Chris Snowdon, author of Velvet Glove, Iron Fist, kicks off the Colloquium About The Cigarette Hypothesis:.
Smoking and lung cancer: The case for the prosecution
I’m as interested as anyone to see what crops up in this discussion. ‘Smoking causes lung cancer’ is regularly cited as one of the strongest findings in epidemiology, and so it is. It is certainly one of the most significant (in both the statistical and conventional sense).
Like most scientific findings, "the smoking theory" (as the tobacco industry used to call it) is taken on trust by those of us outside the field. I was not even born when most of the major studies were published. When writing Velvet Glove, Iron Fist, I sought out every study on secondhand smoke and lung cancer. I can’t say I did the same for primary smoking and lung cancer but I read enough for me to be satisfied that smoking raises the risk of lung cancer for a lifetime smoker by a magnitude of 10 to 20 (somewhat less for some ethnic groups, particularly East Asians).
For most of us, it is proven beyond any reasonable doubt, but that does not put it beyond debate. As long as there are people who question a claim, the debate is not over. Debate is healthy and necessary. Gallileo did not persuade people of his theory by calling them flat-earthers. Darwin did not persuaded people of his theories by calling them deniers. And so I am not going enter this debate by appealing to authority ("every expert agrees that…") or with weasel words ("everyone knows that…"). Nor do I need to. I believe the evidence speaks for itself.
A suitable place to kick things off is Austin Bradford Hill’s famous speech of 1965, which set out what was effectively a check-list of criteria to be met by epidemiologists before they cried "There! That’s the man!". Hill was the co-author of one of the earliest smoking-lung cancer studies in 1950, to which we will doubtless return, and he was acutely aware that statistical correlations were common, but genuine causative associations were not. I’d like to think that contemporary epidemiologists wake on Christmas Eve every year to see the ghost of Hill at the end of their bed, but they probably sleep like babies (the swine).
Anyway, here are his criteria and how they relate to smoking-lung cancer:
1. Strength: Hill gave the example of chimney sweeps and scrotal cancer which found a relative risk (RR) of 200 (ie. they were 200 times more likely to get this rare disease). Such a relative risk was so large that it required no epidemiological study. It was observable to the naked eye, as it were—as obvious as finding the association between mining and coughing, or being a woman and enjoying Sex in the City. The lung cancer-smoking link (from hereafter "the smoking theory" just to wind up any ASH supporters) is not quite as large as that—hardly any are—but it is generally in the region of 5 to 20, always greater than 2 to 3 and sometimes as high as 50. By any standard, this is a strong association.
2. Consistency: As Hill said: "Has it been repeatedly observed by different persons, in different places, circumstances and times?" Clearly the answer is yes. The smoking theory has been demonstrated again and again all over the world since the 1930s.
3. Specificity: In other words, does the disease only affect the exposed group? The fact that there is no malaria without mosquitoes supports the theory that mosquitoes spread malaria. Asbestosis is entirely specific to people who have been exposed to asbestos. Is there the same specificity with smoking and lung cancer? The answer is no. People developed lung cancer before smoking arrived in Europe and nonsmokers still get lung cancer in reasonably large numbers. Other factors are involved—other forms of smoke, radon and several other risk factors. But, as Hill said, people can get scrotal cancer without being chimney sweeps. He continued: "If other causes of death are raised 10, 20 or even 50% in smokers whereas cancer of the lung is raised 900 – 1000% we have specificity – a specificity in the magnitude of the association."
4. Temporality: In other words, cause and effect. Does smoking cause lung cancer or do smokers happen to be people who put themselves at risk of lung cancer more than nonsmokers. This is a valid question that less scrupulous epidemiologists fail to ask. We know today that smokers are more likely to be in lower socio-economic groups. This is a major confounding factor. The fact that lower socio-economic groups are also more likely to end up in prison and are more likely to have a baby die in the first 12 months of life does not prevent junk scientists claiming that secondhand smoke "causes" criminality or cot death. But these associations are very weak whereas the smoking theory is strong. If there was a more significant risk factor for lung cancer that it associated with smoking, but is not smoking, we need to hear what it is. The suggestions put forward—such as vehicle exhaust, asbestos exposure or pollution—are not specific enough to smokers to explain the statistical association between smoking and lung cancer.
5. Biological gradient: Does the risk rise with the number of cigarettes smoked or the number of years of smoking. With a very good degree of consistency, studies have shown the answer to be yes.
6. Plausibility: Is it plausible that filling the lungs with smoke over a hundred times a day could damage them? I would say so. If not that, then what? Sometimes I hear smokers’ rights people disputing the smoking theory while blaming car exhaust fumes. This seems to me to be inconsistent. Either breathing fumes, toxins and carcinogens into the lungs is dangerous or it is not. There is almost certainly a threshold below which the human body can filter and tolerate these fumes (which makes passive smoking and multiple chemical sensitivity less plausible as serious risks), but directly breathing smoke in must be well above that.
7. Coherence: Does it fit the overall pattern? Again, yes. The lung cancer rate rose first amongst men because they were the first to smoke and it rose later amongst women when they started to smoke. It is highest in regions and countries where people smoke and lowest where they do not. In Sweden, the use of snus has led to Europe’s lowest smoking rate and also the lowest lung cancer rate. Is there a more plausible explanation for this than that smoking causes lung cancer?
8. Experiment: This is the most difficult aspect of the smoking theory since lung cancer takes decades to develop and is therefore difficult to demonstrate in a laboratory experiment. Scientists have successfully made animals develop lung cancer by forcing them to smoke, and they have done the same by painting cigarette tar on mice. Does this prove the smoking theory? Not necessarily. The defence will say that the doses are unrealistically high. I have some sympathy with that view, but it certainly does not disprove the theory.
9. Analogy: "In some circumstances it would be fair to judge by analogy." I’ve never quite understood why this should be a scientific criterion so I’m going to ignore it, but if the defence wish to discuss it they should feel free.
This is my starting point. Crucially, why is the association so strong? If it is not smoking, then what? Why does the lung cancer epidemic follow in the footsteps of smoking in terms of location and gender? Or does it? Are we being sold a lemon? Over to you, the defence…
Frank Davis 
No smoking animal studies have produced lung cancer
Scientists have successfully made animals develop lung cancer by forcing them to smoke, and they have done the same by painting cigarette tar on mice.
I don’t think this is true. My understanding is that animals have only got lung cancer through painting, and never through smoking. A lot the studies were reviewed in the McTear case in 2005. In this there are numerous statements along the following lines:
and
and
All if which means that the case against tobacco rests entirely on epidemiological studies like thos of Doll and Hill, Wynder and Graham, etc.
No smoking animal studies have produced lung cancer
Scientists have successfully made animals develop lung cancer by forcing them to smoke, and they have done the same by painting cigarette tar on mice.
I don’t think this is true. My understanding is that animals have only got lung cancer through painting, and never through smoking. A lot the studies were reviewed in the McTear case in 2005. In this there are numerous statements along the following lines:
and
and
All if which means that the case against tobacco rests entirely on epidemiological studies like thos of Doll and Hill, Wynder and Graham, etc.
No smoking animal studies have produced lung cancer
Scientists have successfully made animals develop lung cancer by forcing them to smoke, and they have done the same by painting cigarette tar on mice.
I don’t think this is true. My understanding is that animals have only got lung cancer through painting, and never through smoking. A lot the studies were reviewed in the McTear case in 2005. In this there are numerous statements along the following lines:
and
and
All if which means that the case against tobacco rests entirely on epidemiological studies like thos of Doll and Hill, Wynder and Graham, etc.
Re: No smoking animal studies have produced lung cancer
I agree Frank but thought I would add a little more.
The McTear case was taken out by ASH and they employed the country’s top anti-smoking ‘experts’ such as James Friend and Richard Doll. Their barrister was Mr McEachran and the judge stated:
[6.150] Mr McEachran did not seek to argue that the causal connection between cigarette smoking and lung cancer had been established by any branch of scientific inquiry other than epidemiology. He accepted that it was established on the evidence that the process by which lung cancer developed was not yet known (see para.[6.30]). He also accepted in effect, at para.[6.56], that the averment for ITL at p.16 of the Closed Record was proved, “that over several decades, an enormous research effort has been made to produce in the laboratory the kind of lung cancer reported to be statistically associated with smoking. However, researchers have been unable to produce such cancer in test animals exposed to fresh whole smoke.”
See more on the judge’s summing up in [6.139], [6.151] and [6.153].
I also remember reading somewhere that Dr Elizabeth Whelan of ACSH had stated this as well but I can’t find it now.
Tony
Lung Cancer geographical distribution
It is highest in regions and countries where people smoke and lowest where they do not.
Consider the map below of lung cancer mortality in the USA, which shows the highest mortality in the south-eastern states.
Why is this? Is it because most of the smokers in America are concentrated in this area? I don’t think so (although I don’t have an equivalent map showing US tobacco consumption state by state, and county by county). I’d expect that tobacco consumption would be roughly even across the whole of the USA.
Note the hot spot in the south of Nevada, where most of the nuclear weapons testing was done. The prevailing wind is west to east, and so fallout from weapons tests would have been deposited to the east of Nevada, particularly in regions which have high rainfall. The rainfall map of the USA shows much higher rainfall in the eastern USA than over the Rockies in the west. Which has led me (and Fredrik Eich) to consider a variety of fallout hypotheses.
Lung Cancer geographical distribution
It is highest in regions and countries where people smoke and lowest where they do not.
Consider the map below of lung cancer mortality in the USA, which shows the highest mortality in the south-eastern states.
Why is this? Is it because most of the smokers in America are concentrated in this area? I don’t think so (although I don’t have an equivalent map showing US tobacco consumption state by state, and county by county). I’d expect that tobacco consumption would be roughly even across the whole of the USA.
Note the hot spot in the south of Nevada, where most of the nuclear weapons testing was done. The prevailing wind is west to east, and so fallout from weapons tests would have been deposited to the east of Nevada, particularly in regions which have high rainfall. The rainfall map of the USA shows much higher rainfall in the eastern USA than over the Rockies in the west. Which has led me (and Fredrik Eich) to consider a variety of fallout hypotheses.
Lung Cancer geographical distribution
It is highest in regions and countries where people smoke and lowest where they do not.
Consider the map below of lung cancer mortality in the USA, which shows the highest mortality in the south-eastern states.
Why is this? Is it because most of the smokers in America are concentrated in this area? I don’t think so (although I don’t have an equivalent map showing US tobacco consumption state by state, and county by county). I’d expect that tobacco consumption would be roughly even across the whole of the USA.
Note the hot spot in the south of Nevada, where most of the nuclear weapons testing was done. The prevailing wind is west to east, and so fallout from weapons tests would have been deposited to the east of Nevada, particularly in regions which have high rainfall. The rainfall map of the USA shows much higher rainfall in the eastern USA than over the Rockies in the west. Which has led me (and Fredrik Eich) to consider a variety of fallout hypotheses.
Re: Lung Cancer geographical distribution
Here is a night map
http://www.worldmapsonline.com/SatPosters/NorthAmericaNight.htm for comparison
Fredrik
The Debate
I think that it would not be a good thing, at this stage of the debate, to ‘pick holes’ in the tapestry of the argument. But it may be reasonable to ask for clarification
My concern is Snowden’s statement (in sentence two) that he has read enough “..for me to be satisfied that smoking raises the risk of lung cancer for a lifetime smoker by a magnitude of 10 to 20 (somewhat less for some ethnic groups, particularly East Asians)”.
As I understand it, an ‘order of magnitude’ is a very big quantity. For example, if we take some number, say 10, and increase it by ‘one order of magnitude’, we must square the number 10. Thus, the number 10, increased by ‘one order of magnitude’ becomes 10 times 10, which equals 100. If we increase the number 10 by ‘two orders of magnitude’, we have 10 times 10 times 10, which equals 1000.
Thus, when Snowden says that the risk (of developing lung cancer from smoking) is increased by an ‘order of magnitude’ in the region of 10 to 20, he is saying that the risk increases by between 10 to the power of 10, and/or 10 to the power of 20. 10 to the power of 10 equals 10 000 000 000.
Obviously, I must be wrong in my understanding of the meaning of the phrase ‘orders of magnitude’ – but I have seen this ‘exaggeration’ before. I saw it in an argument between Dave Atherton and Professor Repace on the British Medical Journal site. Prof Repace claimed ‘2 or 3 orders of magnitude’ for ‘passive smoking risk’. Erm…No….one ‘order of magnitude’ is huge, two ‘orders of magnitude’ is enormous.
In my response to Prof Repace’s claim of ‘2 or 3 orders of magnitude’, I suggested the following thought experiment. Let us consider a horse race. Almost always, one horse comes first. Let us call that ‘magnitude one’. But, occasionally, there is a dead heat between two horses. Let us call that ‘magnitude two’ (note that the number of horses in the race is irrelevant at this time). Now, let us progress in our imagination to a dead heat of three horses. that is ‘magnitude three’. We must now ask the question, ‘how often do three horses in a race arrive at a dead heat’? Answer? Very, very rare. But we must go on. We must ask how often do FOUR horses arrive at the finishing line in a dead heat? And, obviously, you could go on to five horses or six horses or seven horses, all arriving at the finishing line in a dead heat.
I think that the above reasonably illustrates the real meaning of the idea of ‘orders of magnitude’.
Needless to say, Prof Repace did not respond to either Dave Atherton’s more erudite submissions or my silly examples.
It is very important to us all that phrases such as ‘orders of magnitude’ should be clearly explained. If they are not, then we will all continue to mess around in the dark.
The Debate
I think that it would not be a good thing, at this stage of the debate, to ‘pick holes’ in the tapestry of the argument. But it may be reasonable to ask for clarification
My concern is Snowden’s statement (in sentence two) that he has read enough “..for me to be satisfied that smoking raises the risk of lung cancer for a lifetime smoker by a magnitude of 10 to 20 (somewhat less for some ethnic groups, particularly East Asians)”.
As I understand it, an ‘order of magnitude’ is a very big quantity. For example, if we take some number, say 10, and increase it by ‘one order of magnitude’, we must square the number 10. Thus, the number 10, increased by ‘one order of magnitude’ becomes 10 times 10, which equals 100. If we increase the number 10 by ‘two orders of magnitude’, we have 10 times 10 times 10, which equals 1000.
Thus, when Snowden says that the risk (of developing lung cancer from smoking) is increased by an ‘order of magnitude’ in the region of 10 to 20, he is saying that the risk increases by between 10 to the power of 10, and/or 10 to the power of 20. 10 to the power of 10 equals 10 000 000 000.
Obviously, I must be wrong in my understanding of the meaning of the phrase ‘orders of magnitude’ – but I have seen this ‘exaggeration’ before. I saw it in an argument between Dave Atherton and Professor Repace on the British Medical Journal site. Prof Repace claimed ‘2 or 3 orders of magnitude’ for ‘passive smoking risk’. Erm…No….one ‘order of magnitude’ is huge, two ‘orders of magnitude’ is enormous.
In my response to Prof Repace’s claim of ‘2 or 3 orders of magnitude’, I suggested the following thought experiment. Let us consider a horse race. Almost always, one horse comes first. Let us call that ‘magnitude one’. But, occasionally, there is a dead heat between two horses. Let us call that ‘magnitude two’ (note that the number of horses in the race is irrelevant at this time). Now, let us progress in our imagination to a dead heat of three horses. that is ‘magnitude three’. We must now ask the question, ‘how often do three horses in a race arrive at a dead heat’? Answer? Very, very rare. But we must go on. We must ask how often do FOUR horses arrive at the finishing line in a dead heat? And, obviously, you could go on to five horses or six horses or seven horses, all arriving at the finishing line in a dead heat.
I think that the above reasonably illustrates the real meaning of the idea of ‘orders of magnitude’.
Needless to say, Prof Repace did not respond to either Dave Atherton’s more erudite submissions or my silly examples.
It is very important to us all that phrases such as ‘orders of magnitude’ should be clearly explained. If they are not, then we will all continue to mess around in the dark.
The Debate
I think that it would not be a good thing, at this stage of the debate, to ‘pick holes’ in the tapestry of the argument. But it may be reasonable to ask for clarification
My concern is Snowden’s statement (in sentence two) that he has read enough “..for me to be satisfied that smoking raises the risk of lung cancer for a lifetime smoker by a magnitude of 10 to 20 (somewhat less for some ethnic groups, particularly East Asians)”.
As I understand it, an ‘order of magnitude’ is a very big quantity. For example, if we take some number, say 10, and increase it by ‘one order of magnitude’, we must square the number 10. Thus, the number 10, increased by ‘one order of magnitude’ becomes 10 times 10, which equals 100. If we increase the number 10 by ‘two orders of magnitude’, we have 10 times 10 times 10, which equals 1000.
Thus, when Snowden says that the risk (of developing lung cancer from smoking) is increased by an ‘order of magnitude’ in the region of 10 to 20, he is saying that the risk increases by between 10 to the power of 10, and/or 10 to the power of 20. 10 to the power of 10 equals 10 000 000 000.
Obviously, I must be wrong in my understanding of the meaning of the phrase ‘orders of magnitude’ – but I have seen this ‘exaggeration’ before. I saw it in an argument between Dave Atherton and Professor Repace on the British Medical Journal site. Prof Repace claimed ‘2 or 3 orders of magnitude’ for ‘passive smoking risk’. Erm…No….one ‘order of magnitude’ is huge, two ‘orders of magnitude’ is enormous.
In my response to Prof Repace’s claim of ‘2 or 3 orders of magnitude’, I suggested the following thought experiment. Let us consider a horse race. Almost always, one horse comes first. Let us call that ‘magnitude one’. But, occasionally, there is a dead heat between two horses. Let us call that ‘magnitude two’ (note that the number of horses in the race is irrelevant at this time). Now, let us progress in our imagination to a dead heat of three horses. that is ‘magnitude three’. We must now ask the question, ‘how often do three horses in a race arrive at a dead heat’? Answer? Very, very rare. But we must go on. We must ask how often do FOUR horses arrive at the finishing line in a dead heat? And, obviously, you could go on to five horses or six horses or seven horses, all arriving at the finishing line in a dead heat.
I think that the above reasonably illustrates the real meaning of the idea of ‘orders of magnitude’.
Needless to say, Prof Repace did not respond to either Dave Atherton’s more erudite submissions or my silly examples.
It is very important to us all that phrases such as ‘orders of magnitude’ should be clearly explained. If they are not, then we will all continue to mess around in the dark.
Re: The Debate
As I understand it, an ‘order of magnitude’ is a very big quantity. For example, if we take some number, say 10, and increase it by ‘one order of magnitude’, we must square the number 10.
I think you’ve got it wrong. An “order of magnitude”, in my understanding, is a factor of 10. So 100 is an order of magnitude larger than 10, and 1000 is an order of magnitude bigger than 100, and so on.
Chris Snowdon is anyway not talking about an order of magnitude, but a magnitude (a “greatness”) of 10 or 20. That means 10 times or 20 times. A magnitude is not the same as an order of magnitude.
OT, but I loved this remark by Dr Ian Dunbar:
Ian Dunbar: Has anyone else noticed that smokers are thinkers while non-smokers are merely dreamers?
OT, but I loved this remark by Dr Ian Dunbar:
Ian Dunbar: Has anyone else noticed that smokers are thinkers while non-smokers are merely dreamers?
OT, but I loved this remark by Dr Ian Dunbar:
Ian Dunbar: Has anyone else noticed that smokers are thinkers while non-smokers are merely dreamers?
Re: The Debate
As I understand it, an ‘order of magnitude’ is a very big quantity. For example, if we take some number, say 10, and increase it by ‘one order of magnitude’, we must square the number 10.
I think you’ve got it wrong. An “order of magnitude”, in my understanding, is a factor of 10. So 100 is an order of magnitude larger than 10, and 1000 is an order of magnitude bigger than 100, and so on.
Chris Snowdon is anyway not talking about an order of magnitude, but a magnitude (a “greatness”) of 10 or 20. That means 10 times or 20 times. A magnitude is not the same as an order of magnitude.
Re: The Debate
As I understand it, an ‘order of magnitude’ is a very big quantity. For example, if we take some number, say 10, and increase it by ‘one order of magnitude’, we must square the number 10.
I think you’ve got it wrong. An “order of magnitude”, in my understanding, is a factor of 10. So 100 is an order of magnitude larger than 10, and 1000 is an order of magnitude bigger than 100, and so on.
Chris Snowdon is anyway not talking about an order of magnitude, but a magnitude (a “greatness”) of 10 or 20. That means 10 times or 20 times. A magnitude is not the same as an order of magnitude.
@frank yes, im curious about nuclear fallout as well.
Also, I’m wondering about the possible connections between cremations (introduced ±1870), and the use of mercury fillings (introduced ±1840).
I mean, we do know mercury is not good for us, surely all those cremated dental fillings released into the air must have had some effect? On a side note this seems to go well with fredriks connection between water/cancer (eg. mercury build-up in fish?)
btw, still very excited by you guys doing this project :)
@frank yes, im curious about nuclear fallout as well.
Also, I’m wondering about the possible connections between cremations (introduced ±1870), and the use of mercury fillings (introduced ±1840).
I mean, we do know mercury is not good for us, surely all those cremated dental fillings released into the air must have had some effect? On a side note this seems to go well with fredriks connection between water/cancer (eg. mercury build-up in fish?)
btw, still very excited by you guys doing this project :)
@frank yes, im curious about nuclear fallout as well.
Also, I’m wondering about the possible connections between cremations (introduced ±1870), and the use of mercury fillings (introduced ±1840).
I mean, we do know mercury is not good for us, surely all those cremated dental fillings released into the air must have had some effect? On a side note this seems to go well with fredriks connection between water/cancer (eg. mercury build-up in fish?)
btw, still very excited by you guys doing this project :)
On the color map of the US – on the State of California there is a big red spot east where Sacramento and Central Valley is located which is to the right of the big blue spot where is San Francisco. San Francisco is constantly refreshed by never-ending ocean breeze blowing inward from west to east and all the smog from San Francisco to East Bay to Silicon Valley to the south is all blown eastward, eventually into Central Valley and Sacramento.
Furthermore, Sacramento is a high densely populated area in the middle of what is California’s agricultural region – and Sacramento is well known for being the most horrible allergy spot in the state because of all the rich pollen that settles over everything.
Everything from the west heads due east, Central Valley and Sacramento heats up and the air stiffles, to the east of that is the Sierra Mountain range extending some 10,000 to 14,000 feet high and keeping everything already settled in Sacramento from blowing much further eastward and so Central Valley is eventually where everything airborne just stops.
And no SHS ever blows from SF into Sacramento – because SF has effectly made smoking illegal, indoors and out. So it’s nothing to do with SHS blowing that far.
So I would suggest that maybe the heavily motoring public of the SF Bay area having their pollution all blown over into Sacramento and Central Valley along with the higher than normal pollen count out there might have something to do with that big red spot being on Sacramento – and red because it’s also a highly populated area, more so than any other smaller cities in Central Valley.
About magnitudes of greatness – in California we get earthquakes and they are measured using the Richter scale. On the Richter scale, each “magnitude of greatness” is an increase by the exponential raising to the power of 10.
Thus an EQ of magnitude 5 is 10x more shaking than one of magnitude 4. An EQ of magnitude 10 would be 10^5 (ten raised to the power of five) or 10x10x10x10x10 or 100,000 more ground movement than one of magnitude 5.
But out here, when one talks about “magnitude of greatness” one usually is refering to the number of times to which 10 is raised as an exponent.
On the color map of the US – on the State of California there is a big red spot east where Sacramento and Central Valley is located which is to the right of the big blue spot where is San Francisco. San Francisco is constantly refreshed by never-ending ocean breeze blowing inward from west to east and all the smog from San Francisco to East Bay to Silicon Valley to the south is all blown eastward, eventually into Central Valley and Sacramento.
Furthermore, Sacramento is a high densely populated area in the middle of what is California’s agricultural region – and Sacramento is well known for being the most horrible allergy spot in the state because of all the rich pollen that settles over everything.
Everything from the west heads due east, Central Valley and Sacramento heats up and the air stiffles, to the east of that is the Sierra Mountain range extending some 10,000 to 14,000 feet high and keeping everything already settled in Sacramento from blowing much further eastward and so Central Valley is eventually where everything airborne just stops.
And no SHS ever blows from SF into Sacramento – because SF has effectly made smoking illegal, indoors and out. So it’s nothing to do with SHS blowing that far.
So I would suggest that maybe the heavily motoring public of the SF Bay area having their pollution all blown over into Sacramento and Central Valley along with the higher than normal pollen count out there might have something to do with that big red spot being on Sacramento – and red because it’s also a highly populated area, more so than any other smaller cities in Central Valley.
About magnitudes of greatness – in California we get earthquakes and they are measured using the Richter scale. On the Richter scale, each “magnitude of greatness” is an increase by the exponential raising to the power of 10.
Thus an EQ of magnitude 5 is 10x more shaking than one of magnitude 4. An EQ of magnitude 10 would be 10^5 (ten raised to the power of five) or 10x10x10x10x10 or 100,000 more ground movement than one of magnitude 5.
But out here, when one talks about “magnitude of greatness” one usually is refering to the number of times to which 10 is raised as an exponent.
On the color map of the US – on the State of California there is a big red spot east where Sacramento and Central Valley is located which is to the right of the big blue spot where is San Francisco. San Francisco is constantly refreshed by never-ending ocean breeze blowing inward from west to east and all the smog from San Francisco to East Bay to Silicon Valley to the south is all blown eastward, eventually into Central Valley and Sacramento.
Furthermore, Sacramento is a high densely populated area in the middle of what is California’s agricultural region – and Sacramento is well known for being the most horrible allergy spot in the state because of all the rich pollen that settles over everything.
Everything from the west heads due east, Central Valley and Sacramento heats up and the air stiffles, to the east of that is the Sierra Mountain range extending some 10,000 to 14,000 feet high and keeping everything already settled in Sacramento from blowing much further eastward and so Central Valley is eventually where everything airborne just stops.
And no SHS ever blows from SF into Sacramento – because SF has effectly made smoking illegal, indoors and out. So it’s nothing to do with SHS blowing that far.
So I would suggest that maybe the heavily motoring public of the SF Bay area having their pollution all blown over into Sacramento and Central Valley along with the higher than normal pollen count out there might have something to do with that big red spot being on Sacramento – and red because it’s also a highly populated area, more so than any other smaller cities in Central Valley.
About magnitudes of greatness – in California we get earthquakes and they are measured using the Richter scale. On the Richter scale, each “magnitude of greatness” is an increase by the exponential raising to the power of 10.
Thus an EQ of magnitude 5 is 10x more shaking than one of magnitude 4. An EQ of magnitude 10 would be 10^5 (ten raised to the power of five) or 10x10x10x10x10 or 100,000 more ground movement than one of magnitude 5.
But out here, when one talks about “magnitude of greatness” one usually is refering to the number of times to which 10 is raised as an exponent.
question for Chris
How does one explain that the type of lung cancer have changed over the last 3 decades from squamous cell cancer to adenocarcinoma cancer.
One theory that I have read is that because of the filter being added to the cigarette allowing the person to inhale deeper. This theory has also been applied to users of very low yield cigarettes who tend to compensate for the lower nicotine levels by inhaling more deeply and frequently.
And if that is so why would non smokers also have higher rates of adenocarcinoma?
question for Chris
How does one explain that the type of lung cancer have changed over the last 3 decades from squamous cell cancer to adenocarcinoma cancer.
One theory that I have read is that because of the filter being added to the cigarette allowing the person to inhale deeper. This theory has also been applied to users of very low yield cigarettes who tend to compensate for the lower nicotine levels by inhaling more deeply and frequently.
And if that is so why would non smokers also have higher rates of adenocarcinoma?
question for Chris
How does one explain that the type of lung cancer have changed over the last 3 decades from squamous cell cancer to adenocarcinoma cancer.
One theory that I have read is that because of the filter being added to the cigarette allowing the person to inhale deeper. This theory has also been applied to users of very low yield cigarettes who tend to compensate for the lower nicotine levels by inhaling more deeply and frequently.
And if that is so why would non smokers also have higher rates of adenocarcinoma?
Regarding these Maps
A couple of years ago, I spent some time pouring over US statistical maps in relation to this topic. In the end, I concluded that, despite how handy and appealing they seem, they are probably more misleading than they are useful.
Look at the Central U.S. or the “midwest”. I’ve noticed that on almost any U.S. statistical distribution map one might look at it, this area of the U.S. is almost always untouched and pristine. Consider that about 1.8 million live in the State of Nebraska and and about 2.8 million live in the State of Kansas. Now, consider that 8 million people live in the very small area at the bottom of a New York map, representing the area of New York City alone. Approximately TWICE the amount of people lived in the cramped space of New York City as live in the central US States of Kansas, Nebraska, South Dakota, and North Dakota COMBINED.
Collecting data on a per 100,000 basis in New York City represents a few city blocks. In more rural states, it means collecting data from several counties with a population spread very far apart.
This fact alone represents myriad challenges to collecting consistent statistical data across populations in a country as large and diverse as the US, especially if the statistics are based on a per 100,000 population basis.
If the data is collected in New York City, for instance, a researcher might visit a hospital that’s had well over 100,000 actual patients in the past year, nonetheless millions of potential patients. The majority of the patients come from within a radius of few miles. This makes for a one-stop source for data on a per 100,000 population basis.
Meanwhile, a researcher in Kansas might have to visit several hospitals, all of which likely interpret their data collection responsibilities differently, to get results representing a population of 100,000. Everything is different, really, from the sophistication of the hospitals to prevailing regional differences.
Even if the data collection methods don’t involve hospitals at all, similar challenges remain.
There’s no consistency at all, really, because there can’t be. There’s simply too much to consider.
Otherwise, it means that if we all want to be safe from from everything, then we should all take up residence in Kansas. Meanwhile, no offense to any Kansans, but most Americans don’t consider moving to Kansas to be an exciting prospect. If they did, the population of that state would be much greater.
-WS
Regarding these Maps
A couple of years ago, I spent some time pouring over US statistical maps in relation to this topic. In the end, I concluded that, despite how handy and appealing they seem, they are probably more misleading than they are useful.
Look at the Central U.S. or the “midwest”. I’ve noticed that on almost any U.S. statistical distribution map one might look at it, this area of the U.S. is almost always untouched and pristine. Consider that about 1.8 million live in the State of Nebraska and and about 2.8 million live in the State of Kansas. Now, consider that 8 million people live in the very small area at the bottom of a New York map, representing the area of New York City alone. Approximately TWICE the amount of people lived in the cramped space of New York City as live in the central US States of Kansas, Nebraska, South Dakota, and North Dakota COMBINED.
Collecting data on a per 100,000 basis in New York City represents a few city blocks. In more rural states, it means collecting data from several counties with a population spread very far apart.
This fact alone represents myriad challenges to collecting consistent statistical data across populations in a country as large and diverse as the US, especially if the statistics are based on a per 100,000 population basis.
If the data is collected in New York City, for instance, a researcher might visit a hospital that’s had well over 100,000 actual patients in the past year, nonetheless millions of potential patients. The majority of the patients come from within a radius of few miles. This makes for a one-stop source for data on a per 100,000 population basis.
Meanwhile, a researcher in Kansas might have to visit several hospitals, all of which likely interpret their data collection responsibilities differently, to get results representing a population of 100,000. Everything is different, really, from the sophistication of the hospitals to prevailing regional differences.
Even if the data collection methods don’t involve hospitals at all, similar challenges remain.
There’s no consistency at all, really, because there can’t be. There’s simply too much to consider.
Otherwise, it means that if we all want to be safe from from everything, then we should all take up residence in Kansas. Meanwhile, no offense to any Kansans, but most Americans don’t consider moving to Kansas to be an exciting prospect. If they did, the population of that state would be much greater.
-WS
Regarding these Maps
A couple of years ago, I spent some time pouring over US statistical maps in relation to this topic. In the end, I concluded that, despite how handy and appealing they seem, they are probably more misleading than they are useful.
Look at the Central U.S. or the “midwest”. I’ve noticed that on almost any U.S. statistical distribution map one might look at it, this area of the U.S. is almost always untouched and pristine. Consider that about 1.8 million live in the State of Nebraska and and about 2.8 million live in the State of Kansas. Now, consider that 8 million people live in the very small area at the bottom of a New York map, representing the area of New York City alone. Approximately TWICE the amount of people lived in the cramped space of New York City as live in the central US States of Kansas, Nebraska, South Dakota, and North Dakota COMBINED.
Collecting data on a per 100,000 basis in New York City represents a few city blocks. In more rural states, it means collecting data from several counties with a population spread very far apart.
This fact alone represents myriad challenges to collecting consistent statistical data across populations in a country as large and diverse as the US, especially if the statistics are based on a per 100,000 population basis.
If the data is collected in New York City, for instance, a researcher might visit a hospital that’s had well over 100,000 actual patients in the past year, nonetheless millions of potential patients. The majority of the patients come from within a radius of few miles. This makes for a one-stop source for data on a per 100,000 population basis.
Meanwhile, a researcher in Kansas might have to visit several hospitals, all of which likely interpret their data collection responsibilities differently, to get results representing a population of 100,000. Everything is different, really, from the sophistication of the hospitals to prevailing regional differences.
Even if the data collection methods don’t involve hospitals at all, similar challenges remain.
There’s no consistency at all, really, because there can’t be. There’s simply too much to consider.
Otherwise, it means that if we all want to be safe from from everything, then we should all take up residence in Kansas. Meanwhile, no offense to any Kansans, but most Americans don’t consider moving to Kansas to be an exciting prospect. If they did, the population of that state would be much greater.
-WS
Re: Regarding these Maps
I agree that data collection methods probably differ from state to state, and that affects the figures.
Also, since this is a map of mortality, rather than incidence, it may be that in some states people get better treatment for cancer than in others. Or (because it’s the USA) in some states more people have health insurance than in others, so that poorer states have higher mortality.
But the much higher population densities and better hospitals in NY would seem to me to suggest that the lung cancer mortality is measured more accurately there.
It’s a bit like weather stations across the USA. There are probably lots more of them in NY than in Oklahoma. That should mean that NY figures are more accurate, not that they’re distorted (leaving aside urban heat island effects).
Frank
Re: Regarding these Maps
One might also super-impose other maps upon this map, maps showing all sorts of situations particular to the entire US, including location of nuclear power plants. On the map above showing the US, the comment about Sacramento east of San Francisco receiving all their smog from auto and diesel exhaust could also have said that Sacramento was home to a large nuclear power generating facility at one time, that has since been shut down, but operated for decades, a power plant that was similar to the one operating at Three Mile Island in the eastern US. If one is going to correlate cause and effect using statistics, then two maps superimposed could say increase in lung cancer is correlated (or not) with proximity of nuclear power plants having operated in the same area and come up with the same conclusions as automatically pronounced against tobacco usage as it’s really just the same conjecture.
Re: Regarding these Maps
“But the much higher population densities and better hospitals in NY would seem to me to suggest that the lung cancer mortality is measured more accurately there.”
Yes, I would agree. That’s why I’m skeptical that central states always seem to be less affected when one looks at almost any per 100,000 analysis. Not only in health statistics, but in employment and economic analysis as well. Then again, perhaps it just seems that way to me.
-WS
The Debate
OK, Frank.
First, can I say that I refer to Chris Snowden as ‘Snowden’ only to reduce the number of characters – just as I would say ‘Cameron’ rather that ‘Dave Cameron’. Can I also say that I accept that Snowden did not mean ‘orders of magnitude’ but meant ‘multiples’ – in the sense of ‘multiplied by two, or three’ rather than ‘squared’ and ‘cubed’.
But we can see, can we not, how phrases which the common man is not familiar with, can be used to exaggerate? NB I am not saying that Snowden has deliberately done any such thing!
May I suggest something?
The essentials of ‘a debate’ are that the ‘proposer’ makes a statement. In this case, the subject of our debate is, “that smokng causes lung cancer”, and so Swowden makes an argument that this is so.
The second phase is that the ‘opposer’ makes his statement. In this particular case, ‘Davis’ outlines the reasons that smoking is not the cause of lung cancer. Subsequent speakers, on each side, expand upon the argument that the principal speaker outlined.
Frank, in the nature of DEBATE, you should not have ‘replied’ to Snowden’s arguments – that must come later.
Today, Snowden has made his opening statement. Commenters, such as myself, have queried Snowden’s assumptions. But you must have arguments which show that smoking IS NOT the cause of lung cancer and, if possible, show that smoking CANNOT be the cause of lung cancer.
Tomorrow, Davis, make your opening statement.
Finally, I do not agree that it is impossible to prove a negative, although I do not quite understand as yet how this appertains to smoking. May I give an example?
Suppose that a person said that, in the last war, the Germans were preparing to invade England. How could one prove that it was not so – IE, prove that the Germans were NOT intent upon invading England. IE prove a negative. Well, it is quite simple, is it not? Just send out a couple of planes and see what is happening on the French coast. If there are no troops massing and no boats massing, then there is invasion imminent.
Thus, it is possible to prove, by virtue of THE LACK OF lung cancer deaths among smokers who have died over the years, that there is no certainty or direct cause,
We have only just started. every facet of smoking/lung cancer must be examined carefully.
I am sorry that my arguments are a bit disjointed. I hope that the essence is sufficiently clear.
The Debate
OK, Frank.
First, can I say that I refer to Chris Snowden as ‘Snowden’ only to reduce the number of characters – just as I would say ‘Cameron’ rather that ‘Dave Cameron’. Can I also say that I accept that Snowden did not mean ‘orders of magnitude’ but meant ‘multiples’ – in the sense of ‘multiplied by two, or three’ rather than ‘squared’ and ‘cubed’.
But we can see, can we not, how phrases which the common man is not familiar with, can be used to exaggerate? NB I am not saying that Snowden has deliberately done any such thing!
May I suggest something?
The essentials of ‘a debate’ are that the ‘proposer’ makes a statement. In this case, the subject of our debate is, “that smokng causes lung cancer”, and so Swowden makes an argument that this is so.
The second phase is that the ‘opposer’ makes his statement. In this particular case, ‘Davis’ outlines the reasons that smoking is not the cause of lung cancer. Subsequent speakers, on each side, expand upon the argument that the principal speaker outlined.
Frank, in the nature of DEBATE, you should not have ‘replied’ to Snowden’s arguments – that must come later.
Today, Snowden has made his opening statement. Commenters, such as myself, have queried Snowden’s assumptions. But you must have arguments which show that smoking IS NOT the cause of lung cancer and, if possible, show that smoking CANNOT be the cause of lung cancer.
Tomorrow, Davis, make your opening statement.
Finally, I do not agree that it is impossible to prove a negative, although I do not quite understand as yet how this appertains to smoking. May I give an example?
Suppose that a person said that, in the last war, the Germans were preparing to invade England. How could one prove that it was not so – IE, prove that the Germans were NOT intent upon invading England. IE prove a negative. Well, it is quite simple, is it not? Just send out a couple of planes and see what is happening on the French coast. If there are no troops massing and no boats massing, then there is invasion imminent.
Thus, it is possible to prove, by virtue of THE LACK OF lung cancer deaths among smokers who have died over the years, that there is no certainty or direct cause,
We have only just started. every facet of smoking/lung cancer must be examined carefully.
I am sorry that my arguments are a bit disjointed. I hope that the essence is sufficiently clear.
The Debate
OK, Frank.
First, can I say that I refer to Chris Snowden as ‘Snowden’ only to reduce the number of characters – just as I would say ‘Cameron’ rather that ‘Dave Cameron’. Can I also say that I accept that Snowden did not mean ‘orders of magnitude’ but meant ‘multiples’ – in the sense of ‘multiplied by two, or three’ rather than ‘squared’ and ‘cubed’.
But we can see, can we not, how phrases which the common man is not familiar with, can be used to exaggerate? NB I am not saying that Snowden has deliberately done any such thing!
May I suggest something?
The essentials of ‘a debate’ are that the ‘proposer’ makes a statement. In this case, the subject of our debate is, “that smokng causes lung cancer”, and so Swowden makes an argument that this is so.
The second phase is that the ‘opposer’ makes his statement. In this particular case, ‘Davis’ outlines the reasons that smoking is not the cause of lung cancer. Subsequent speakers, on each side, expand upon the argument that the principal speaker outlined.
Frank, in the nature of DEBATE, you should not have ‘replied’ to Snowden’s arguments – that must come later.
Today, Snowden has made his opening statement. Commenters, such as myself, have queried Snowden’s assumptions. But you must have arguments which show that smoking IS NOT the cause of lung cancer and, if possible, show that smoking CANNOT be the cause of lung cancer.
Tomorrow, Davis, make your opening statement.
Finally, I do not agree that it is impossible to prove a negative, although I do not quite understand as yet how this appertains to smoking. May I give an example?
Suppose that a person said that, in the last war, the Germans were preparing to invade England. How could one prove that it was not so – IE, prove that the Germans were NOT intent upon invading England. IE prove a negative. Well, it is quite simple, is it not? Just send out a couple of planes and see what is happening on the French coast. If there are no troops massing and no boats massing, then there is invasion imminent.
Thus, it is possible to prove, by virtue of THE LACK OF lung cancer deaths among smokers who have died over the years, that there is no certainty or direct cause,
We have only just started. every facet of smoking/lung cancer must be examined carefully.
I am sorry that my arguments are a bit disjointed. I hope that the essence is sufficiently clear.
Re: The Debate
I’m sorry, but where did I pick you up for calling him Snowden? I don’t remember doing that. My only comment in response to you has been about the order of magnitude business.
As for the structure of the debate, I do have a response in preparation, but along quite different lines than my comments above. My remarks above about animal studies, and geographic distributions of lung cancer, would not have been contained in that response. So I thought I’d raise them from the floor. I don’t see any particular reason why myself, or Chris Snowdon, or Rich White, or other contributors (e.g. Phil Button) shouldn’t post comments as well as more formal arguments.
The idea, as I see it, is to air a few arguments, not to stick to some sort of rigid format. After all, in setting out the ‘terms and conditions’ in the previous post, I left things very loose. I did this so as to allow the discussion to develop as it may, playing it by ear.
Next up, anyway, will be Rich White. I’ll probably come in after that.
Frank
I would be interested if there has been a change in the manufacture of cigarettes from the 1950’s or earlier to the present day. Many people seem to remember there grandparents smoking Senior Service and Players and living to a ripe age.
I started on Woodbines and have recently gone back onto rolling tobacco due to ‘ready mades’ tasting strange.
I also seem not alone in noticing that in my own small group of colleagues two have sadly died of cancer and both life time non smokers.
I would be interested if there has been a change in the manufacture of cigarettes from the 1950’s or earlier to the present day. Many people seem to remember there grandparents smoking Senior Service and Players and living to a ripe age.
I started on Woodbines and have recently gone back onto rolling tobacco due to ‘ready mades’ tasting strange.
I also seem not alone in noticing that in my own small group of colleagues two have sadly died of cancer and both life time non smokers.
I would be interested if there has been a change in the manufacture of cigarettes from the 1950’s or earlier to the present day. Many people seem to remember there grandparents smoking Senior Service and Players and living to a ripe age.
I started on Woodbines and have recently gone back onto rolling tobacco due to ‘ready mades’ tasting strange.
I also seem not alone in noticing that in my own small group of colleagues two have sadly died of cancer and both life time non smokers.
“Boyette said that before World War II wood was the preferred fuel for curing barns.
A wood fire burned just outside the barn. The heat and combustion gases flowed through a flue, usually made of brick, that snaked across the floor of the barn, then rose up through the barn. Because the gases moved through the flue, the tobacco was never exposed to them.
The barns were heated, and the tobacco cured, but the heat was indirect.”
“After World War II, Boyette added, tobacco growers began to switch from wood to fuel oil as a heating source, but they still used flues that carried the combustion gases through the barn.
Then, with the energy crisis of the early 1970s, growers began to switch to natural or propane gas, which was more readily available than fuel oil. Because gas burns so cleanly, growers were able to get rid of flues, and began using direct-fired barns.”
http://www.cals.ncsu.edu/agcomm/magazine/winter01/back.htm
What About Existing Diesel Burners??
“Large numbers of barns with fuel oil burners continue to be used to cure tobacco throughout the flue cured production area.”
“Original fuel oil heat exchanger models were not solid welded and have the potential for leaking combustion gases in the curing chamber. Current models are solid welded.”
http://www.cpes.peachnet.edu/tobacco/fueloil.htm
“One would have expected the results of such definitive experiments to have been published by 1957 or 1958, or by 1960 at the very latest.
Instead, publication of papers on the subject suddenly ceased; funds for research on the effects of diesel smoke were withdrawn; lawyers issued instructions on how to confuse a court should an action for damages be initiated; and articles on diesel fuel tended to have the unsupported statement “diesel smoke is harmless” as a frequent non sequitor.”
http://legacy.library.ucsf.edu/action/document/page;jsessionid=1A622975CD35D2F66C01526368B52B33?tid=yth67a99&page=17
An old retired US sailor once commented to me that his personal observation was that lung cancers didn’t start becoming prevalent until people stopped using sulfur matches and flint cigarette lighters and began using propane lighters to light cigarettes as their popularity and availability grew.
In the manufacture of cigarettes, stale cartons are sent back to the tobacco companies who credit the retailers for unsold goods – the filling inside those cigarettes are extracted, run through a slurry of chemicals of all sorts, sliced down into tiny bits and recombined with the fresh tobacco on the assembly line. Thus some brands (cheaper) are a high percentage of recombined chemically reconstituted unsold tobacco returned to the manufacturer while other brands (premium priced) have less of the recombined chemically treated filler and more genuine tobacco added to them.
Maybe all those chemicals from the reconstituted products makes a difference, especially after it’s been recycled over and over and over again – then it’s not even tobacco at some point but a chemical soup that is being manufactured.
Popular in some parts of the US these days is a wholly organic, non-chemically treated, tobacco cigarette product into which no reconstituted product is added, being marketed out of New Mexico by a company owned by RJ Reynolds, who is one of the major manufacturers over there, by the name of Spirit brand.
They never seem to ask smokers in these studies what brand of tobacco they habitually smoke (and most smokers do habitually smoke one brand).
And I’ve occasionally wondered whether the means of lighting a cigarette might be relevant. When I used matches, I’d quite often light a cigarette with the flaring ignition of whatever compound was on the end of the match, rather than wait for the match to be well alight. And I didn’t like what I was inhaling, because it left a nasty taste.
I suspect that gas lighters are probably the cleanest, in that the gas usually burns to produce CO2 and water. But before I used gas lighters, I’d use fuel lighters, which almost certainly produced a lot of combustion products.
What did they use before matches and lighters? Candles, probably, I imagine.
Frank
Frumusetea este promisiunea fericirii
Frumusetea este promisiunea fericirii
Frumusetea este promisiunea fericirii
Distribution map of smokers
There is a distribution map of smokers in the US here. Sorry I don’t know how to reproduce it on the page but it might be useful to someone. http://labs.slate.com/articles/cigarette-map/ (it seems to have been produced by a clinic)
Distribution map of smokers
There is a distribution map of smokers in the US here. Sorry I don’t know how to reproduce it on the page but it might be useful to someone. http://labs.slate.com/articles/cigarette-map/ (it seems to have been produced by a clinic)
Distribution map of smokers
There is a distribution map of smokers in the US here. Sorry I don’t know how to reproduce it on the page but it might be useful to someone. http://labs.slate.com/articles/cigarette-map/ (it seems to have been produced by a clinic)
Re: Distribution map of smokers
Thanks for that. I’d not seen it before. Unfortunately it’s for 2009. It would have been more interesting to see the distribution 50 years earlier.
Nevertheless, it’s fairly even, with a range from roughly 5% to 15% or so over the USA.
Frank
“Boyette said that before World War II wood was the preferred fuel for curing barns.
A wood fire burned just outside the barn. The heat and combustion gases flowed through a flue, usually made of brick, that snaked across the floor of the barn, then rose up through the barn. Because the gases moved through the flue, the tobacco was never exposed to them.
The barns were heated, and the tobacco cured, but the heat was indirect.”
“After World War II, Boyette added, tobacco growers began to switch from wood to fuel oil as a heating source, but they still used flues that carried the combustion gases through the barn.
Then, with the energy crisis of the early 1970s, growers began to switch to natural or propane gas, which was more readily available than fuel oil. Because gas burns so cleanly, growers were able to get rid of flues, and began using direct-fired barns.”
http://www.cals.ncsu.edu/agcomm/magazine/winter01/back.htm
What About Existing Diesel Burners??
“Large numbers of barns with fuel oil burners continue to be used to cure tobacco throughout the flue cured production area.”
“Original fuel oil heat exchanger models were not solid welded and have the potential for leaking combustion gases in the curing chamber. Current models are solid welded.”
http://www.cpes.peachnet.edu/tobacco/fueloil.htm
“One would have expected the results of such definitive experiments to have been published by 1957 or 1958, or by 1960 at the very latest.
Instead, publication of papers on the subject suddenly ceased; funds for research on the effects of diesel smoke were withdrawn; lawyers issued instructions on how to confuse a court should an action for damages be initiated; and articles on diesel fuel tended to have the unsupported statement “diesel smoke is harmless” as a frequent non sequitor.”
http://legacy.library.ucsf.edu/action/document/page;jsessionid=1A622975CD35D2F66C01526368B52B33?tid=yth67a99&page=17
“Boyette said that before World War II wood was the preferred fuel for curing barns.
A wood fire burned just outside the barn. The heat and combustion gases flowed through a flue, usually made of brick, that snaked across the floor of the barn, then rose up through the barn. Because the gases moved through the flue, the tobacco was never exposed to them.
The barns were heated, and the tobacco cured, but the heat was indirect.”
“After World War II, Boyette added, tobacco growers began to switch from wood to fuel oil as a heating source, but they still used flues that carried the combustion gases through the barn.
Then, with the energy crisis of the early 1970s, growers began to switch to natural or propane gas, which was more readily available than fuel oil. Because gas burns so cleanly, growers were able to get rid of flues, and began using direct-fired barns.”
http://www.cals.ncsu.edu/agcomm/magazine/winter01/back.htm
What About Existing Diesel Burners??
“Large numbers of barns with fuel oil burners continue to be used to cure tobacco throughout the flue cured production area.”
“Original fuel oil heat exchanger models were not solid welded and have the potential for leaking combustion gases in the curing chamber. Current models are solid welded.”
http://www.cpes.peachnet.edu/tobacco/fueloil.htm
“One would have expected the results of such definitive experiments to have been published by 1957 or 1958, or by 1960 at the very latest.
Instead, publication of papers on the subject suddenly ceased; funds for research on the effects of diesel smoke were withdrawn; lawyers issued instructions on how to confuse a court should an action for damages be initiated; and articles on diesel fuel tended to have the unsupported statement “diesel smoke is harmless” as a frequent non sequitor.”
http://legacy.library.ucsf.edu/action/document/page;jsessionid=1A622975CD35D2F66C01526368B52B33?tid=yth67a99&page=17
Lying about the reasons for lung cancer
This blog post points out that our lung and respiratory conditions are higher than in Europe but smoking rates lower than many European states.
I blame the wet climate. This will make damp problems in substandard housing worse and we have plenty of that too.
That might explain respiratory conditions but not sure about lung cancer.
http://www.ecigarettedirect.co.uk/ashtray-blog/2010/11/uk-is-the-worst-for-lung-disease-and-charities-are-lying-about-the-reasons.html
Lying about the reasons for lung cancer
This blog post points out that our lung and respiratory conditions are higher than in Europe but smoking rates lower than many European states.
I blame the wet climate. This will make damp problems in substandard housing worse and we have plenty of that too.
That might explain respiratory conditions but not sure about lung cancer.
http://www.ecigarettedirect.co.uk/ashtray-blog/2010/11/uk-is-the-worst-for-lung-disease-and-charities-are-lying-about-the-reasons.html
Lying about the reasons for lung cancer
This blog post points out that our lung and respiratory conditions are higher than in Europe but smoking rates lower than many European states.
I blame the wet climate. This will make damp problems in substandard housing worse and we have plenty of that too.
That might explain respiratory conditions but not sure about lung cancer.
http://www.ecigarettedirect.co.uk/ashtray-blog/2010/11/uk-is-the-worst-for-lung-disease-and-charities-are-lying-about-the-reasons.html
Hmm, I think for reasons already mentioned (relative population densities) the map of the US isn’t that useful. If you look at Belinda’s map and click on the different age ranges you’ll see that amongst young and middle aged people the high smoking rates do seem to correlate with the Eastern US’s high cancer rates. (That said, there is a lot of smoking in the centre and north west but no similar link there). But whether that means anything when that area is the most densely populated is hard to say. What we need is a picture of a densely populated country like Japan or the UK.
Hmm, I think for reasons already mentioned (relative population densities) the map of the US isn’t that useful. If you look at Belinda’s map and click on the different age ranges you’ll see that amongst young and middle aged people the high smoking rates do seem to correlate with the Eastern US’s high cancer rates. (That said, there is a lot of smoking in the centre and north west but no similar link there). But whether that means anything when that area is the most densely populated is hard to say. What we need is a picture of a densely populated country like Japan or the UK.
Hmm, I think for reasons already mentioned (relative population densities) the map of the US isn’t that useful. If you look at Belinda’s map and click on the different age ranges you’ll see that amongst young and middle aged people the high smoking rates do seem to correlate with the Eastern US’s high cancer rates. (That said, there is a lot of smoking in the centre and north west but no similar link there). But whether that means anything when that area is the most densely populated is hard to say. What we need is a picture of a densely populated country like Japan or the UK.
Then again, there are soem weird discrepancies. There are some chunks in the centre/North west of the US with high smoking rates and low cancer incidence which could indicate another cause. But it seems doubtful if that other cause is traffic fumes, otherwise why does California have a low cancer rate when it is relatively densely populated and LA is famous for its smogs. It also has a low smoking rate which seems to support the smoking/cancer hypothesis. Then again the central/northwest high smokers/low cancer rates seem to disprove it.
There must be another factor – not smoking, and seemingly not traffic pollution (although what someone posted about winds on the West coast is interesting), that is the cause. But what?
Mr A
Then again, there are soem weird discrepancies. There are some chunks in the centre/North west of the US with high smoking rates and low cancer incidence which could indicate another cause. But it seems doubtful if that other cause is traffic fumes, otherwise why does California have a low cancer rate when it is relatively densely populated and LA is famous for its smogs. It also has a low smoking rate which seems to support the smoking/cancer hypothesis. Then again the central/northwest high smokers/low cancer rates seem to disprove it.
There must be another factor – not smoking, and seemingly not traffic pollution (although what someone posted about winds on the West coast is interesting), that is the cause. But what?
Mr A
Then again, there are soem weird discrepancies. There are some chunks in the centre/North west of the US with high smoking rates and low cancer incidence which could indicate another cause. But it seems doubtful if that other cause is traffic fumes, otherwise why does California have a low cancer rate when it is relatively densely populated and LA is famous for its smogs. It also has a low smoking rate which seems to support the smoking/cancer hypothesis. Then again the central/northwest high smokers/low cancer rates seem to disprove it.
There must be another factor – not smoking, and seemingly not traffic pollution (although what someone posted about winds on the West coast is interesting), that is the cause. But what?
Mr A
Hmmm. Someone mentioned Mercury. Here, from an unrelated study on Mercury and autism is a map of Mercury sensitivity in the US. Look familiar?
http://blog.imva.info/medicine/confrontations-with-mad-mercury-doctors
Mr A
Hmmm. Someone mentioned Mercury. Here, from an unrelated study on Mercury and autism is a map of Mercury sensitivity in the US. Look familiar?
http://blog.imva.info/medicine/confrontations-with-mad-mercury-doctors
Mr A
Hmmm. Someone mentioned Mercury. Here, from an unrelated study on Mercury and autism is a map of Mercury sensitivity in the US. Look familiar?
http://blog.imva.info/medicine/confrontations-with-mad-mercury-doctors
Mr A
Or this one from a study linking air pollution with daibetes (?). Again, you’ll see the two maps (diabetes and air pollution) correlate with the cancer map.
http://www.treehugger.com/files/2010/09/particulate-air-pollution-strongly-linked-increased-diabetes-prevalence.php
Do these links just demonstrate the uselessness of using such maps of the US as has already been suggested? Or do they point to some other factor?
Mr A
Or this one from a study linking air pollution with daibetes (?). Again, you’ll see the two maps (diabetes and air pollution) correlate with the cancer map.
http://www.treehugger.com/files/2010/09/particulate-air-pollution-strongly-linked-increased-diabetes-prevalence.php
Do these links just demonstrate the uselessness of using such maps of the US as has already been suggested? Or do they point to some other factor?
Mr A
Or this one from a study linking air pollution with daibetes (?). Again, you’ll see the two maps (diabetes and air pollution) correlate with the cancer map.
http://www.treehugger.com/files/2010/09/particulate-air-pollution-strongly-linked-increased-diabetes-prevalence.php
Do these links just demonstrate the uselessness of using such maps of the US as has already been suggested? Or do they point to some other factor?
Mr A
Re: The Debate
I’m sorry, but where did I pick you up for calling him Snowden? I don’t remember doing that. My only comment in response to you has been about the order of magnitude business.
As for the structure of the debate, I do have a response in preparation, but along quite different lines than my comments above. My remarks above about animal studies, and geographic distributions of lung cancer, would not have been contained in that response. So I thought I’d raise them from the floor. I don’t see any particular reason why myself, or Chris Snowdon, or Rich White, or other contributors (e.g. Phil Button) shouldn’t post comments as well as more formal arguments.
The idea, as I see it, is to air a few arguments, not to stick to some sort of rigid format. After all, in setting out the ‘terms and conditions’ in the previous post, I left things very loose. I did this so as to allow the discussion to develop as it may, playing it by ear.
Next up, anyway, will be Rich White. I’ll probably come in after that.
Frank
Re: The Debate
I’m sorry, but where did I pick you up for calling him Snowden? I don’t remember doing that. My only comment in response to you has been about the order of magnitude business.
As for the structure of the debate, I do have a response in preparation, but along quite different lines than my comments above. My remarks above about animal studies, and geographic distributions of lung cancer, would not have been contained in that response. So I thought I’d raise them from the floor. I don’t see any particular reason why myself, or Chris Snowdon, or Rich White, or other contributors (e.g. Phil Button) shouldn’t post comments as well as more formal arguments.
The idea, as I see it, is to air a few arguments, not to stick to some sort of rigid format. After all, in setting out the ‘terms and conditions’ in the previous post, I left things very loose. I did this so as to allow the discussion to develop as it may, playing it by ear.
Next up, anyway, will be Rich White. I’ll probably come in after that.
Frank
Other sources
“Diesel fumes from the ports of Los Angeles and Long Beach are elevating the risk of cancer not only adjacent to the ports but many miles inland, a new study shows.
It is the first state study that shows that air pollution from the ports is increasing cancer risk in the Los Angeles Basin, said Jerry Martin, spokesman for the California Air Resources Board, which released a draft of the study Tuesday.”
“The sources of much of the diesel exhaust, however, are not covered by those rules because ships, trains, trucks and cargo equipment are considered “mobile sources” that are regulated less stringently.”
“Earlier research had found that diesel fumes accounted for 71% of the cancer risk associated with air pollution in the Los Angeles region.”
“One surprise in the study is that pollution from within the two ports extends so far inland, Ospital said.”
http://articles.latimes.com/2005/oct/05/local/me-air4
“The two-year public health inquiry covered a large swath of the Bay Area – an area of 3,800 square miles that is home to 3.1 million people. The residents had an elevated risk of cancer – nearly 1,200 additional cancers per million people due to long-term exposure to diesel particulate matter than people living elsewhere, the study reported in preliminary findings”
“The study concentrated on three sources of the toxic air contaminant: the Port of Oakland, the Union Pacific Railroad near the port, and freeway truck traffic and nonport-related marine vessel traffic in and around West Oakland in general. Diesel trucks accounted for 70 percent of the elevated health risks – amounting to 850 potential cancer cases per million above the expected rate of cancer in the general population”
http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2008/03/20/BA1PVMN0O.DTL
Proposed wood burning ban draws fire
“A proposed ban on burning wood in the Bay Area’s 1 million fireplaces and stoves on bad-air days has drawn praise – and heat – from hundreds of residents as regulators consider how to balance the health risks of inhaling smoke against the need to stay warm.”
“it is even worse to allow these chronic and abusive wood-burners to needlessly pump our lungs full of … fumes and particulates which bring great risks to our immediate and long term health.”
“The Bay Area Air Quality Management District’s plan to restrict wood burning comes after federal officials imposed tighter limits on emissions of fine particles, a move that regional officials say could lead them to declare 20 Spare the Air days during the winter season.”
http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2008/01/20/MNGQUGD16.DTL
Other sources
“Diesel fumes from the ports of Los Angeles and Long Beach are elevating the risk of cancer not only adjacent to the ports but many miles inland, a new study shows.
It is the first state study that shows that air pollution from the ports is increasing cancer risk in the Los Angeles Basin, said Jerry Martin, spokesman for the California Air Resources Board, which released a draft of the study Tuesday.”
“The sources of much of the diesel exhaust, however, are not covered by those rules because ships, trains, trucks and cargo equipment are considered “mobile sources” that are regulated less stringently.”
“Earlier research had found that diesel fumes accounted for 71% of the cancer risk associated with air pollution in the Los Angeles region.”
“One surprise in the study is that pollution from within the two ports extends so far inland, Ospital said.”
http://articles.latimes.com/2005/oct/05/local/me-air4
“The two-year public health inquiry covered a large swath of the Bay Area – an area of 3,800 square miles that is home to 3.1 million people. The residents had an elevated risk of cancer – nearly 1,200 additional cancers per million people due to long-term exposure to diesel particulate matter than people living elsewhere, the study reported in preliminary findings”
“The study concentrated on three sources of the toxic air contaminant: the Port of Oakland, the Union Pacific Railroad near the port, and freeway truck traffic and nonport-related marine vessel traffic in and around West Oakland in general. Diesel trucks accounted for 70 percent of the elevated health risks – amounting to 850 potential cancer cases per million above the expected rate of cancer in the general population”
http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2008/03/20/BA1PVMN0O.DTL
Proposed wood burning ban draws fire
“A proposed ban on burning wood in the Bay Area’s 1 million fireplaces and stoves on bad-air days has drawn praise – and heat – from hundreds of residents as regulators consider how to balance the health risks of inhaling smoke against the need to stay warm.”
“it is even worse to allow these chronic and abusive wood-burners to needlessly pump our lungs full of … fumes and particulates which bring great risks to our immediate and long term health.”
“The Bay Area Air Quality Management District’s plan to restrict wood burning comes after federal officials imposed tighter limits on emissions of fine particles, a move that regional officials say could lead them to declare 20 Spare the Air days during the winter season.”
http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2008/01/20/MNGQUGD16.DTL
Other sources
“Diesel fumes from the ports of Los Angeles and Long Beach are elevating the risk of cancer not only adjacent to the ports but many miles inland, a new study shows.
It is the first state study that shows that air pollution from the ports is increasing cancer risk in the Los Angeles Basin, said Jerry Martin, spokesman for the California Air Resources Board, which released a draft of the study Tuesday.”
“The sources of much of the diesel exhaust, however, are not covered by those rules because ships, trains, trucks and cargo equipment are considered “mobile sources” that are regulated less stringently.”
“Earlier research had found that diesel fumes accounted for 71% of the cancer risk associated with air pollution in the Los Angeles region.”
“One surprise in the study is that pollution from within the two ports extends so far inland, Ospital said.”
http://articles.latimes.com/2005/oct/05/local/me-air4
“The two-year public health inquiry covered a large swath of the Bay Area – an area of 3,800 square miles that is home to 3.1 million people. The residents had an elevated risk of cancer – nearly 1,200 additional cancers per million people due to long-term exposure to diesel particulate matter than people living elsewhere, the study reported in preliminary findings”
“The study concentrated on three sources of the toxic air contaminant: the Port of Oakland, the Union Pacific Railroad near the port, and freeway truck traffic and nonport-related marine vessel traffic in and around West Oakland in general. Diesel trucks accounted for 70 percent of the elevated health risks – amounting to 850 potential cancer cases per million above the expected rate of cancer in the general population”
http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2008/03/20/BA1PVMN0O.DTL
Proposed wood burning ban draws fire
“A proposed ban on burning wood in the Bay Area’s 1 million fireplaces and stoves on bad-air days has drawn praise – and heat – from hundreds of residents as regulators consider how to balance the health risks of inhaling smoke against the need to stay warm.”
“it is even worse to allow these chronic and abusive wood-burners to needlessly pump our lungs full of … fumes and particulates which bring great risks to our immediate and long term health.”
“The Bay Area Air Quality Management District’s plan to restrict wood burning comes after federal officials imposed tighter limits on emissions of fine particles, a move that regional officials say could lead them to declare 20 Spare the Air days during the winter season.”
http://www.sfgate.com/cgi-bin/article.cgi?f=/c/a/2008/01/20/MNGQUGD16.DTL
Debate
Hi Frank I hope you are well.
Happy to join in the debate tonight what time is kick off andf where do I sign in?
Dave Atherton
Debate
Hi Frank I hope you are well.
Happy to join in the debate tonight what time is kick off andf where do I sign in?
Dave Atherton
Debate
Hi Frank I hope you are well.
Happy to join in the debate tonight what time is kick off andf where do I sign in?
Dave Atherton
Re: Debate
It’s already kicked off, with the contribution from Chris Snowdon above. Rich White is next up. If you’d like to make a contribution to the debate other than a comment, compose something, and send it to me at cfrankdavis@googlemail.com, and I’ll put it up (perhaps with minor edits).
This is a bit of an informal and experimental ‘debate’. I’m hoping that it’ll give the subject of smoking and lung cancer a fairly good airing.
I hope you are well too.
Frank
Re: Debate
I should have added that the debate isn’t ‘tonight’, but will be spread over several days or more, as and when contributions come in.
Frank
Bradford Hill again
Returning to Chris Snowdon’s original submission, in particular concerning strength of association, Bradford Hill had this to say:
‘To explain the pronounced excess of cancer of the lung in any other environmental terms [i.e. other than smoking] requires some feature of life so intimately linked with cigarette smoking and with the amount of smoking that such a feature should be easily detectable. If we cannot detect it or reasonably infer a specific one, then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic “you can’t prove it, there may be such a feature”.’
There may be evidence for other candidate ‘causes’, e.g. diesel fumes, nuclear fallout, the human papillomavirus, etc, but can we reasonably say that any of these are as strongly ‘associated’ with lung cancer as smoking? This is the challenge that the sceptic (and I count myself as one) has to answer: come up with a credible alternative. As Jerome Cornfield, writing in the 1950s, put it:
‘It would be desirable to have a set of findings on the subject of smoking and lung cancer so clear-cut and unequivocal that they were self-interpreting. The findings now available on tobacco, as in most other fields of science, particularly biologic science, do not meet this ideal. Nevertheless, if the findings had been made on a new agent, to which hundreds of millions of adults were not already addicted, and on one which did not support a large industry, skilled in the arts of mass persuasion, the evidence for the hazardous nature of the agent would be generally regarded as beyond dispute.’
One final quote from Bradford Hill:
‘What I do not believe – and this has been suggested – that we can usefully lay down some hard and fast rules of evidence that must be obeyed before we can accept cause and effect. None of my nine viewpoints can bring indisputable evidence for or against the cause-and-effect hypothesis and none can be required as a sine qua non. What they can do, with greater or less strength, is to help us to make up our minds on the fundamental question – is there any other way of explaining the set of facts before us, is there any other answer equally, or more, likely than cause and effect?’
DW
Bradford Hill again
Returning to Chris Snowdon’s original submission, in particular concerning strength of association, Bradford Hill had this to say:
‘To explain the pronounced excess of cancer of the lung in any other environmental terms [i.e. other than smoking] requires some feature of life so intimately linked with cigarette smoking and with the amount of smoking that such a feature should be easily detectable. If we cannot detect it or reasonably infer a specific one, then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic “you can’t prove it, there may be such a feature”.’
There may be evidence for other candidate ‘causes’, e.g. diesel fumes, nuclear fallout, the human papillomavirus, etc, but can we reasonably say that any of these are as strongly ‘associated’ with lung cancer as smoking? This is the challenge that the sceptic (and I count myself as one) has to answer: come up with a credible alternative. As Jerome Cornfield, writing in the 1950s, put it:
‘It would be desirable to have a set of findings on the subject of smoking and lung cancer so clear-cut and unequivocal that they were self-interpreting. The findings now available on tobacco, as in most other fields of science, particularly biologic science, do not meet this ideal. Nevertheless, if the findings had been made on a new agent, to which hundreds of millions of adults were not already addicted, and on one which did not support a large industry, skilled in the arts of mass persuasion, the evidence for the hazardous nature of the agent would be generally regarded as beyond dispute.’
One final quote from Bradford Hill:
‘What I do not believe – and this has been suggested – that we can usefully lay down some hard and fast rules of evidence that must be obeyed before we can accept cause and effect. None of my nine viewpoints can bring indisputable evidence for or against the cause-and-effect hypothesis and none can be required as a sine qua non. What they can do, with greater or less strength, is to help us to make up our minds on the fundamental question – is there any other way of explaining the set of facts before us, is there any other answer equally, or more, likely than cause and effect?’
DW
Bradford Hill again
Returning to Chris Snowdon’s original submission, in particular concerning strength of association, Bradford Hill had this to say:
‘To explain the pronounced excess of cancer of the lung in any other environmental terms [i.e. other than smoking] requires some feature of life so intimately linked with cigarette smoking and with the amount of smoking that such a feature should be easily detectable. If we cannot detect it or reasonably infer a specific one, then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic “you can’t prove it, there may be such a feature”.’
There may be evidence for other candidate ‘causes’, e.g. diesel fumes, nuclear fallout, the human papillomavirus, etc, but can we reasonably say that any of these are as strongly ‘associated’ with lung cancer as smoking? This is the challenge that the sceptic (and I count myself as one) has to answer: come up with a credible alternative. As Jerome Cornfield, writing in the 1950s, put it:
‘It would be desirable to have a set of findings on the subject of smoking and lung cancer so clear-cut and unequivocal that they were self-interpreting. The findings now available on tobacco, as in most other fields of science, particularly biologic science, do not meet this ideal. Nevertheless, if the findings had been made on a new agent, to which hundreds of millions of adults were not already addicted, and on one which did not support a large industry, skilled in the arts of mass persuasion, the evidence for the hazardous nature of the agent would be generally regarded as beyond dispute.’
One final quote from Bradford Hill:
‘What I do not believe – and this has been suggested – that we can usefully lay down some hard and fast rules of evidence that must be obeyed before we can accept cause and effect. None of my nine viewpoints can bring indisputable evidence for or against the cause-and-effect hypothesis and none can be required as a sine qua non. What they can do, with greater or less strength, is to help us to make up our minds on the fundamental question – is there any other way of explaining the set of facts before us, is there any other answer equally, or more, likely than cause and effect?’
DW
Re: Bradford Hill again
‘To explain the pronounced excess of cancer of the lung in any other environmental terms [i.e. other than smoking] requires some feature of life so intimately linked with cigarette smoking and with the amount of smoking that such a feature should be easily detectable. If we cannot detect it or reasonably infer a specific one, then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic “you can’t prove it, there may be such a feature”.’
I can think of two – matches and lighters. Maybe it’s people who use sulpher encrusted matches to light their cigarettes, or those who inhale the first puff which contains the gas/sulpher.
Re: Distribution map of smokers
Thanks for that. I’d not seen it before. Unfortunately it’s for 2009. It would have been more interesting to see the distribution 50 years earlier.
Nevertheless, it’s fairly even, with a range from roughly 5% to 15% or so over the USA.
Frank
Re: Distribution map of smokers
Thanks for that. I’d not seen it before. Unfortunately it’s for 2009. It would have been more interesting to see the distribution 50 years earlier.
Nevertheless, it’s fairly even, with a range from roughly 5% to 15% or so over the USA.
Frank
Re: Regarding these Maps
I agree that data collection methods probably differ from state to state, and that affects the figures.
Also, since this is a map of mortality, rather than incidence, it may be that in some states people get better treatment for cancer than in others. Or (because it’s the USA) in some states more people have health insurance than in others, so that poorer states have higher mortality.
But the much higher population densities and better hospitals in NY would seem to me to suggest that the lung cancer mortality is measured more accurately there.
It’s a bit like weather stations across the USA. There are probably lots more of them in NY than in Oklahoma. That should mean that NY figures are more accurate, not that they’re distorted (leaving aside urban heat island effects).
Frank
Re: Regarding these Maps
I agree that data collection methods probably differ from state to state, and that affects the figures.
Also, since this is a map of mortality, rather than incidence, it may be that in some states people get better treatment for cancer than in others. Or (because it’s the USA) in some states more people have health insurance than in others, so that poorer states have higher mortality.
But the much higher population densities and better hospitals in NY would seem to me to suggest that the lung cancer mortality is measured more accurately there.
It’s a bit like weather stations across the USA. There are probably lots more of them in NY than in Oklahoma. That should mean that NY figures are more accurate, not that they’re distorted (leaving aside urban heat island effects).
Frank
Re: Debate
It’s already kicked off, with the contribution from Chris Snowdon above. Rich White is next up. If you’d like to make a contribution to the debate other than a comment, compose something, and send it to me at cfrankdavis@googlemail.com, and I’ll put it up (perhaps with minor edits).
This is a bit of an informal and experimental ‘debate’. I’m hoping that it’ll give the subject of smoking and lung cancer a fairly good airing.
I hope you are well too.
Frank
Re: Debate
It’s already kicked off, with the contribution from Chris Snowdon above. Rich White is next up. If you’d like to make a contribution to the debate other than a comment, compose something, and send it to me at cfrankdavis@googlemail.com, and I’ll put it up (perhaps with minor edits).
This is a bit of an informal and experimental ‘debate’. I’m hoping that it’ll give the subject of smoking and lung cancer a fairly good airing.
I hope you are well too.
Frank
Re: Debate
I should have added that the debate isn’t ‘tonight’, but will be spread over several days or more, as and when contributions come in.
Frank
Re: Debate
I should have added that the debate isn’t ‘tonight’, but will be spread over several days or more, as and when contributions come in.
Frank
“Scientists have successfully made animals develop lung cancer by forcing them to smoke, and they have done the same by painting cigarette tar on mice. Does this prove the smoking theory? Not necessarily. The defence will say that the doses are unrealistically high. I have some sympathy with that view, but it certainly does not disprove the theory.”
Quite apart from the fact that, as Frank points out above, they have not done so, even with the aforementioned “unrealistically high” doses, even if the doses used had been of a “normal” level, (and I am not aware of any tests which have ever used a “normal” level in any case, which is in and of itself somewhat suspect) the lack of development of lung cancer in laboratory animals after the application of the hypothetised “cause,” in scientific terms, actually does effectively “disprove the theory.”
It’s standard scientific protocol – the final step in any scientific test for the cause of an ailment is just that – after finding a link and a statistical indication amongst your subjects when compared to a control group, you then apply the cause to an uninfected group of subjects and they must develop that ailment in order to claim “proof” that it is the cause so that statement such as “X causes Y” can be made without the danger of misleading the public. This final step in the chain was established by the scientific community itself in order to maintain its integrity and to protect itself from falling into disrepute through the unsubstatiated claims of those who wished to use their discipline in order to further their own agendas. By allowing this departure from protocol, science has enabled the very attitudes which it tried so hard to avoid (mistrust, scepticism, disregard) to befall their own field of endeavour.
Of course there is nothing to stop anyone, like Chris, from continuing to “believe” that smoking causes lung cancer, any more than the lack of proof of an all-seeing all-knowing God should prevent Christians from believing that there is one, but this is a matter of personal faith and should be stated as such and adhered to for its own sake, rather than attempting to shore itself up and win “converts” by allusions to scientific “proof” which believers know is a more convincing “take”, in this day and age, than faith alone.
“Smoking causes lung cancer” is no less a statement of belief than are claims that God created the world in six days, that only Christian believers may enter the gates of heaven or that Islamists who give their lives for their religion will go to heaven and be served eternally by virgins. The difference is that the last three are at least honest enough to present themselves just as beliefs, rather than masquerading as some kind of scientifically-proven facts.
“Scientists have successfully made animals develop lung cancer by forcing them to smoke, and they have done the same by painting cigarette tar on mice. Does this prove the smoking theory? Not necessarily. The defence will say that the doses are unrealistically high. I have some sympathy with that view, but it certainly does not disprove the theory.”
Quite apart from the fact that, as Frank points out above, they have not done so, even with the aforementioned “unrealistically high” doses, even if the doses used had been of a “normal” level, (and I am not aware of any tests which have ever used a “normal” level in any case, which is in and of itself somewhat suspect) the lack of development of lung cancer in laboratory animals after the application of the hypothetised “cause,” in scientific terms, actually does effectively “disprove the theory.”
It’s standard scientific protocol – the final step in any scientific test for the cause of an ailment is just that – after finding a link and a statistical indication amongst your subjects when compared to a control group, you then apply the cause to an uninfected group of subjects and they must develop that ailment in order to claim “proof” that it is the cause so that statement such as “X causes Y” can be made without the danger of misleading the public. This final step in the chain was established by the scientific community itself in order to maintain its integrity and to protect itself from falling into disrepute through the unsubstatiated claims of those who wished to use their discipline in order to further their own agendas. By allowing this departure from protocol, science has enabled the very attitudes which it tried so hard to avoid (mistrust, scepticism, disregard) to befall their own field of endeavour.
Of course there is nothing to stop anyone, like Chris, from continuing to “believe” that smoking causes lung cancer, any more than the lack of proof of an all-seeing all-knowing God should prevent Christians from believing that there is one, but this is a matter of personal faith and should be stated as such and adhered to for its own sake, rather than attempting to shore itself up and win “converts” by allusions to scientific “proof” which believers know is a more convincing “take”, in this day and age, than faith alone.
“Smoking causes lung cancer” is no less a statement of belief than are claims that God created the world in six days, that only Christian believers may enter the gates of heaven or that Islamists who give their lives for their religion will go to heaven and be served eternally by virgins. The difference is that the last three are at least honest enough to present themselves just as beliefs, rather than masquerading as some kind of scientifically-proven facts.
“Scientists have successfully made animals develop lung cancer by forcing them to smoke, and they have done the same by painting cigarette tar on mice. Does this prove the smoking theory? Not necessarily. The defence will say that the doses are unrealistically high. I have some sympathy with that view, but it certainly does not disprove the theory.”
Quite apart from the fact that, as Frank points out above, they have not done so, even with the aforementioned “unrealistically high” doses, even if the doses used had been of a “normal” level, (and I am not aware of any tests which have ever used a “normal” level in any case, which is in and of itself somewhat suspect) the lack of development of lung cancer in laboratory animals after the application of the hypothetised “cause,” in scientific terms, actually does effectively “disprove the theory.”
It’s standard scientific protocol – the final step in any scientific test for the cause of an ailment is just that – after finding a link and a statistical indication amongst your subjects when compared to a control group, you then apply the cause to an uninfected group of subjects and they must develop that ailment in order to claim “proof” that it is the cause so that statement such as “X causes Y” can be made without the danger of misleading the public. This final step in the chain was established by the scientific community itself in order to maintain its integrity and to protect itself from falling into disrepute through the unsubstatiated claims of those who wished to use their discipline in order to further their own agendas. By allowing this departure from protocol, science has enabled the very attitudes which it tried so hard to avoid (mistrust, scepticism, disregard) to befall their own field of endeavour.
Of course there is nothing to stop anyone, like Chris, from continuing to “believe” that smoking causes lung cancer, any more than the lack of proof of an all-seeing all-knowing God should prevent Christians from believing that there is one, but this is a matter of personal faith and should be stated as such and adhered to for its own sake, rather than attempting to shore itself up and win “converts” by allusions to scientific “proof” which believers know is a more convincing “take”, in this day and age, than faith alone.
“Smoking causes lung cancer” is no less a statement of belief than are claims that God created the world in six days, that only Christian believers may enter the gates of heaven or that Islamists who give their lives for their religion will go to heaven and be served eternally by virgins. The difference is that the last three are at least honest enough to present themselves just as beliefs, rather than masquerading as some kind of scientifically-proven facts.
To Chris and Frank
I think it would be important when you’re citing the different studies you to support your respective positions, to first examine a few important details in the studies that are all too often ignored.
Hill is an older study but the newer junk studies qualify a smoker as anyone who has smoked 100 cigarettes in a lifetime and lumps him further with ex-smokers of 100 or more cigarettes in a lifetime no matter how long ago the current smokers have started smoking and how log ago the former smokers stopped.
What does Hill say? What was a smoker according to him? (I haven’t read the study by the way, I did more extensive research on SHS, just like Chris accepting as truth that smoking causes lung cancer). Were pipe smokers who hardly inhale part of his cohort? How about cigarette smokers that didn’t inhale at all which was quite comme at the time. How many cigarettes did one have to smoke to be part of the study? Is any of this spelled out in his methodology?
I feel that before we throw around the sweeping statement that ”smoking causes lung cancer”, it would be important to know what smoking is. We might end up with the contention that ”abusively and deeply inhaling smoke over long periods of time causes lung cancer” instead.
Iro
To Chris and Frank
I think it would be important when you’re citing the different studies you to support your respective positions, to first examine a few important details in the studies that are all too often ignored.
Hill is an older study but the newer junk studies qualify a smoker as anyone who has smoked 100 cigarettes in a lifetime and lumps him further with ex-smokers of 100 or more cigarettes in a lifetime no matter how long ago the current smokers have started smoking and how log ago the former smokers stopped.
What does Hill say? What was a smoker according to him? (I haven’t read the study by the way, I did more extensive research on SHS, just like Chris accepting as truth that smoking causes lung cancer). Were pipe smokers who hardly inhale part of his cohort? How about cigarette smokers that didn’t inhale at all which was quite comme at the time. How many cigarettes did one have to smoke to be part of the study? Is any of this spelled out in his methodology?
I feel that before we throw around the sweeping statement that ”smoking causes lung cancer”, it would be important to know what smoking is. We might end up with the contention that ”abusively and deeply inhaling smoke over long periods of time causes lung cancer” instead.
Iro
To Chris and Frank
I think it would be important when you’re citing the different studies you to support your respective positions, to first examine a few important details in the studies that are all too often ignored.
Hill is an older study but the newer junk studies qualify a smoker as anyone who has smoked 100 cigarettes in a lifetime and lumps him further with ex-smokers of 100 or more cigarettes in a lifetime no matter how long ago the current smokers have started smoking and how log ago the former smokers stopped.
What does Hill say? What was a smoker according to him? (I haven’t read the study by the way, I did more extensive research on SHS, just like Chris accepting as truth that smoking causes lung cancer). Were pipe smokers who hardly inhale part of his cohort? How about cigarette smokers that didn’t inhale at all which was quite comme at the time. How many cigarettes did one have to smoke to be part of the study? Is any of this spelled out in his methodology?
I feel that before we throw around the sweeping statement that ”smoking causes lung cancer”, it would be important to know what smoking is. We might end up with the contention that ”abusively and deeply inhaling smoke over long periods of time causes lung cancer” instead.
Iro
Re: To Chris and Frank
In the 1954 British Doctors study, it states how the doctors were asked to classify themselves:
In addition to giving their name, address, and age, the doctors were asked to classify themselves into one of three groups – namely, (a) whether they were, at that time, smoking; (b) whether they had smoked but had given up; (c) whether they had never smoked regularly (that is, had never smoked as much as one cigarette a day, or its equivalent in pipe tobacco, for as long as one year).
I have spent many happy hours considering how these questions might be misunderstood or misrepresented. For example, (a) could be misinterpreted as meaning, are you smoking a cigarette right this second? (b) is also open to misinterpretation. And I defy anybody to say exactly what the convoluted question (c) means.
The definition of what a ‘smoker’ is seems to have changed from year to year, almost. The current view seems to be that you’re a smoker if you’ve smoked more than 100 cigarettes in your lifetime. Why 100? Why not 50, or 500?
Similar problems arise in defining an ‘ex-smoker’. How long do you have to have given up smoking before you can call yourself an ex-smoker? 5 years? 1 year? 3 months? 2 days? 15 minutes?
I think Doll and Hill probably realised that if they simply said the obvious, that a non-smoker was someone who had never smoked a single cigarette in their life, they would have had precious few non-smokers. So they relaxed the definition. But they could have relaxed it to the point that a non-smoker was someone who didn’t currently have a cigarette in their mouth.
In these days of passive smoking when there is the category of the ‘never-smoker’, we also have to wonder how much secondhand smoke these never smokers have inhaled. I’ve forgotten what the cigarette-equivalent of sitting in a smoky bar all evening is, but I can well imagine that over a few years or decades it could well add up to more than 100 cigarettes – so that even ‘never-smokers’ are smokers.
Frank
My last sentence should have read:
”abusively and deeply inhaling smoke over long periods of time may cause lung cancer”
Because even the 2 or 3 pack a day smokers don’t necessarily end up with lung cancer.
Iro
My last sentence should have read:
”abusively and deeply inhaling smoke over long periods of time may cause lung cancer”
Because even the 2 or 3 pack a day smokers don’t necessarily end up with lung cancer.
Iro
My last sentence should have read:
”abusively and deeply inhaling smoke over long periods of time may cause lung cancer”
Because even the 2 or 3 pack a day smokers don’t necessarily end up with lung cancer.
Iro
Iro,
Hope this helps:
Wynder’s 1950 study:
‘Nonsmokers (less than 1 cigaret per day for more than twenty years)'”
…
“If a patient smoked for less than twenty years, his amount of smoking was adjusted to a twenty year period. Thus a patient smoking 20 cigarets for ten years only was classified as smoking 10 cigarets daily. ”
…
Pipe and cigar smokers were recast as cigaret equivalents. My copy is rather illegible but I think it makes a cigar equivalent to 3 cigarets and a pipe equivalent to 2.5 cigarets.
Doll’s 1950 Hospital study and Doll’s ‘British Doctors Study’:
(Hill was Doll’s supervisor and co-author on these papers)
“A smoker was therefore defined in this inquiry as a person who had smoked as much as one cigarette a day for as long as a year.” Pipe and cigar smoker consumption was based on grams of tobacco smoked with 1g = 1 cigarette.
So Wynder’s definition of a non-smoker was less than 20 X 365 X 1 = 7300 cigarettes or equivalent in a lifetime. Doll and Hill’s definition was 365 cigarettes in a lifetime.
Quite a difference but both are very small and Doll’s figure is very similar to the cut-off of 100 cigarettes in a lifetime that seems in common use today.
As to inhaling, smokers who inhaled were found to be significantly LESS likely to die of lung cancer.
Tony
My apologies if this appears twice. It seems the first time I posted it it didn’t appear:
All this is very wishy washy and makes any and all of these studies hard to believe especially when one reads in one particular study that I came across by accident that 280,000 cigarettes is considered the cut-off point in many studies of when tumors are noticed http://www.ncbi.nlm.nih.gov/pubmed/15207443 . I tried to find other references to this 280,000 cigarette contention but couldn’t. Did anyone ever come across anything that refers to it?
In my opinion, as long as they don’t do studies that target more narrowed down categories of smokers i.e. occasional, light, moderate, heavy, very heavy, any of the conclusions they come up with are suspect. I would like to see a study that had a complete distinct cohort of smokers who only smoked 1 to 5 or even 10 a day compared to a control group of non-smokers. Bets are the RR will be null or maybe very slightly increased for those who smoked 10. This is my opinion based on every day observations, not some theoretical figures thrown around by acamedics splitting hairs in 4.
Iro
OK
I have to ask.
7. Coherence: Does it fit the overall pattern? Again, yes. The lung cancer rate rose first amongst men because they were the first to smoke and it rose later amongst women when they started to smoke.
“In fact the first observations on an appreciable rise in the frequency of lung cancer were reported from the highly industrialized cities of densely populated Saxony during the first two decades of this century.
Some years later it was found that high lung cancer rates existed for the population of the industrialized territory of the Ruhr valley, while they were below average for the agricultural region of the Main valley.”
http://www.chestjournal.org/cgi/reprint/30/2/141
Court testimony
“Q Actually Dr. when was an increase in lung cancer first noted?
A The pathologists of central Europe, particularly in Germany where autopsies were performed for many years in hospital institutes of pathology, the University institutes of pathology on the majority of patients who died in these hospitals, the percentage rate ran between 90% and 95% of the deaths which occurred, and showed around 1920 that there had been a gradual, and progressive increase in lung cancer deaths observed in autopsies since the turn of the Century.
Q Since about 1900?
A Around 1900
Q And then it gradually started to increase,
A the number of cases increased.
Having in mind that you were living in Central Europe, at that time, was there any increase in smoking during that period of time that parallelled the increase in lung cancer from 1900 to 1920?
A It is pretty well established from statements in the literature that a wide spread and general use of the cigarette among the people of industrialized countries started with the first World War.
That means there was an increase in the lung cancer incidence before the custom of smoking cigarettes became a widespread habit.”
http://tobaccodocuments.org/industry_depositions/503243231-3367.html?zoom=750&ocr_position=above_foramatted&start_page=1
“The dramatic growth of lung cancer in the 1920s and 1930s was not at first attributed to smoking: the influenza pandemic of 1919 was sometimes blamed, as were automobile exhaust, dust from newly tarred roads, diverse occupational exposures (including tar and diverse polycyclic hydrocarbons), increasing exposure to X rays, exposure to chemical warfare agents during the First World War,..”
http://toxicology.usu.edu/endnote/Proctor-Nazi-war-tobacco.htm
1957
“Soon after World War 1 when mustard gas had been used extensively for war purposes on both sides,the claim was advanced by some investigators that the corrosive trauma to the respiratory system resulting from a single exposure to mustard gas might have causal relation to this subsequent development of cancer of the larynx and of the lung among veterans of the various armies”.
“Japanese investigators observed and reported during recent years that employees of war gas factories in Japan, exposed to mustard gas, died from chronic respiratory diseases which, for a number of years, had been clinically diagnosed as tuberculosis of the lung.
When subsequently on some of these death cases autopsies were performed, it was found that every one of these workers …….dying from tuberculosis of the lung had a cancer of the lung and in more recent years the Japanese observer also clinically confirmed the diagnosis, confirmed by biopsies, of cancer of the larynx among those workers.”
There is; moreover, a large scale English study on the relative frequency of cancer of the lung among English veterans of World War I on record in which the relative frequency of cancer of the lung among this population group in relation to the standard values was determined.”
http://tobaccodocuments.org/rjr/503243231-3367.html?zoom=750&ocr_position=above_foramatted&start_page=21
Mustard Gas Poisoning, Chronic Bronchitis and Lung Cancer – 1955
Click to access Case%20RAM%20and%20Lea%20AJ%201955%20mustard%20gas%20poisoning,%20chronic%20bronchitis.pdf
I would imagine that would contribute to a massive rise in male lung cancers from 1920 onward.
Did they allow for this in the original studies, or just lump everything together?
Rose
OK
I have to ask.
7. Coherence: Does it fit the overall pattern? Again, yes. The lung cancer rate rose first amongst men because they were the first to smoke and it rose later amongst women when they started to smoke.
“In fact the first observations on an appreciable rise in the frequency of lung cancer were reported from the highly industrialized cities of densely populated Saxony during the first two decades of this century.
Some years later it was found that high lung cancer rates existed for the population of the industrialized territory of the Ruhr valley, while they were below average for the agricultural region of the Main valley.”
http://www.chestjournal.org/cgi/reprint/30/2/141
Court testimony
“Q Actually Dr. when was an increase in lung cancer first noted?
A The pathologists of central Europe, particularly in Germany where autopsies were performed for many years in hospital institutes of pathology, the University institutes of pathology on the majority of patients who died in these hospitals, the percentage rate ran between 90% and 95% of the deaths which occurred, and showed around 1920 that there had been a gradual, and progressive increase in lung cancer deaths observed in autopsies since the turn of the Century.
Q Since about 1900?
A Around 1900
Q And then it gradually started to increase,
A the number of cases increased.
Having in mind that you were living in Central Europe, at that time, was there any increase in smoking during that period of time that parallelled the increase in lung cancer from 1900 to 1920?
A It is pretty well established from statements in the literature that a wide spread and general use of the cigarette among the people of industrialized countries started with the first World War.
That means there was an increase in the lung cancer incidence before the custom of smoking cigarettes became a widespread habit.”
http://tobaccodocuments.org/industry_depositions/503243231-3367.html?zoom=750&ocr_position=above_foramatted&start_page=1
“The dramatic growth of lung cancer in the 1920s and 1930s was not at first attributed to smoking: the influenza pandemic of 1919 was sometimes blamed, as were automobile exhaust, dust from newly tarred roads, diverse occupational exposures (including tar and diverse polycyclic hydrocarbons), increasing exposure to X rays, exposure to chemical warfare agents during the First World War,..”
http://toxicology.usu.edu/endnote/Proctor-Nazi-war-tobacco.htm
1957
“Soon after World War 1 when mustard gas had been used extensively for war purposes on both sides,the claim was advanced by some investigators that the corrosive trauma to the respiratory system resulting from a single exposure to mustard gas might have causal relation to this subsequent development of cancer of the larynx and of the lung among veterans of the various armies”.
“Japanese investigators observed and reported during recent years that employees of war gas factories in Japan, exposed to mustard gas, died from chronic respiratory diseases which, for a number of years, had been clinically diagnosed as tuberculosis of the lung.
When subsequently on some of these death cases autopsies were performed, it was found that every one of these workers …….dying from tuberculosis of the lung had a cancer of the lung and in more recent years the Japanese observer also clinically confirmed the diagnosis, confirmed by biopsies, of cancer of the larynx among those workers.”
There is; moreover, a large scale English study on the relative frequency of cancer of the lung among English veterans of World War I on record in which the relative frequency of cancer of the lung among this population group in relation to the standard values was determined.”
http://tobaccodocuments.org/rjr/503243231-3367.html?zoom=750&ocr_position=above_foramatted&start_page=21
Mustard Gas Poisoning, Chronic Bronchitis and Lung Cancer – 1955
Click to access Case%20RAM%20and%20Lea%20AJ%201955%20mustard%20gas%20poisoning,%20chronic%20bronchitis.pdf
I would imagine that would contribute to a massive rise in male lung cancers from 1920 onward.
Did they allow for this in the original studies, or just lump everything together?
Rose
OK
I have to ask.
7. Coherence: Does it fit the overall pattern? Again, yes. The lung cancer rate rose first amongst men because they were the first to smoke and it rose later amongst women when they started to smoke.
“In fact the first observations on an appreciable rise in the frequency of lung cancer were reported from the highly industrialized cities of densely populated Saxony during the first two decades of this century.
Some years later it was found that high lung cancer rates existed for the population of the industrialized territory of the Ruhr valley, while they were below average for the agricultural region of the Main valley.”
http://www.chestjournal.org/cgi/reprint/30/2/141
Court testimony
“Q Actually Dr. when was an increase in lung cancer first noted?
A The pathologists of central Europe, particularly in Germany where autopsies were performed for many years in hospital institutes of pathology, the University institutes of pathology on the majority of patients who died in these hospitals, the percentage rate ran between 90% and 95% of the deaths which occurred, and showed around 1920 that there had been a gradual, and progressive increase in lung cancer deaths observed in autopsies since the turn of the Century.
Q Since about 1900?
A Around 1900
Q And then it gradually started to increase,
A the number of cases increased.
Having in mind that you were living in Central Europe, at that time, was there any increase in smoking during that period of time that parallelled the increase in lung cancer from 1900 to 1920?
A It is pretty well established from statements in the literature that a wide spread and general use of the cigarette among the people of industrialized countries started with the first World War.
That means there was an increase in the lung cancer incidence before the custom of smoking cigarettes became a widespread habit.”
http://tobaccodocuments.org/industry_depositions/503243231-3367.html?zoom=750&ocr_position=above_foramatted&start_page=1
“The dramatic growth of lung cancer in the 1920s and 1930s was not at first attributed to smoking: the influenza pandemic of 1919 was sometimes blamed, as were automobile exhaust, dust from newly tarred roads, diverse occupational exposures (including tar and diverse polycyclic hydrocarbons), increasing exposure to X rays, exposure to chemical warfare agents during the First World War,..”
http://toxicology.usu.edu/endnote/Proctor-Nazi-war-tobacco.htm
1957
“Soon after World War 1 when mustard gas had been used extensively for war purposes on both sides,the claim was advanced by some investigators that the corrosive trauma to the respiratory system resulting from a single exposure to mustard gas might have causal relation to this subsequent development of cancer of the larynx and of the lung among veterans of the various armies”.
“Japanese investigators observed and reported during recent years that employees of war gas factories in Japan, exposed to mustard gas, died from chronic respiratory diseases which, for a number of years, had been clinically diagnosed as tuberculosis of the lung.
When subsequently on some of these death cases autopsies were performed, it was found that every one of these workers …….dying from tuberculosis of the lung had a cancer of the lung and in more recent years the Japanese observer also clinically confirmed the diagnosis, confirmed by biopsies, of cancer of the larynx among those workers.”
There is; moreover, a large scale English study on the relative frequency of cancer of the lung among English veterans of World War I on record in which the relative frequency of cancer of the lung among this population group in relation to the standard values was determined.”
http://tobaccodocuments.org/rjr/503243231-3367.html?zoom=750&ocr_position=above_foramatted&start_page=21
Mustard Gas Poisoning, Chronic Bronchitis and Lung Cancer – 1955
Click to access Case%20RAM%20and%20Lea%20AJ%201955%20mustard%20gas%20poisoning,%20chronic%20bronchitis.pdf
I would imagine that would contribute to a massive rise in male lung cancers from 1920 onward.
Did they allow for this in the original studies, or just lump everything together?
Rose
They were all lumped together. As I put in Catch-2 response, smoking has never been singled out as a lone factor for investigation, ‘smokers’ were studied rather than ‘smoking’ if you like. The 50s was, I think, a particularly difficult time to investgiate lung cancer precisely for the reasons you mentioned.
Causality
Chris opened quite rightly, in my opinion, with Hill’s criteria for good epidemiology. Rightly because it is the accuracy of the epidemiological evidence which is at the heart of the debate. Epidemiology can, at best, only identify an association. It is for the biological scientists to then elucidate a mechanism which explains the association.
An association between smoking and lung cancer has been demonstrated beyond any doubt. So the debate has two areas of discussion to pursue:
1. A scientific area: Is the association produced by an unknown confounder? That is: does something else that is present in the smoking group cause the association rather than the smoking? This is almost impossible to rule out with absolute certainty.
2. A semantic area: Does smoking cause lung cancer or does it increase the risk of an individual developing lung cancer? This area is the one where I have most of my concern. The use of the word cause presents the information to us as a straight forward statement that implies:
a. If you smoke you get lung cancer.
b. If you don’t smoke you won’t get lung cancer.
This is clearly far from the truth. In actuality lung cancer has a multifactorial causality. This is demonstrated by some smokers not developing the disease and some non-smokers developing the disease.
My position in summary is that what is true is that:
Smoking is associated with an increased risk of developing lung cancer in an individual.
What is not true:
Smoking causes lung cancer.
Causality
Chris opened quite rightly, in my opinion, with Hill’s criteria for good epidemiology. Rightly because it is the accuracy of the epidemiological evidence which is at the heart of the debate. Epidemiology can, at best, only identify an association. It is for the biological scientists to then elucidate a mechanism which explains the association.
An association between smoking and lung cancer has been demonstrated beyond any doubt. So the debate has two areas of discussion to pursue:
1. A scientific area: Is the association produced by an unknown confounder? That is: does something else that is present in the smoking group cause the association rather than the smoking? This is almost impossible to rule out with absolute certainty.
2. A semantic area: Does smoking cause lung cancer or does it increase the risk of an individual developing lung cancer? This area is the one where I have most of my concern. The use of the word cause presents the information to us as a straight forward statement that implies:
a. If you smoke you get lung cancer.
b. If you don’t smoke you won’t get lung cancer.
This is clearly far from the truth. In actuality lung cancer has a multifactorial causality. This is demonstrated by some smokers not developing the disease and some non-smokers developing the disease.
My position in summary is that what is true is that:
Smoking is associated with an increased risk of developing lung cancer in an individual.
What is not true:
Smoking causes lung cancer.
Causality
Chris opened quite rightly, in my opinion, with Hill’s criteria for good epidemiology. Rightly because it is the accuracy of the epidemiological evidence which is at the heart of the debate. Epidemiology can, at best, only identify an association. It is for the biological scientists to then elucidate a mechanism which explains the association.
An association between smoking and lung cancer has been demonstrated beyond any doubt. So the debate has two areas of discussion to pursue:
1. A scientific area: Is the association produced by an unknown confounder? That is: does something else that is present in the smoking group cause the association rather than the smoking? This is almost impossible to rule out with absolute certainty.
2. A semantic area: Does smoking cause lung cancer or does it increase the risk of an individual developing lung cancer? This area is the one where I have most of my concern. The use of the word cause presents the information to us as a straight forward statement that implies:
a. If you smoke you get lung cancer.
b. If you don’t smoke you won’t get lung cancer.
This is clearly far from the truth. In actuality lung cancer has a multifactorial causality. This is demonstrated by some smokers not developing the disease and some non-smokers developing the disease.
My position in summary is that what is true is that:
Smoking is associated with an increased risk of developing lung cancer in an individual.
What is not true:
Smoking causes lung cancer.
Re: Causality
Dear Gasdoc
You say that it is almost impossible to rule out with absolute certainty the existence of an unknown confounder. That is, of course, true, and would be assented to by the most ardent supporter of the smoking/lung cancer hypothesis. But we can’t leave it at that. As I pointed out in an earlier post, quoting Bradford Hill, ‘If we cannot detect it or reasonably infer a specific one [confounder], then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic “you can’t prove it, there may be such a feature”.’ There can always be an unknown confounder.
Your other point is that smoking can’t be a cause of lung cancer because (a) some (I would say many, in fact) smokers don’t get lung cancer, and (b) some non-smokers do get the disease. Both (a) and (b) are indisputably true, but your conclusion does not follow. Just because C is not always the cause of E doesn’t mean that it never is or never can be. Nor does it follow that because E sometimes happens when C is absent that C can’t cause E. Surely the causes of many chronic diseases fit into this ‘neither necessary nor sufficient’ category?
DW
Re: Causality
My confounder would be diet. It can certainly be detected and reasonably be infered as specific.
I did not say smoking can’t be a cause of lung cancer.
Re: Causality
My confounder would be diet. It can certainly be detected and reasonably be infered as specific.
You may well be right. It was your talk of ‘unknown’ confounders that confused me.
I did not say smoking can’t be a cause of lung cancer.
Does that mean that you think it can be a cause or do you mean that it is associated with an increased risk of developing the disease? My problem with the latter formulation is that ‘is associated with’ and ‘increased risk of’ are just too vague. I prefer to couch the discussion in terms of causation and my feeling is (and at this stage it is only a feeling) that smoking is either a cause of lung cancer or it isn’t. Of course this doesn’t rule out other causes.
We are on the same side – I’m just seeking clarification in my own mind as much as anything else.
DW
Re: Causality
I feel at present that my position is one of “sitting on the fence”. I can only apologise for that as it doesn’t help the debate and nor assist you with clarification.
My original post is pedantic in the extreme, but seeks to describe the current state of medical knowledge as I see it. That is “smoking is associated with an increased risk of lung cancer” states exactly the results of the epidemiology. So I’m saying the epidemiology doesn’t prove smoking is a cause of lung cancer. My position is that as diet is undoubtedly a cause of cancer it could well be the explanation of the association between smoking and lung cancer because smokers generally have poor/different diet.
An illustration of this is that red hair is associated with heart disease. But the real cause is some influence of diet and lifestyle. The reason for the association between red hair and heart disease is that the Scottish people both have a higher than average prevalence of read hair, poor diet and heart disease. It is easy to eliminate the red hair “confounder” in epidemiology but less so the diet.
So I’m saying that the epidemiology does not prove that smoking causes lung cancer and that assuming it does diverts resources away from elucidating the real situation. That is that many factors influence an individuals risk and these deserve further study.
I hope this helps. I realise that sometimes I may sound arrogant or confrontational in my writing style or short answers. I can assure you that this is not the case and I apologise if my short reply earlier seemed curt.
Re: Causality
So I’m saying that the epidemiology does not prove that smoking causes lung cancer and that assuming it does diverts resources away from elucidating the real situation. That is that many factors influence an individuals risk and these deserve further study.
I couldn’t agree more. You see, we are on the same side.
I realise that sometimes I may sound arrogant or confrontational in my writing style or short answers. I can assure you that this is not the case and I apologise if my short reply earlier seemed curt.
Not at all.
Best wishes
DW
Re: Causality
Dear Gasdoc
You say that it is almost impossible to rule out with absolute certainty the existence of an unknown confounder. That is, of course, true, and would be assented to by the most ardent supporter of the smoking/lung cancer hypothesis. But we can’t leave it at that. As I pointed out in an earlier post, quoting Bradford Hill, ‘If we cannot detect it or reasonably infer a specific one [confounder], then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic “you can’t prove it, there may be such a feature”.’ There can always be an unknown confounder.
Your other point is that smoking can’t be a cause of lung cancer because (a) some (I would say many, in fact) smokers don’t get lung cancer, and (b) some non-smokers do get the disease. Both (a) and (b) are indisputably true, but your conclusion does not follow. Just because C is not always the cause of E doesn’t mean that it never is or never can be. Nor does it follow that because E sometimes happens when C is absent that C can’t cause E. Surely the causes of many chronic diseases fit into this ‘neither necessary nor sufficient’ category?
DW
Re: Causality
Dear Gasdoc
You say that it is almost impossible to rule out with absolute certainty the existence of an unknown confounder. That is, of course, true, and would be assented to by the most ardent supporter of the smoking/lung cancer hypothesis. But we can’t leave it at that. As I pointed out in an earlier post, quoting Bradford Hill, ‘If we cannot detect it or reasonably infer a specific one [confounder], then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic “you can’t prove it, there may be such a feature”.’ There can always be an unknown confounder.
Your other point is that smoking can’t be a cause of lung cancer because (a) some (I would say many, in fact) smokers don’t get lung cancer, and (b) some non-smokers do get the disease. Both (a) and (b) are indisputably true, but your conclusion does not follow. Just because C is not always the cause of E doesn’t mean that it never is or never can be. Nor does it follow that because E sometimes happens when C is absent that C can’t cause E. Surely the causes of many chronic diseases fit into this ‘neither necessary nor sufficient’ category?
DW
CATCH 1
5. Biological gradient: Does the risk rise with the number of cigarettes smoked or the number of years of smoking. With a very good degree of consistency, studies have shown the answer to be yes.
———————–
This excludes 1 important factor – Biological Variation. Including the biological variation of a healthy individual as well as biological variation of an individual affected by an acute/chronic condition would perhaps provide a more accurate picture of the process by which active smoking can be said to be the direct cause of lung cancer (small cell carcinoma, squamous cell carcinoma and adenocarcinoma) and also provide an area of investigation into why a large number of people do not develop this disease.
CATCH 1
5. Biological gradient: Does the risk rise with the number of cigarettes smoked or the number of years of smoking. With a very good degree of consistency, studies have shown the answer to be yes.
———————–
This excludes 1 important factor – Biological Variation. Including the biological variation of a healthy individual as well as biological variation of an individual affected by an acute/chronic condition would perhaps provide a more accurate picture of the process by which active smoking can be said to be the direct cause of lung cancer (small cell carcinoma, squamous cell carcinoma and adenocarcinoma) and also provide an area of investigation into why a large number of people do not develop this disease.
CATCH 1
5. Biological gradient: Does the risk rise with the number of cigarettes smoked or the number of years of smoking. With a very good degree of consistency, studies have shown the answer to be yes.
———————–
This excludes 1 important factor – Biological Variation. Including the biological variation of a healthy individual as well as biological variation of an individual affected by an acute/chronic condition would perhaps provide a more accurate picture of the process by which active smoking can be said to be the direct cause of lung cancer (small cell carcinoma, squamous cell carcinoma and adenocarcinoma) and also provide an area of investigation into why a large number of people do not develop this disease.
Re: CATCH 1
There was a genuine biological, non-statistical, non-epidemological, study done in Japan a few years back in which scientists were able to show there is a gene marker in some individuals that makes them especially need intake of tobacco or else nicotine, and it had nothing to do with “addiction”. It had to do with their genetic make-up and some part on their DNA actually “craved” or needed tobacco/nicotine in order to fulfill a natural desire for individuals for whom this gene pattern existed. I cannot find the link which I thought I had saved – but this was within 2 years ago that this was reported briefly, in the MSM, then quickly disappeared. It was reported in a peer-reviewed medical journal at the time. So there may be something to the idea that some people “were born to smoke” and may or may not receive any ill-effects from it, where-as others might be the opposite and should be forewarned not to smoke, becuase of genetic composition. Anti-smoking politics would of course not allow such type of research to continue and the article was quickly hushed up shortly after its announcement. It’s too bad, because if that were the case, then like with diabetes testing resulting in some persons knowing they shouldn’t over-indulge in sugar, then maybe a similar test would indicate which people should, by their genetic make-up, be actively smoking and indicate for some, that they absolutely should not be.
Re: CATCH 1
Biological variation does not only apply to any particular genetic markers, it applies to every process occurring in our body at any given time with variations throughout the day, as well as those processes caused by acute/chronic diseases.
http://books.google.com/books?id=1YsDPMABuwEC&pg=PA82&lpg=PA82&dq=calculation+of+biological+variation&source=bl&ots=FdaiV0Csiq&sig=a8neqIK1vj1wGjvgOY0zAs5xSlY&hl=en&ei=YbTyTJrEPIyGhQe7k9XZDA&sa=X&oi=book_result&ct=result&resnum=3&sqi=2&ved=0CCQQ6AEwAg#v=onepage&q=calculation%20of%20biological%20variation&f=false
(hope the link works, happy perusal)
Clearly biological variation is an aspect for any investigation to be taken into account.
Re: CATCH 1
Sorry for the faulty link, here the book:
Biological Variation: From Principles to Practice
By Callum G. Fraser
Re: CATCH 1
There was a genuine biological, non-statistical, non-epidemological, study done in Japan a few years back in which scientists were able to show there is a gene marker in some individuals that makes them especially need intake of tobacco or else nicotine, and it had nothing to do with “addiction”. It had to do with their genetic make-up and some part on their DNA actually “craved” or needed tobacco/nicotine in order to fulfill a natural desire for individuals for whom this gene pattern existed. I cannot find the link which I thought I had saved – but this was within 2 years ago that this was reported briefly, in the MSM, then quickly disappeared. It was reported in a peer-reviewed medical journal at the time. So there may be something to the idea that some people “were born to smoke” and may or may not receive any ill-effects from it, where-as others might be the opposite and should be forewarned not to smoke, becuase of genetic composition. Anti-smoking politics would of course not allow such type of research to continue and the article was quickly hushed up shortly after its announcement. It’s too bad, because if that were the case, then like with diabetes testing resulting in some persons knowing they shouldn’t over-indulge in sugar, then maybe a similar test would indicate which people should, by their genetic make-up, be actively smoking and indicate for some, that they absolutely should not be.
Re: CATCH 1
There was a genuine biological, non-statistical, non-epidemological, study done in Japan a few years back in which scientists were able to show there is a gene marker in some individuals that makes them especially need intake of tobacco or else nicotine, and it had nothing to do with “addiction”. It had to do with their genetic make-up and some part on their DNA actually “craved” or needed tobacco/nicotine in order to fulfill a natural desire for individuals for whom this gene pattern existed. I cannot find the link which I thought I had saved – but this was within 2 years ago that this was reported briefly, in the MSM, then quickly disappeared. It was reported in a peer-reviewed medical journal at the time. So there may be something to the idea that some people “were born to smoke” and may or may not receive any ill-effects from it, where-as others might be the opposite and should be forewarned not to smoke, becuase of genetic composition. Anti-smoking politics would of course not allow such type of research to continue and the article was quickly hushed up shortly after its announcement. It’s too bad, because if that were the case, then like with diabetes testing resulting in some persons knowing they shouldn’t over-indulge in sugar, then maybe a similar test would indicate which people should, by their genetic make-up, be actively smoking and indicate for some, that they absolutely should not be.
Re: Regarding these Maps
One might also super-impose other maps upon this map, maps showing all sorts of situations particular to the entire US, including location of nuclear power plants. On the map above showing the US, the comment about Sacramento east of San Francisco receiving all their smog from auto and diesel exhaust could also have said that Sacramento was home to a large nuclear power generating facility at one time, that has since been shut down, but operated for decades, a power plant that was similar to the one operating at Three Mile Island in the eastern US. If one is going to correlate cause and effect using statistics, then two maps superimposed could say increase in lung cancer is correlated (or not) with proximity of nuclear power plants having operated in the same area and come up with the same conclusions as automatically pronounced against tobacco usage as it’s really just the same conjecture.
Re: Regarding these Maps
One might also super-impose other maps upon this map, maps showing all sorts of situations particular to the entire US, including location of nuclear power plants. On the map above showing the US, the comment about Sacramento east of San Francisco receiving all their smog from auto and diesel exhaust could also have said that Sacramento was home to a large nuclear power generating facility at one time, that has since been shut down, but operated for decades, a power plant that was similar to the one operating at Three Mile Island in the eastern US. If one is going to correlate cause and effect using statistics, then two maps superimposed could say increase in lung cancer is correlated (or not) with proximity of nuclear power plants having operated in the same area and come up with the same conclusions as automatically pronounced against tobacco usage as it’s really just the same conjecture.
An old retired US sailor once commented to me that his personal observation was that lung cancers didn’t start becoming prevalent until people stopped using sulfur matches and flint cigarette lighters and began using propane lighters to light cigarettes as their popularity and availability grew.
In the manufacture of cigarettes, stale cartons are sent back to the tobacco companies who credit the retailers for unsold goods – the filling inside those cigarettes are extracted, run through a slurry of chemicals of all sorts, sliced down into tiny bits and recombined with the fresh tobacco on the assembly line. Thus some brands (cheaper) are a high percentage of recombined chemically reconstituted unsold tobacco returned to the manufacturer while other brands (premium priced) have less of the recombined chemically treated filler and more genuine tobacco added to them.
Maybe all those chemicals from the reconstituted products makes a difference, especially after it’s been recycled over and over and over again – then it’s not even tobacco at some point but a chemical soup that is being manufactured.
Popular in some parts of the US these days is a wholly organic, non-chemically treated, tobacco cigarette product into which no reconstituted product is added, being marketed out of New Mexico by a company owned by RJ Reynolds, who is one of the major manufacturers over there, by the name of Spirit brand.
An old retired US sailor once commented to me that his personal observation was that lung cancers didn’t start becoming prevalent until people stopped using sulfur matches and flint cigarette lighters and began using propane lighters to light cigarettes as their popularity and availability grew.
In the manufacture of cigarettes, stale cartons are sent back to the tobacco companies who credit the retailers for unsold goods – the filling inside those cigarettes are extracted, run through a slurry of chemicals of all sorts, sliced down into tiny bits and recombined with the fresh tobacco on the assembly line. Thus some brands (cheaper) are a high percentage of recombined chemically reconstituted unsold tobacco returned to the manufacturer while other brands (premium priced) have less of the recombined chemically treated filler and more genuine tobacco added to them.
Maybe all those chemicals from the reconstituted products makes a difference, especially after it’s been recycled over and over and over again – then it’s not even tobacco at some point but a chemical soup that is being manufactured.
Popular in some parts of the US these days is a wholly organic, non-chemically treated, tobacco cigarette product into which no reconstituted product is added, being marketed out of New Mexico by a company owned by RJ Reynolds, who is one of the major manufacturers over there, by the name of Spirit brand.
Re: CATCH 1
Biological variation does not only apply to any particular genetic markers, it applies to every process occurring in our body at any given time with variations throughout the day, as well as those processes caused by acute/chronic diseases.
http://books.google.com/books?id=1YsDPMABuwEC&pg=PA82&lpg=PA82&dq=calculation+of+biological+variation&source=bl&ots=FdaiV0Csiq&sig=a8neqIK1vj1wGjvgOY0zAs5xSlY&hl=en&ei=YbTyTJrEPIyGhQe7k9XZDA&sa=X&oi=book_result&ct=result&resnum=3&sqi=2&ved=0CCQQ6AEwAg#v=onepage&q=calculation%20of%20biological%20variation&f=false
(hope the link works, happy perusal)
Clearly biological variation is an aspect for any investigation to be taken into account.
Re: CATCH 1
Biological variation does not only apply to any particular genetic markers, it applies to every process occurring in our body at any given time with variations throughout the day, as well as those processes caused by acute/chronic diseases.
http://books.google.com/books?id=1YsDPMABuwEC&pg=PA82&lpg=PA82&dq=calculation+of+biological+variation&source=bl&ots=FdaiV0Csiq&sig=a8neqIK1vj1wGjvgOY0zAs5xSlY&hl=en&ei=YbTyTJrEPIyGhQe7k9XZDA&sa=X&oi=book_result&ct=result&resnum=3&sqi=2&ved=0CCQQ6AEwAg#v=onepage&q=calculation%20of%20biological%20variation&f=false
(hope the link works, happy perusal)
Clearly biological variation is an aspect for any investigation to be taken into account.
Re: CATCH 1
Sorry for the faulty link, here the book:
Biological Variation: From Principles to Practice
By Callum G. Fraser
Re: CATCH 1
Sorry for the faulty link, here the book:
Biological Variation: From Principles to Practice
By Callum G. Fraser
Re: To Chris and Frank
In the 1954 British Doctors study, it states how the doctors were asked to classify themselves:
In addition to giving their name, address, and age, the doctors were asked to classify themselves into one of three groups – namely, (a) whether they were, at that time, smoking; (b) whether they had smoked but had given up; (c) whether they had never smoked regularly (that is, had never smoked as much as one cigarette a day, or its equivalent in pipe tobacco, for as long as one year).
I have spent many happy hours considering how these questions might be misunderstood or misrepresented. For example, (a) could be misinterpreted as meaning, are you smoking a cigarette right this second? (b) is also open to misinterpretation. And I defy anybody to say exactly what the convoluted question (c) means.
The definition of what a ‘smoker’ is seems to have changed from year to year, almost. The current view seems to be that you’re a smoker if you’ve smoked more than 100 cigarettes in your lifetime. Why 100? Why not 50, or 500?
Similar problems arise in defining an ‘ex-smoker’. How long do you have to have given up smoking before you can call yourself an ex-smoker? 5 years? 1 year? 3 months? 2 days? 15 minutes?
I think Doll and Hill probably realised that if they simply said the obvious, that a non-smoker was someone who had never smoked a single cigarette in their life, they would have had precious few non-smokers. So they relaxed the definition. But they could have relaxed it to the point that a non-smoker was someone who didn’t currently have a cigarette in their mouth.
In these days of passive smoking when there is the category of the ‘never-smoker’, we also have to wonder how much secondhand smoke these never smokers have inhaled. I’ve forgotten what the cigarette-equivalent of sitting in a smoky bar all evening is, but I can well imagine that over a few years or decades it could well add up to more than 100 cigarettes – so that even ‘never-smokers’ are smokers.
Frank
Re: To Chris and Frank
In the 1954 British Doctors study, it states how the doctors were asked to classify themselves:
In addition to giving their name, address, and age, the doctors were asked to classify themselves into one of three groups – namely, (a) whether they were, at that time, smoking; (b) whether they had smoked but had given up; (c) whether they had never smoked regularly (that is, had never smoked as much as one cigarette a day, or its equivalent in pipe tobacco, for as long as one year).
I have spent many happy hours considering how these questions might be misunderstood or misrepresented. For example, (a) could be misinterpreted as meaning, are you smoking a cigarette right this second? (b) is also open to misinterpretation. And I defy anybody to say exactly what the convoluted question (c) means.
The definition of what a ‘smoker’ is seems to have changed from year to year, almost. The current view seems to be that you’re a smoker if you’ve smoked more than 100 cigarettes in your lifetime. Why 100? Why not 50, or 500?
Similar problems arise in defining an ‘ex-smoker’. How long do you have to have given up smoking before you can call yourself an ex-smoker? 5 years? 1 year? 3 months? 2 days? 15 minutes?
I think Doll and Hill probably realised that if they simply said the obvious, that a non-smoker was someone who had never smoked a single cigarette in their life, they would have had precious few non-smokers. So they relaxed the definition. But they could have relaxed it to the point that a non-smoker was someone who didn’t currently have a cigarette in their mouth.
In these days of passive smoking when there is the category of the ‘never-smoker’, we also have to wonder how much secondhand smoke these never smokers have inhaled. I’ve forgotten what the cigarette-equivalent of sitting in a smoky bar all evening is, but I can well imagine that over a few years or decades it could well add up to more than 100 cigarettes – so that even ‘never-smokers’ are smokers.
Frank
Iro,
Hope this helps:
Wynder’s 1950 study:
‘Nonsmokers (less than 1 cigaret per day for more than twenty years)'”
…
“If a patient smoked for less than twenty years, his amount of smoking was adjusted to a twenty year period. Thus a patient smoking 20 cigarets for ten years only was classified as smoking 10 cigarets daily. ”
…
Pipe and cigar smokers were recast as cigaret equivalents. My copy is rather illegible but I think it makes a cigar equivalent to 3 cigarets and a pipe equivalent to 2.5 cigarets.
Doll’s 1950 Hospital study and Doll’s ‘British Doctors Study’:
(Hill was Doll’s supervisor and co-author on these papers)
“A smoker was therefore defined in this inquiry as a person who had smoked as much as one cigarette a day for as long as a year.” Pipe and cigar smoker consumption was based on grams of tobacco smoked with 1g = 1 cigarette.
So Wynder’s definition of a non-smoker was less than 20 X 365 X 1 = 7300 cigarettes or equivalent in a lifetime. Doll and Hill’s definition was 365 cigarettes in a lifetime.
Quite a difference but both are very small and Doll’s figure is very similar to the cut-off of 100 cigarettes in a lifetime that seems in common use today.
As to inhaling, smokers who inhaled were found to be significantly LESS likely to die of lung cancer.
Tony
Iro,
Hope this helps:
Wynder’s 1950 study:
‘Nonsmokers (less than 1 cigaret per day for more than twenty years)'”
…
“If a patient smoked for less than twenty years, his amount of smoking was adjusted to a twenty year period. Thus a patient smoking 20 cigarets for ten years only was classified as smoking 10 cigarets daily. ”
…
Pipe and cigar smokers were recast as cigaret equivalents. My copy is rather illegible but I think it makes a cigar equivalent to 3 cigarets and a pipe equivalent to 2.5 cigarets.
Doll’s 1950 Hospital study and Doll’s ‘British Doctors Study’:
(Hill was Doll’s supervisor and co-author on these papers)
“A smoker was therefore defined in this inquiry as a person who had smoked as much as one cigarette a day for as long as a year.” Pipe and cigar smoker consumption was based on grams of tobacco smoked with 1g = 1 cigarette.
So Wynder’s definition of a non-smoker was less than 20 X 365 X 1 = 7300 cigarettes or equivalent in a lifetime. Doll and Hill’s definition was 365 cigarettes in a lifetime.
Quite a difference but both are very small and Doll’s figure is very similar to the cut-off of 100 cigarettes in a lifetime that seems in common use today.
As to inhaling, smokers who inhaled were found to be significantly LESS likely to die of lung cancer.
Tony
They never seem to ask smokers in these studies what brand of tobacco they habitually smoke (and most smokers do habitually smoke one brand).
And I’ve occasionally wondered whether the means of lighting a cigarette might be relevant. When I used matches, I’d quite often light a cigarette with the flaring ignition of whatever compound was on the end of the match, rather than wait for the match to be well alight. And I didn’t like what I was inhaling, because it left a nasty taste.
I suspect that gas lighters are probably the cleanest, in that the gas usually burns to produce CO2 and water. But before I used gas lighters, I’d use fuel lighters, which almost certainly produced a lot of combustion products.
What did they use before matches and lighters? Candles, probably, I imagine.
Frank
They never seem to ask smokers in these studies what brand of tobacco they habitually smoke (and most smokers do habitually smoke one brand).
And I’ve occasionally wondered whether the means of lighting a cigarette might be relevant. When I used matches, I’d quite often light a cigarette with the flaring ignition of whatever compound was on the end of the match, rather than wait for the match to be well alight. And I didn’t like what I was inhaling, because it left a nasty taste.
I suspect that gas lighters are probably the cleanest, in that the gas usually burns to produce CO2 and water. But before I used gas lighters, I’d use fuel lighters, which almost certainly produced a lot of combustion products.
What did they use before matches and lighters? Candles, probably, I imagine.
Frank
They were all lumped together. As I put in Catch-2 response, smoking has never been singled out as a lone factor for investigation, ‘smokers’ were studied rather than ‘smoking’ if you like. The 50s was, I think, a particularly difficult time to investgiate lung cancer precisely for the reasons you mentioned.
They were all lumped together. As I put in Catch-2 response, smoking has never been singled out as a lone factor for investigation, ‘smokers’ were studied rather than ‘smoking’ if you like. The 50s was, I think, a particularly difficult time to investgiate lung cancer precisely for the reasons you mentioned.
Lung cancer in smokers looks different than in non-smoker
http://www.montrealgazette.com/health/Lung+cancer+smokers+looks+different+than+smoker/3806044/story.html
Lung cancer in smokers looks different than in non-smoker
http://www.montrealgazette.com/health/Lung+cancer+smokers+looks+different+than+smoker/3806044/story.html
Lung cancer in smokers looks different than in non-smoker
http://www.montrealgazette.com/health/Lung+cancer+smokers+looks+different+than+smoker/3806044/story.html
Mesothelioma has been associated with the exposure to asbestos. It is also associated with “Exposure to a particular virus – A virus called simian virus 40 (SV 40) has been linked with some cases of mesothelioma
# Exposure to radiation”
This should affect smokers and non-smokers alike.
Types of Lung Cancer in Non-Smokers
While over half of lung cancers in smokers are classified as squamous cell lung cancers (a type of non-small cell lung cancer), the majority of lung cancers in non-smokers are adenocarcinomas (another type of non-small cell lung cancer).
Squamous cell lung cancers tend to grow near the airways and cause symptoms early on, such as coughing or coughing up blood (hemoptysis).
“Adenocarcinomas often grow in the outer regions of the lungs and can be present for a long time before symptoms occur. Symptoms such as shortness of breath, fatigue, or symptoms due to spread of the cancer to other regions of the body (such as bone pain) may be more common”.
I’m sorry – I did read that these were the cancers associated with smokers….
Re: No smoking animal studies have produced lung cancer
I agree Frank but thought I would add a little more.
The McTear case was taken out by ASH and they employed the country’s top anti-smoking ‘experts’ such as James Friend and Richard Doll. Their barrister was Mr McEachran and the judge stated:
[6.150] Mr McEachran did not seek to argue that the causal connection between cigarette smoking and lung cancer had been established by any branch of scientific inquiry other than epidemiology. He accepted that it was established on the evidence that the process by which lung cancer developed was not yet known (see para.[6.30]). He also accepted in effect, at para.[6.56], that the averment for ITL at p.16 of the Closed Record was proved, “that over several decades, an enormous research effort has been made to produce in the laboratory the kind of lung cancer reported to be statistically associated with smoking. However, researchers have been unable to produce such cancer in test animals exposed to fresh whole smoke.”
See more on the judge’s summing up in [6.139], [6.151] and [6.153].
I also remember reading somewhere that Dr Elizabeth Whelan of ACSH had stated this as well but I can’t find it now.
Tony
Re: No smoking animal studies have produced lung cancer
I agree Frank but thought I would add a little more.
The McTear case was taken out by ASH and they employed the country’s top anti-smoking ‘experts’ such as James Friend and Richard Doll. Their barrister was Mr McEachran and the judge stated:
[6.150] Mr McEachran did not seek to argue that the causal connection between cigarette smoking and lung cancer had been established by any branch of scientific inquiry other than epidemiology. He accepted that it was established on the evidence that the process by which lung cancer developed was not yet known (see para.[6.30]). He also accepted in effect, at para.[6.56], that the averment for ITL at p.16 of the Closed Record was proved, “that over several decades, an enormous research effort has been made to produce in the laboratory the kind of lung cancer reported to be statistically associated with smoking. However, researchers have been unable to produce such cancer in test animals exposed to fresh whole smoke.”
See more on the judge’s summing up in [6.139], [6.151] and [6.153].
I also remember reading somewhere that Dr Elizabeth Whelan of ACSH had stated this as well but I can’t find it now.
Tony
Mesothelioma has been associated with the exposure to asbestos. It is also associated with “Exposure to a particular virus – A virus called simian virus 40 (SV 40) has been linked with some cases of mesothelioma
# Exposure to radiation”
This should affect smokers and non-smokers alike.
Types of Lung Cancer in Non-Smokers
While over half of lung cancers in smokers are classified as squamous cell lung cancers (a type of non-small cell lung cancer), the majority of lung cancers in non-smokers are adenocarcinomas (another type of non-small cell lung cancer).
Squamous cell lung cancers tend to grow near the airways and cause symptoms early on, such as coughing or coughing up blood (hemoptysis).
“Adenocarcinomas often grow in the outer regions of the lungs and can be present for a long time before symptoms occur. Symptoms such as shortness of breath, fatigue, or symptoms due to spread of the cancer to other regions of the body (such as bone pain) may be more common”.
I’m sorry – I did read that these were the cancers associated with smokers….
Mesothelioma has been associated with the exposure to asbestos. It is also associated with “Exposure to a particular virus – A virus called simian virus 40 (SV 40) has been linked with some cases of mesothelioma
# Exposure to radiation”
This should affect smokers and non-smokers alike.
Types of Lung Cancer in Non-Smokers
While over half of lung cancers in smokers are classified as squamous cell lung cancers (a type of non-small cell lung cancer), the majority of lung cancers in non-smokers are adenocarcinomas (another type of non-small cell lung cancer).
Squamous cell lung cancers tend to grow near the airways and cause symptoms early on, such as coughing or coughing up blood (hemoptysis).
“Adenocarcinomas often grow in the outer regions of the lungs and can be present for a long time before symptoms occur. Symptoms such as shortness of breath, fatigue, or symptoms due to spread of the cancer to other regions of the body (such as bone pain) may be more common”.
I’m sorry – I did read that these were the cancers associated with smokers….
My apologies if this appears twice. It seems the first time I posted it it didn’t appear:
All this is very wishy washy and makes any and all of these studies hard to believe especially when one reads in one particular study that I came across by accident that 280,000 cigarettes is considered the cut-off point in many studies of when tumors are noticed http://www.ncbi.nlm.nih.gov/pubmed/15207443 . I tried to find other references to this 280,000 cigarette contention but couldn’t. Did anyone ever come across anything that refers to it?
In my opinion, as long as they don’t do studies that target more narrowed down categories of smokers i.e. occasional, light, moderate, heavy, very heavy, any of the conclusions they come up with are suspect. I would like to see a study that had a complete distinct cohort of smokers who only smoked 1 to 5 or even 10 a day compared to a control group of non-smokers. Bets are the RR will be null or maybe very slightly increased for those who smoked 10. This is my opinion based on every day observations, not some theoretical figures thrown around by acamedics splitting hairs in 4.
Iro
My apologies if this appears twice. It seems the first time I posted it it didn’t appear:
All this is very wishy washy and makes any and all of these studies hard to believe especially when one reads in one particular study that I came across by accident that 280,000 cigarettes is considered the cut-off point in many studies of when tumors are noticed http://www.ncbi.nlm.nih.gov/pubmed/15207443 . I tried to find other references to this 280,000 cigarette contention but couldn’t. Did anyone ever come across anything that refers to it?
In my opinion, as long as they don’t do studies that target more narrowed down categories of smokers i.e. occasional, light, moderate, heavy, very heavy, any of the conclusions they come up with are suspect. I would like to see a study that had a complete distinct cohort of smokers who only smoked 1 to 5 or even 10 a day compared to a control group of non-smokers. Bets are the RR will be null or maybe very slightly increased for those who smoked 10. This is my opinion based on every day observations, not some theoretical figures thrown around by acamedics splitting hairs in 4.
Iro
Re: Causality
My confounder would be diet. It can certainly be detected and reasonably be infered as specific.
I did not say smoking can’t be a cause of lung cancer.
Re: Causality
My confounder would be diet. It can certainly be detected and reasonably be infered as specific.
I did not say smoking can’t be a cause of lung cancer.
Re: Regarding these Maps
“But the much higher population densities and better hospitals in NY would seem to me to suggest that the lung cancer mortality is measured more accurately there.”
Yes, I would agree. That’s why I’m skeptical that central states always seem to be less affected when one looks at almost any per 100,000 analysis. Not only in health statistics, but in employment and economic analysis as well. Then again, perhaps it just seems that way to me.
-WS
Re: Regarding these Maps
“But the much higher population densities and better hospitals in NY would seem to me to suggest that the lung cancer mortality is measured more accurately there.”
Yes, I would agree. That’s why I’m skeptical that central states always seem to be less affected when one looks at almost any per 100,000 analysis. Not only in health statistics, but in employment and economic analysis as well. Then again, perhaps it just seems that way to me.
-WS
Re: Bradford Hill again
‘To explain the pronounced excess of cancer of the lung in any other environmental terms [i.e. other than smoking] requires some feature of life so intimately linked with cigarette smoking and with the amount of smoking that such a feature should be easily detectable. If we cannot detect it or reasonably infer a specific one, then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic “you can’t prove it, there may be such a feature”.’
I can think of two – matches and lighters. Maybe it’s people who use sulpher encrusted matches to light their cigarettes, or those who inhale the first puff which contains the gas/sulpher.
Re: Bradford Hill again
‘To explain the pronounced excess of cancer of the lung in any other environmental terms [i.e. other than smoking] requires some feature of life so intimately linked with cigarette smoking and with the amount of smoking that such a feature should be easily detectable. If we cannot detect it or reasonably infer a specific one, then in such circumstances I think we are reasonably entitled to reject the vague contention of the armchair critic “you can’t prove it, there may be such a feature”.’
I can think of two – matches and lighters. Maybe it’s people who use sulpher encrusted matches to light their cigarettes, or those who inhale the first puff which contains the gas/sulpher.
Have there ever been any studies looking at matches/lighters? Wondering if inhaling these fumes could be a culprit.
Have there ever been any studies looking at matches/lighters? Wondering if inhaling these fumes could be a culprit.
Have there ever been any studies looking at matches/lighters? Wondering if inhaling these fumes could be a culprit.
Re: Causality
My confounder would be diet. It can certainly be detected and reasonably be infered as specific.
You may well be right. It was your talk of ‘unknown’ confounders that confused me.
I did not say smoking can’t be a cause of lung cancer.
Does that mean that you think it can be a cause or do you mean that it is associated with an increased risk of developing the disease? My problem with the latter formulation is that ‘is associated with’ and ‘increased risk of’ are just too vague. I prefer to couch the discussion in terms of causation and my feeling is (and at this stage it is only a feeling) that smoking is either a cause of lung cancer or it isn’t. Of course this doesn’t rule out other causes.
We are on the same side – I’m just seeking clarification in my own mind as much as anything else.
DW
Re: Causality
My confounder would be diet. It can certainly be detected and reasonably be infered as specific.
You may well be right. It was your talk of ‘unknown’ confounders that confused me.
I did not say smoking can’t be a cause of lung cancer.
Does that mean that you think it can be a cause or do you mean that it is associated with an increased risk of developing the disease? My problem with the latter formulation is that ‘is associated with’ and ‘increased risk of’ are just too vague. I prefer to couch the discussion in terms of causation and my feeling is (and at this stage it is only a feeling) that smoking is either a cause of lung cancer or it isn’t. Of course this doesn’t rule out other causes.
We are on the same side – I’m just seeking clarification in my own mind as much as anything else.
DW
Re: Causality
I feel at present that my position is one of “sitting on the fence”. I can only apologise for that as it doesn’t help the debate and nor assist you with clarification.
My original post is pedantic in the extreme, but seeks to describe the current state of medical knowledge as I see it. That is “smoking is associated with an increased risk of lung cancer” states exactly the results of the epidemiology. So I’m saying the epidemiology doesn’t prove smoking is a cause of lung cancer. My position is that as diet is undoubtedly a cause of cancer it could well be the explanation of the association between smoking and lung cancer because smokers generally have poor/different diet.
An illustration of this is that red hair is associated with heart disease. But the real cause is some influence of diet and lifestyle. The reason for the association between red hair and heart disease is that the Scottish people both have a higher than average prevalence of read hair, poor diet and heart disease. It is easy to eliminate the red hair “confounder” in epidemiology but less so the diet.
So I’m saying that the epidemiology does not prove that smoking causes lung cancer and that assuming it does diverts resources away from elucidating the real situation. That is that many factors influence an individuals risk and these deserve further study.
I hope this helps. I realise that sometimes I may sound arrogant or confrontational in my writing style or short answers. I can assure you that this is not the case and I apologise if my short reply earlier seemed curt.
Re: Causality
I feel at present that my position is one of “sitting on the fence”. I can only apologise for that as it doesn’t help the debate and nor assist you with clarification.
My original post is pedantic in the extreme, but seeks to describe the current state of medical knowledge as I see it. That is “smoking is associated with an increased risk of lung cancer” states exactly the results of the epidemiology. So I’m saying the epidemiology doesn’t prove smoking is a cause of lung cancer. My position is that as diet is undoubtedly a cause of cancer it could well be the explanation of the association between smoking and lung cancer because smokers generally have poor/different diet.
An illustration of this is that red hair is associated with heart disease. But the real cause is some influence of diet and lifestyle. The reason for the association between red hair and heart disease is that the Scottish people both have a higher than average prevalence of read hair, poor diet and heart disease. It is easy to eliminate the red hair “confounder” in epidemiology but less so the diet.
So I’m saying that the epidemiology does not prove that smoking causes lung cancer and that assuming it does diverts resources away from elucidating the real situation. That is that many factors influence an individuals risk and these deserve further study.
I hope this helps. I realise that sometimes I may sound arrogant or confrontational in my writing style or short answers. I can assure you that this is not the case and I apologise if my short reply earlier seemed curt.
Re: Causality
So I’m saying that the epidemiology does not prove that smoking causes lung cancer and that assuming it does diverts resources away from elucidating the real situation. That is that many factors influence an individuals risk and these deserve further study.
I couldn’t agree more. You see, we are on the same side.
I realise that sometimes I may sound arrogant or confrontational in my writing style or short answers. I can assure you that this is not the case and I apologise if my short reply earlier seemed curt.
Not at all.
Best wishes
DW
Re: Causality
So I’m saying that the epidemiology does not prove that smoking causes lung cancer and that assuming it does diverts resources away from elucidating the real situation. That is that many factors influence an individuals risk and these deserve further study.
I couldn’t agree more. You see, we are on the same side.
I realise that sometimes I may sound arrogant or confrontational in my writing style or short answers. I can assure you that this is not the case and I apologise if my short reply earlier seemed curt.
Not at all.
Best wishes
DW
Re: Lung Cancer geographical distribution
Here is a night map
http://www.worldmapsonline.com/SatPosters/NorthAmericaNight.htm for comparison
Fredrik
Re: Lung Cancer geographical distribution
Here is a night map
http://www.worldmapsonline.com/SatPosters/NorthAmericaNight.htm for comparison
Fredrik
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This variant does not approach me. Perhaps there are still variants?
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This variant does not approach me. Perhaps there are still variants?
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This variant does not approach me. Perhaps there are still variants?