In an ironic twist, David Schuman will be paying monthly co-op fees that have risen to help pay insurance costs related to the co-ops fight against Schuman’s secondhand smoke case.

    “The cow is way out of the barn at this point. I have spent my retirement. I have $20,000 I have to pay my lawyer and expert witness,” Schuman said, in response to a question about why he would not appeal to the membership.

    http://greenbelt.patch.com/articles/schuman-s-to-pay-fees-used-to-fight-against-his-secondhand-smoke-case

  25. They say more than 60% of lifestyle-related cancers are due to smoking’

    So if we take the notion that more than 60% of lifestyle-related cancers are due to smoking,considering:

    – the overall reduction in smoking prevalence which initiated in the early 80’s and continued through the 90’s (talking about uk)
    – the time lag of 20 -30 years between smoking and developing cancer from smoking

    that means that we would be able to see in 2011 a huge overall reduction in the number of cancers

    Instead we see a stability for men and a rise for women in overall cancers.

    Something does not add up Frank…

    http://info.cancerresearchuk.org/cancerstats/incidence/all-cancers-combined/

    http://old.rcplondon.ac.uk/pubs/books/nicotine/1-overview.htm#2

  26. waltc says:

    Better minds than mine (Gary? Frank?) may know what to do with these stats, but they’ve all got official sources. Somehow they’d be connected to mortality rates, but that’s above my pay grade.

    US total pop in 2009 (2010 census): Just over 307 mil. 24% of whom were under 18 so the total officially adult pop was 228+ mill. Officially 21% smoked: about 46 million, tho apparently when you add in all kinds of smoked tobacco and underage smokers, the CDC claims it was 60 mil, at least in one report. The same year, 12.8% of the US pop. was over age 65, (39 mil+)

    Us total pop in 1960, just under 180 mil. Seems to me there were more people with larger families back then, but if we go with roughly the same % of under-18’s, that’s 45 million “kids” (some of whom smoked but I guess they’re not counted) leaving 135 million adults. If 60% smoked (accepting Frank’s postulate) that’d be about 80 million adult smokers. Recalling the era, I’d guess at least 30% of the “kids” aged 16-18 smoked, too.)

    Then there’s this: Official figures for 1965 (the year after the first Surgeon General’s “smoking causes cancer” report), there were 50.1 million adult smokers. But again, that’s not counting the under-18’s or the pipes and cigars.

    So– you mathematical geniuses– go forth and multiply (or divide, or subtract, or whatever).

    • garyk30 says:

      “So– you mathematical geniuses– go forth and multiply (or divide, or subtract, or whatever).”

      Genius????
      Frank = yes, I do not go much beyond adding and subtracting.

      I can not “go forth and multiply ” as I am toooo old and had that function fixed years ago. :)

      • Frank Davis says:

        Genius????
        Frank = yes

        I’m no mathematical genius. I can do quite a lot of mathematics, but there’s plenty I can’t do (e.g. vector algebra, complex numbers, the list is endless). I have a pretty basic mathematical toolkit, and also I crack a lot of problems with brute-force computer methods (computers don’t really do much more than add and subtract).

  27. The Man With Many Chins says:

    For quite some time, I have been of the opinion that smoking does not cause lung cancer. COPD, yes certainly, but cancer no.

    Why else would the rate of LC have not changed (and other cancers increased), when smoking prevalence has dropped so much.

    Question 1. How many nuclear weapons have been air tested since 1945? A lot. Consider that it could only take ONE particle of highly radioactive dust lodging in a lung to start LC. (A good vid on nuclear tests is here http://www.youtube.com/watch?v=WAnqRQg-W0k). Aforementioned dust could be everywhere and anywhere on the planet.

    Question 2. Other environmental factors. Consider the vast increase (especially recently) in diesel powered vehicles, and diesel particulates are known to be highly carcinogenic. I would rather suck up a lot of second hand smoke than DPM!

    Question 3. Other chemical factors. Consider the vast increase in chemical usage, in our daily lives. Cleaning products, polish, artificial materials including plastic etc. Many of these products also contain known carcinogens.

    Question 4. Food additives. Consider the vast array of additives that are added to our food. Many of these have also been shown to be carcinogenic, but they gaily add them too our foodstuffs when processing.

    Question 5. Fluoridation of water supplies. There is much discussion over the cumulative carcinogenic effect of adding sodium fluoride to our water supplies. This could also be a serious causative factor IMO.

    Question 6. Vaccinations. Big Pharma love giving us vaccinations. Especially those with mercury as the carrier (another known carcinogen). Far be it from me to consider a conspiracy theory, but as cancer treatment is so expensive, and genetic research is moving towards individually tailored (expensive) treatment but it’s in Big Pharma’s best interests to keep lifelong customers on their drugs that don’t actually cure anything.

    Thats my tuppence worth, and looking at my questions above, it strikes me that tobacco was singled out as an easy target to blame all manner of illnesses on.

    • Frank Davis says:

      I agree with pretty much all that. The 20th century produced so many real or potential carcinogens that it’s very strange that a traditional product, that had been around for centuries, took the rap for lung cancer.

      Tobacco was an easy target because tobacco smoke got visibly inhaled into lungs. They got round the ‘traditional product’ objection by pinning the blame on new-fangled cigarettes, which only began to be manufactured in quantity with the invention of machines in about 1870 (I think). But these days that early distinction has been lost, and it’s just tobacco in general. And maybe even inhaling anything at all, so even e-cigs which look like cigarettes are believed to be dangerous.

      • Rose says:

        Memo Re: General Motors Press Conference With Doll R Discussing Link Between Cancer and Chemicals 1979

        “I attended General Motors’ press conference this morning for Sir Richard. He should have had on a GM blue blazer. Doll said it is a mistake to attribute cancer to recent developments in industrial countries. “I don’t expect much trouble from chemicals – introduced in the last 30 years,” he said.

        “Industrial development and high standard of living are not necessarily associated with a high incidence of cancer.” Doll said a decrease in total number of cancers among both men and women in industrialized Japan proves industrial causes are not important. Cigarettes cause 40 percent of all fatal cancers in Britain, Doll said. These would be eliminated if the population did not smoke.

        He also blames dietetic factors, such as amount of fat eaten. TTO asked Doll: “Do you have any second thoughts at all — since your work does deal with cancer and the environment — about accepting an award from an industry which is having its own controversies concerning polluting the environment.

        ” Doll: “No ……. To be honest with you, No.”
        (Another scribe to me: “He’s blushing.”)

        GM Cancer Foundation Pres. then jumped in to explain that “great pains” are taken to separate GM the company from the foundation.”
        http://tobaccodocuments.org/ti/TIMN0110278-0279.html

        Injurywatch discovers secret payments for anti-smoking cancer-link by Oxford academic Sir Richard Doll by asbestos and chemical industry

        Click to access doll.pdf

      • garyk30 says:

        Question 3
        Indeed, Here is a list of 33 of the 188 toxic pollutants the EPA has found will be in CLEAN smoke free,urban air.

        Some you may recognize as being in cigarette smoke and there are some that are not found in cigarette smoke.

        http://www.epa.gov/ttn/atw/nata/mapconc.html

        Acetaldehyde-Acrolein-Acrylonitrile-Arsenic Compounds-Benzene-Beryllium Compounds-1,3-Butadiene-Cadmium Compounds-Carbon tetrachloride-Chloroform-Chromium Compounds-Coke Oven Emissions- 1,3-Dichloropropene-Diesel Particulate Matter-Ethylene dibromide-Ethylene dichloride-Ethylene oxide-Formaldehyde-Hexachlorobenzene- Hydrazine-Lead Compounds-Manganese Compounds-Mercury Compounds-Methylene chloride-Nickel Compounds-Perchloroethylene-Polychlorinated biphenyls (PCB)-Polycyclic Organic Matter (POM)-Polycyclic Aromatic Hydrocarbons (7-PAH)-Propylene dichloride-Quinoline-1,1,2,2-Tetrachloroethane- Trichloroethylene-Vinyl chloride

        And,as was mentioned, the radioactive particles from all of the nuclear tests.

    • fredrikeich says:

      “But I think that the trouble with it may be that quite a few of these fallout products have quite short half-lives.” – Frank

      I think I am right in saying that the shorter the half life the more damage is done, they would be bieng produced all the time, especially with alpha emitters located internally eg the lung.

      http://en.wikipedia.org/wiki/Relative_biological_effectiveness#Dependence_on_source_location

  28. garyk30 says:

    Snoking status by age group
    http://apps.nccd.cdc.gov/brfss/age.asp?yr=2006&state=US&qkey=4394&grp=0

    Early 20th century smoking rates:
    Cigarette smoking in the USA
    http://www.pnlee.co.uk/ISS.htm

    Web Edition
    Countries S-Y

    United States(pdf)

    Table 4M Prevalence of smoking, males: selected surveys by age, 1935-2005 ……………….page 18

    1935 = 53%

    1947 = 64%

    1955 = 52%

    Additional information (not presented in tables) page 57

    Kellogg (2002, reprinted from 1922)
    reported that “It is claimed that 90% of all men smoke, while comparatively few women do
    so. ….

    Howe (1984) and US Surgeon General (1980) quoting the Milwaukee Journal presented
    data from an annual survey in the Greater Milwaukee area, of adult (age 18+) men from
    1923 and also of women from 1934. In 1923, 87% of men smoked some form of tobacco,
    and 60% of male cigarette smokers also smoked pipe or cigars. The prevalence of cigarette
    smoking was as follows (selected years, mostly read from graph):
    Males… Females
    1923… 51.8
    1930…. 57
    1934.. 61.. 16.7
    1935 ..62.5… 20
    1940.. 64… 27
    1945.. 66.. 32
    1948 67.1.. 38
    1950.. 65.. 38
    1953.. 69.. 42.9
    1955.. 69… 43
    1958.. 73.. 45.4
    1960.. 63.. 50
    1965.. 54.. 45
    1970.. 38.. 36
    Male cigarette smokers smoked 3.7 packs per week in 1923, and 4.8 packs in 1935
    (equivalent to 10.6 and 13.7 cigarettes/smoker/day respectively). Women smokers smoked
    about half as many as male smokers in 1934.

    page 58
    In addition to the Milwaukee and Columbus surveys (reported above and as source 10), US
    Surgeon General (1980) gave estimates of the prevalence of adult smoking from other local
    consumer surveys of urban areas in 1948:
    Males %…… Females %
    Omaha.. 69.1… 34.3
    Birmingham.. 67.4…. 35.6
    Philadelphia.. 69.4… 46.7
    Seattle… 63.9….. 38.3
    San Jose… 63.4…. 34.0

  29. garyk30 says:

    Mortality Trends for Selected Smoking-Related Cancers and Breast Cancer — United States, 1950-1990
    http://www.cdc.gov/mmwr/preview/mmwrhtml/00022160.htm
    Editorial Note
    Editorial Note: The findings in this report indicate that, in the United States, the overall age-adjusted death rate for lung cancer increased nearly fourfold from 1950 to 1990

    Males = 21.6 to 75.6 per 100,000
    Female = 4.8 to 31.8 per 100,000

    total = 13 to 50.3 per 100,000

  30. garyk30 says:

    Smokers and never smokers are diagnosed with lung cancer at about the same age!!

    http://jco.ascopubs.org/cgi/content/full/25/5/472
    RESULTS
    Although never smokers were slightly older at lung cancer diagnosis than current smokers in two population-based cohorts (MEC and NHEFS), this difference was not observed in the majority of cohorts evaluated (NHS, HPFS, CTS, and U/OLCR; Table 2).

  31. garyk30 says:

    The 20 year time lag between smoking and lung cancer seems to be based on this chart.
    http://en.wikipedia.org/wiki/File:Cancer_smoking_lung_cancer_correlation_from_NIH.svg

    The chart compares apples to oranges.
    The chart gives NO indication of the male smoking rates.
    As shown in previous posts, the male smoking rate was relatively constant over the period of time that lung cancer rates increased greatly.

    Besides the graphs are actually not the same.
    Consumption increased from about 800 to 4,200 and that is a slope of about 1 to 5.
    Lung cancer deaths increased from about 10 to 170 and that is a slope of about 1 to 17.

    Lung cancer deaths increased at a rate that is 3 times as great as the increase in consumption!!!

    Besides, male lung cancer deaths have NEVER gotten anywhere near the 170/100,000 the chart indicates.

  32. Then again, how much can we trust any of the so-called scientific ‘evidence’…..http://www.clinicalpsychology.net/bad-science/

  33. DOES SMOKING KILL WORKERS OR WORKING KILL SMOKERS?

    THE MUTUAL RELATIONSHIP BETWEEN SMOKING, OCCUPATION AND RESPIRATORY DISEASE

    Theodor D. Sterling, Ph.D. – Simon Fraser University, Canada, April 1977

    http://legacy.library.ucsf.edu/tid/czd3aa00/pdf

    “As the proportion of all cancer deaths among smokers and non-smoking asbestos workers is identical, and as smoking asbestos workers have a much higher proportion of deaths from lung cancer than non-smoking asbestos workers, it follows that the proportion of deaths from other cancer among non-smoking asbestos workers is higher than that of smoking asbestos workers.

    Indeed we can see this in the upper right and lower left parts of Figure 1: The proportion of death from mesothelloma and from cancer of all “other sites” is much higher among non-smoking than among smoking asbestos workers.

    How can we interpret such peculiar findings? Is it possible that smoking protects asbestos workers against mesothileoma or against cancer of any other site except the lung? Obviously as the proportions of deaths from cancer among smoking and non-smoking asbestos workers are the same, there is something peculiar about the excess death due to lung cancer among smoking asbestos workers.

    We suggest the obvious interpretation that the diagnosing physician knowing of the smoking habits of an asbestos worker, will diagnose a primary lung cancer-if the worker smokes, but will make a more thorough examination as to the source of cancer when the asbestos worker does not smoke. Also, because the conviction is so strong that smoking is the cause of lung cancer, non-smoking asbestos workers may be diagnosed as having primary cancer from some site other than the lung, in line with prevailing opinions.”
    ….
    “Smoking appears to have been used to divert attention away from the effects of occupational and of environmental exposures. We need to ask the very serious question of whether or not the evidence relating smoking to disease is really acceptable without a thorough re-evaluation of this evidence with respect to the effect of occupation.

    In this connection, we point out that new as well as old studies on smoking and health continue to ignore occupation. A new study from Sweden which did collect information on occupations never bothered to produce an analysis of its effects. Also a recent claim by Dr. Hammond needs to be clarified that he has examined and not found an effect of occupation in his data.

    It is of the greatest importance in this connection that to our knowledge not one Cancer Registry in Canada and the U.S. bothers to determine the occupation of lung or other cancer cases although information on smoking always is included. In this way the effects of occupation on lung disease vis a vis that of smoking may continue to be denied simply because information on occupation is neglected.”

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