Chris Snowdon responds to Rich White and Frank Davis.
Epidemiological studies:
Frank points out that 98% of the (male) patients in the first Doll/Hill study were smokers. This is true, but we know that even in 1950, 98% was not the general smoking rate amongst men (it was around 75%). So how did Doll end up with such a disproportionately large group of smokers in his sample? He didn’t grab them off the street. They were in the sample because it was a study of hospital patients, half of whom had lung cancer. The fact that a random sample of seriously ill people had an unusually large number of smokers amongst them is not the best advertisement for smoking! Doll and Hill weren’t to know that smoking causes all sorts of other diseases that would land smokers in hospital, such as heart disease. Had they known, they might have picked healthy controls from the general population, which had a lower smoking rate and would, therefore, have strengthened their findings.
As it happened, they had no need to. Even with the very high rate of smoking amongst the patients, a clear difference was found. Only 2 of the 647 lung cancer patients were not smokers (0.3%), compared with 27 of the 647 non-cancer patients (4.2%). The lung cancer patients were 13.5 times more likely to be smokers.
Rich brings up the issue of inhalation, which has been doing the rounds since the arch-sceptic Ronald A. Fisher raised it in 1950. Doll and Hill asked patients whether or not they inhaled their cigarettes. 61.6% of the lung cancer patients said they did compared to 67.2% of the non-cancer patients. The difference between the two figures is actually pretty slight. The main thing it tells us is that there were a lot of liars in both groups, as the large number of supposed non-inhalers is difficult to believe. Subsequent (larger) studies in Canada and USA found the proportion of non-inhalers to be 11% and 6% respectively (Surgeon General’s Report, 1964; p. 91 – see Figure 1 below). Both of these studies found the non-inhalers to have the lowest risk. The Doll study is a slight outlier in this respect, although the difference in responses from the two groups is not great, and, as Doll and Hill say in the text of the study, it is not statistically significant once adjusted for confounding.
 |
| Figure 1 |
Fisher didn’t have to get the raw data to see any of this, by the way, Doll and Hill drew attention to it themselves on p. 744, which they are unlikely to have done if they were trying to trick anybody. This brings me nicely on to the question of reliability. It has already been noted that Doll was a smoker himself, as was Evarts Graham (whose study with Ernst Wynder predated Doll’s by a few months). As indeed were several members of the Surgeon General’s panel and many senior doctors. These were not people who were fanatical haters of tobacco and it is difficult to see what their motive might be if—as is being suggested—they twisted the evidence. Like all scientists who do newsworthy research they could be accused of careerism and publicity-seeking, but this is not sufficient either to explain a “scam” that has lasted sixty years, nor why they would choose to demonise their own pleasures.
Many researchers working in tobacco control today can be justly accused of egotism, rent-seeking, being in the pay of pharmaceutical companies, having a background in anti-smoking fanaticism and—not uncommonly—having a personal obsession with smokers and smoking legislation. The same was not true in the 1950s and 1960s. It is a sad reflection on the state of the academic field that, as a result of the biases that have grown up over the years, research written decades ago is more likely to be unbiased and reliable than studies published today.
Neither of the Doll and Hill studies were perfect, just as no epidemiological study is perfect, but the case against smoking hangs on much more than two articles. In 1964, the Surgeon General evaluated 7 prospective studies, including the massive American Cancer Society study of men in 25 US states. The number of people included in these studies totalled over 1,100,000 (Doll’s doctors study was the smallest of them). All of them found higher rates of mortality amongst smokers, higher rates of lung cancer amongst smokers and—with remarkable consistency—found that the risk increased with the amount smoked.
This was supported by 9 case-control studies (see Figure 2 below) which again found a consistent raising of risk and a consistent dose-response relationship. Lung cancer risk was elevated from 2.4 for light smokers to 34.1 for the heaviest smokers.
 |
| Figure 2 |
As has been pointed out, epidemiology can never prove causation, but the correlation is undeniable (even Fisher never denied that there was a correlation). Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.
Animal studies:
It is difficult to force animals to develop lung cancer because it’s difficult (a) to get animals to smoke, and (b) to have the necessary time-frame for lung cancer to develop (a major risk factor for all cancers is ageing). It takes several decades for human beings to smoke and it is therefore very hard to replicate the human experience of chronic, long-term smoking on animals. A bigger problem is that animals breathe through their nose, thereby filtering the smoke. Most experiments with animals are really showing the effect of secondhand smoke (albeit in unrealistically high doses) and, yes, most of them fail. However, Oscar Auerbach did manage it with beagles in 1970, by giving them tracheotomies. 12 of the 86 dogs did get lung cancer over an 18 month period, although Auerbach was criticised by animal rights campaigners and the experiment wasn’t repeated (and tobacco testing with animals was banned in the UK in 1997). Privately, the tobacco industry accepted the experiment as valid. A memo from a Philip Morris scientist read: “I would say that the experiment is a crude one but effective in that carcinoma in dogs has been produced.” A scientist at Gallagher wrote a memo saying: “We believe the Auerbach work proves beyond all reasonable doubt that fresh whole cigarette smoke is carcinogenic to dog lungs and therefore it is highly likely that it would be carcinogenic to human lungs… the results of the research would appear to remove the controversy regarding the causation of the majority of human lung cancer.”
Ecological studies:
The geographical spread of lung cancer follows several decades behind the geographical spread of smoking. For the lung cancer epidemic to begin, you need to have a sizeable group of people who have been smoking for at least 20 years. Rich says that the “highest smoking rates tend to have the lowest lung cancer rates and vice versa” and uses Greece, Japan, China and Hungary as examples. In fact, Hungary has one of the highest rates of lung cancer mortality and Greece’s rate is medium to high (see these graphs). You can see that nearly every country has a higher rate of lung cancer for men than for women, and that in most cases the female rate is going up while the male rate is flattening off or falling. This is simply a reflection of what happened in the second half of the last century when smoking rates went down for men and up for women. Notice also the experience in Sweden, where snus use by men since the 1960s has helped the male smoking rate fall below that of women, resulting in Sweden being the only European country where men have a lower lung cancer mortality than women. Again, if smoking isn’t the primary cause, what other factor fits the specific experiences of each country?
Rates of lung cancer have always been somewhat lower in Asian countries due to an assumed biological resistance. Nevertheless, it is worth comparing the lung cancer incidence for Japanese men of 44.6 per 100,000 against the rate for Japanese women (few of whom smoke) of 13.3 per 100,000. It is a similar story in China (67.5 for men against 26.6 women). In India, where smoking is fairly uncommon amongst men and very rare amongst women, the incidence rates are just 12.1 and 3.8 respectively.
What we are looking for, then, is an unknown factor which is as strong or stronger than the statistical correlation between smoking and lung cancer, which causes lung cancer to rise and fall several decades after smoking rises and falls, which affects men first and then women and which is less common in countries where smoking is less common. Over to the defence…
PS. A few quick points in reply to several comments:
[Rich] MRFIT was primarily a study into cholesterol and heart disease. I’m not aware that they stratified the results to show smoking and lung cancer but I’m happy to be corrected on it.
[Rich] “People have been smoking for millennia.” Yes, but not cigarettes. It is the deep inhaling of cigarettes that poses the hazard. The Surgeon General found little or no elevated risk for pipe and cigar smokers. Really, this debate should be called ‘Does cigarette smoking cause lung cancer.’
[Anon]: “How does one explain that the type of lung cancer have changed over the last 3 decades from squamous cell cancer to adenocarcinoma cancer?” Nonsmokers have always been much more likely to get adenocarcinoma if they get lung cancer at all, and smokers have always had higher rates of other forms of lung cancer. Recent decades have seen more smokers getting adenocarcinoma and the reason you give in your comment is the most common explanation, ie. ‘light’ cigarettes allow (or require, even) the smoke to go deeper into the lungs. Old, unfiltered heavy cigarettes were not inhaled so deeply and so the tumour would form higher up the lung.
[Rich] “We know most cigarette smokers come from the lower classes, and those people tend to be die younger and suffer more disease than the richer in society also.” That is true today but not back then. In the first half of the century and beyond, cigarette smoking was not class-sensitive. Today, it is quite obvious when you see a study which purports to show that maternal smoking breeds criminality in unborn children that mothers who smoke during pregnancy are simply more likely to be from socio-economic classes where criminality is more common. This was not the case when the landmark studies were being conducted and it is another reason why older studies can be more reliable than modern studies.
[Frank]: Definition of a smoker. Doll and Hill were looking for ever-smokers and asking if they’d smoked 100 cigarettes in their life was as good a measure as any. Obviously they wanted to avoid people who bought one pack when they were 15, or had one cigarette every New Years’ Eve. Whether it was 50, 100 or 200 makes little difference. Other studies have found similar results after stratifying for current smokers, ex-smokers and never-smokers. Only counting current smokers would be a poorer system, especially with lung cancer patients who often, and understandably, give up smoking when they develop symptoms.
[Rich] “The quantities of the chemicals and toxins [in cigarettes] are tiny, less than we inhale in normal air.” This statement requires some support and explanation!
Frank Davis 
Smoking prevalence in 1947
I’ll respond to one or two of Chris’ points here, if I may. Chris writes:
Frank points out that 98% of the (male) patients in the first Doll/Hill study were smokers. This is true, but we know that even in 1950, 98% was not the general smoking rate amongst men (it was around 75%).
It would appear that Doll and Hill were unaware of this, judging from the following on p746:
Neither do Doll and Hill suggest, as Chris suggests, that the high prevalence of smoking among hospital patients isn’t a good advert for smoking.
I think we have to accept that male smoking prevalence was very high in 1947-48 when the study began. Furthermore, we know that 87% of the British doctors study in 1951 were smokers. And this would have been a year after these doctors had learned that smoking had been linked with lung cancer, and some of them (like Doll) had given up smoking.
Both of these figures are well above the 75% smoking prevalence that Chris suggests. Where does this 75% come from?
If it’s accepted that smoking is a response to stress, then we should bear in mind that Britons had just been through 5 years of war, during which many people had died and London had been heavily bombed. In the aftermath of that war life didn’t get very much better (there was rationing for several years after the war). It may well be that smoking was at the 96% level in London, but more like 50% in country towns and villages, where life was less stressful, and this where the 75% comes from – averaging across the whole country.
Even with the very high rate of smoking amongst the patients, a clear difference was found. Only 2 of the 647 lung cancer patients were not smokers (0.3%), compared with 27 of the 647 non-cancer patients (4.2%). The lung cancer patients were 13.5 times more likely to be smokers.
Is it that clear? You are simply dividing one number by another, and ignoring the absolute size of the percentages, both of which are small.
And if you can divide 4.2% by 0.3% to get 13.5, I can divide 99.7% by 98% to get 1.017 – a 1.7% higher figure for the number of smokers in the lung cancer group than would be expected on the null hypothesis – and clearly nothing to be concerned about.
Even with the very high rate of smoking amongst the patients, a clear difference was found. Only 2 of the 647 lung cancer patients were not smokers (0.3%), compared with 27 of the 647 non-cancer patients (4.2%). The lung cancer patients were 13.5 times more likely to be smokers.
Is it that clear? You are simply dividing one number by another, and ignoring the absolute size of the percentages, both of which are small.
And if you can divide 4.2% by 0.3% to get 13.5, I can divide 99.7% by 98% to get 1.017 – a 1.7% higher figure for the number of smokers in the lung cancer group than would be expected on the null hypothesis – and clearly nothing to be concerned about.
Chris, Frank is right here (well, almost; the actual division should be 99.7% by 95.8% to get 1.04).
Your final sentence doesn’t follow from the numbers that you quoted. It should actually state:
….. The non-lung cancer patients were 13.5 times more likely to be non-smokers.
but equally true, would be this version:
….. The lung cancer patients were 1.04 times more likely to be smokers.
Of these two statements, the likeliest to achieve statistical confidence is the latter, since it is derived from much larger subsamples (27/2 vs 620/645), so Frank is correct again, ie the null hypothesis (that lung cancer is not strongly associated with smoking) would stand.
All of which is fairly meaningless in isolation, but it does demonstrate just how easy it is to misread statistics.
Brian Bond
Brian,
I divided by 98% because that was the percentage of smokers in the whole study, and that seemed to me to be the real base from which to calculate the variation.
Frank
Frank
In that case, the statement would have been:
…The lung cancer patients were 1.017 times more likely than the general population to be smokers.
whereas Chris’s original position was based on a comparison of the effect group (lung cancer patients) against the control group (non-lung cancer).
This is actually a good example of how the Odds Ratio (RR) differs from Relative Risk in epidemiological calculations, the 1.04 is numerically similar to the OR calculation, whereas your 1.017 is equivalent to RR (not the exact calculations, but mathematically equivalent). It demonstrates that an OR will always be larger than the RR calculated from the same data. This is worth remembering when looking at epi studies; OR and RR are not the same.
Sorry if I seem to be nit-picking, but I have a long professional history in this area, which results in arguably more despair in myself than in others, because I see people who really should know better (epidemiologists) abusing my discipline (statistics) in order to influence the gullible and thick (politicians).
Good debate though – I am currently quite agnostic on the main topic, but as someone who actually did some work for Richard Doll in the early part of my career, that is quite some movement of position.
Brian Bond
Frank
In that case, the statement would have been:
…The lung cancer patients were 1.017 times more likely than the general population to be smokers.
whereas Chris’s original position was based on a comparison of the effect group (lung cancer patients) against the control group (non-lung cancer).
This is actually a good example of how the Odds Ratio (RR) differs from Relative Risk in epidemiological calculations, the 1.04 is numerically similar to the OR calculation, whereas your 1.017 is equivalent to RR (not the exact calculations, but mathematically equivalent). It demonstrates that an OR will always be larger than the RR calculated from the same data. This is worth remembering when looking at epi studies; OR and RR are not the same.
Sorry if I seem to be nit-picking, but I have a long professional history in this area, which results in arguably more despair in myself than in others, because I see people who really should know better (epidemiologists) abusing my discipline (statistics) in order to influence the gullible and thick (politicians).
Good debate though – I am currently quite agnostic on the main topic, but as someone who actually did some work for Richard Doll in the early part of my career, that is quite some movement of position.
Brian Bond
Brian,
I divided by 98% because that was the percentage of smokers in the whole study, and that seemed to me to be the real base from which to calculate the variation.
Frank
Chris, Frank is right here (well, almost; the actual division should be 99.7% by 95.8% to get 1.04).
Your final sentence doesn’t follow from the numbers that you quoted. It should actually state:
….. The non-lung cancer patients were 13.5 times more likely to be non-smokers.
but equally true, would be this version:
….. The lung cancer patients were 1.04 times more likely to be smokers.
Of these two statements, the likeliest to achieve statistical confidence is the latter, since it is derived from much larger subsamples (27/2 vs 620/645), so Frank is correct again, ie the null hypothesis (that lung cancer is not strongly associated with smoking) would stand.
All of which is fairly meaningless in isolation, but it does demonstrate just how easy it is to misread statistics.
Brian Bond
What is being compared here is relative and absolute risk. The former is used by epidemiologists to argue for a causal connection between smoking and lung cancer. This is understandable: you want to compare the number of incidences of a disease (lung cancer) where certain conditions apply (smoking) against the number of incidences where the same conditions do not apply, and use that as evidence for a causal link. Bradford Hill, to be fair to him, was aware of this:
‘I would reject the argument sometimes advanced that what matters is the absolute difference between the death rates of our various groups and not the ratio of one to the other. That depends upon what we want to know. If we want to know how many extra deaths from cancer of the lung will take place through smoking (i.e. presuming causation), then obviously we must use the absolute differences between the death rates – 0.07 per 1,000 per year in nonsmoking doctors, 0.57 in those smoking 1–14 and 2.27 for 25 or more daily. But it does not follow here, or in more specifically occupational problems, that this best measure of the effect upon mortality is also the best measure in relation to etiology. In this respect the ratios of 8, 20 and 32 to 1 are far more informative. It does not, of course, follow that the differences revealed by ratios are of any practical importance. Maybe they are, maybe they are not; but that is another point altogether. We may recall John Snow’s classic analysis of the opening weeks of the cholera epidemic of 1854. The death rate that he recorded in the customers supplied with the grossly polluted water of the Southwark and Vauxhall Company was in truth quite low – 71 deaths in each 10,000 houses. What stands out vividly is the fact that the small rate is 14 times the figure of 5 deaths per 10,000 houses supplied with the sewage free water of the Lambeth Company.’
It might be possible, then, to argue for a causal connection between smoking and lung cancer (by means of the high relative risk), but then to go on to say that actually it doesn’t cause it all that often (by means of the low absolute risk). Both statements can be true – smoking can be a cause of lung cancer, but it’s no where near as harmful as we have been led to believe. Questions concerning causation and those concerning harmfulness are thus quite separate, and there is a danger that the two can become entwined.
DW
What is being compared here is relative and absolute risk. The former is used by epidemiologists to argue for a causal connection between smoking and lung cancer. This is understandable: you want to compare the number of incidences of a disease (lung cancer) where certain conditions apply (smoking) against the number of incidences where the same conditions do not apply, and use that as evidence for a causal link. Bradford Hill, to be fair to him, was aware of this:
‘I would reject the argument sometimes advanced that what matters is the absolute difference between the death rates of our various groups and not the ratio of one to the other. That depends upon what we want to know. If we want to know how many extra deaths from cancer of the lung will take place through smoking (i.e. presuming causation), then obviously we must use the absolute differences between the death rates – 0.07 per 1,000 per year in nonsmoking doctors, 0.57 in those smoking 1–14 and 2.27 for 25 or more daily. But it does not follow here, or in more specifically occupational problems, that this best measure of the effect upon mortality is also the best measure in relation to etiology. In this respect the ratios of 8, 20 and 32 to 1 are far more informative. It does not, of course, follow that the differences revealed by ratios are of any practical importance. Maybe they are, maybe they are not; but that is another point altogether. We may recall John Snow’s classic analysis of the opening weeks of the cholera epidemic of 1854. The death rate that he recorded in the customers supplied with the grossly polluted water of the Southwark and Vauxhall Company was in truth quite low – 71 deaths in each 10,000 houses. What stands out vividly is the fact that the small rate is 14 times the figure of 5 deaths per 10,000 houses supplied with the sewage free water of the Lambeth Company.’
It might be possible, then, to argue for a causal connection between smoking and lung cancer (by means of the high relative risk), but then to go on to say that actually it doesn’t cause it all that often (by means of the low absolute risk). Both statements can be true – smoking can be a cause of lung cancer, but it’s no where near as harmful as we have been led to believe. Questions concerning causation and those concerning harmfulness are thus quite separate, and there is a danger that the two can become entwined.
DW
Even with the very high rate of smoking amongst the patients, a clear difference was found. Only 2 of the 647 lung cancer patients were not smokers (0.3%), compared with 27 of the 647 non-cancer patients (4.2%). The lung cancer patients were 13.5 times more likely to be smokers.
Is it that clear? You are simply dividing one number by another, and ignoring the absolute size of the percentages, both of which are small.
And if you can divide 4.2% by 0.3% to get 13.5, I can divide 99.7% by 98% to get 1.017 – a 1.7% higher figure for the number of smokers in the lung cancer group than would be expected on the null hypothesis – and clearly nothing to be concerned about.
Re: Smoking prevalence in 1947
Chris says:
Frank points out that 98% of the (male) patients in the first Doll/Hill study were smokers. This is true, but we know that even in 1950, 98% was not the general smoking rate amongst men (it was around 75%).
But as I pointed out in the comments on CATCH-1:
In Doll’s 1950 Hospital study and Doll’s ‘British Doctors Study’:
“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 Doll and Hill’s definition of a smoker was 365 cigarettes in a lifetime.
Assuming the estimate of 75% applies to current active smokers then Doll’s definition for his Hospital study would produce a much higher proportion as it included ex-smokers and 98% seems a fairly likely rate.
Tony
Re: Smoking prevalence in 1947
Chris says:
Frank points out that 98% of the (male) patients in the first Doll/Hill study were smokers. This is true, but we know that even in 1950, 98% was not the general smoking rate amongst men (it was around 75%).
But as I pointed out in the comments on CATCH-1:
In Doll’s 1950 Hospital study and Doll’s ‘British Doctors Study’:
“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 Doll and Hill’s definition of a smoker was 365 cigarettes in a lifetime.
Assuming the estimate of 75% applies to current active smokers then Doll’s definition for his Hospital study would produce a much higher proportion as it included ex-smokers and 98% seems a fairly likely rate.
Tony
Re: Smoking prevalence in 1947
Chris says:
Frank points out that 98% of the (male) patients in the first Doll/Hill study were smokers. This is true, but we know that even in 1950, 98% was not the general smoking rate amongst men (it was around 75%).
But as I pointed out in the comments on CATCH-1:
In Doll’s 1950 Hospital study and Doll’s ‘British Doctors Study’:
“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 Doll and Hill’s definition of a smoker was 365 cigarettes in a lifetime.
Assuming the estimate of 75% applies to current active smokers then Doll’s definition for his Hospital study would produce a much higher proportion as it included ex-smokers and 98% seems a fairly likely rate.
Tony
Chris,
Would be pleased if you could address:
A) The issue of detection bias in the official figures. For example: “Feinstein & Wells (1974) found that, regarding a US investigation, a physician is more likely to diagnose lung cancer in smokers than in nonsmokers and in heavy than in light smokers.” (Ann W. also has a post – in CATCH-2 – alluding to the same issue) Epidemiological studies into LC have not been altogether investigating a rise in LC but have been investigating, at least in part, an antismoking bias within the medical establishment.
B) The fact that, in proportional terms, overall cancer mortality for smokers/nonsmokers is very similar – around a third of all mortality, i.e., smoking is not statistically associated with higher overall cancer mortality. Further, what is the reasoning behind going all out to stop people smoking to avoid lung cancer (in only a small subgroup of smokers) when the high likelihood is that this group will contract fatal cancer originating at a site other than the lung but that will probably also spread (metastasized tumors) to the lung?
C) “Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.”
Chris, you’re using the standard, clumsy, epidemiological idea of “causal explanation” where there is the constant attempt to attribute causation on the basis of single factors. The “argument” is that if some other single factor cannot be identified to explain the correlation, then we’ll just continue to blame, causally and singularly, smoking. Rather, the idea of high predictive strength of an antecedent(s) for a consequent should be used. A sub-10% incidence of LC for smokers may be significant in statistical terms but it is not significant in terms of the requirements of coherent causal argument. Remember that 90%+ of lifelong smokers, above a baseline, will not develop LC. Why do they NOT develop LC? Why does only a small subgroup of smokers develop LC? It is by addressing these issues and adding other antecedent factors that will provide a set of antecedents with much, much higher predictive strength for LC. Unless the role of other factors is understood, the role of smoking is not understood. (See also post by “Magnetic” Re:Ditto in CATCH-3)
Magnetic
Chris,
Would be pleased if you could address:
A) The issue of detection bias in the official figures. For example: “Feinstein & Wells (1974) found that, regarding a US investigation, a physician is more likely to diagnose lung cancer in smokers than in nonsmokers and in heavy than in light smokers.” (Ann W. also has a post – in CATCH-2 – alluding to the same issue) Epidemiological studies into LC have not been altogether investigating a rise in LC but have been investigating, at least in part, an antismoking bias within the medical establishment.
B) The fact that, in proportional terms, overall cancer mortality for smokers/nonsmokers is very similar – around a third of all mortality, i.e., smoking is not statistically associated with higher overall cancer mortality. Further, what is the reasoning behind going all out to stop people smoking to avoid lung cancer (in only a small subgroup of smokers) when the high likelihood is that this group will contract fatal cancer originating at a site other than the lung but that will probably also spread (metastasized tumors) to the lung?
C) “Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.”
Chris, you’re using the standard, clumsy, epidemiological idea of “causal explanation” where there is the constant attempt to attribute causation on the basis of single factors. The “argument” is that if some other single factor cannot be identified to explain the correlation, then we’ll just continue to blame, causally and singularly, smoking. Rather, the idea of high predictive strength of an antecedent(s) for a consequent should be used. A sub-10% incidence of LC for smokers may be significant in statistical terms but it is not significant in terms of the requirements of coherent causal argument. Remember that 90%+ of lifelong smokers, above a baseline, will not develop LC. Why do they NOT develop LC? Why does only a small subgroup of smokers develop LC? It is by addressing these issues and adding other antecedent factors that will provide a set of antecedents with much, much higher predictive strength for LC. Unless the role of other factors is understood, the role of smoking is not understood. (See also post by “Magnetic” Re:Ditto in CATCH-3)
Magnetic
Chris,
Would be pleased if you could address:
A) The issue of detection bias in the official figures. For example: “Feinstein & Wells (1974) found that, regarding a US investigation, a physician is more likely to diagnose lung cancer in smokers than in nonsmokers and in heavy than in light smokers.” (Ann W. also has a post – in CATCH-2 – alluding to the same issue) Epidemiological studies into LC have not been altogether investigating a rise in LC but have been investigating, at least in part, an antismoking bias within the medical establishment.
B) The fact that, in proportional terms, overall cancer mortality for smokers/nonsmokers is very similar – around a third of all mortality, i.e., smoking is not statistically associated with higher overall cancer mortality. Further, what is the reasoning behind going all out to stop people smoking to avoid lung cancer (in only a small subgroup of smokers) when the high likelihood is that this group will contract fatal cancer originating at a site other than the lung but that will probably also spread (metastasized tumors) to the lung?
C) “Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.”
Chris, you’re using the standard, clumsy, epidemiological idea of “causal explanation” where there is the constant attempt to attribute causation on the basis of single factors. The “argument” is that if some other single factor cannot be identified to explain the correlation, then we’ll just continue to blame, causally and singularly, smoking. Rather, the idea of high predictive strength of an antecedent(s) for a consequent should be used. A sub-10% incidence of LC for smokers may be significant in statistical terms but it is not significant in terms of the requirements of coherent causal argument. Remember that 90%+ of lifelong smokers, above a baseline, will not develop LC. Why do they NOT develop LC? Why does only a small subgroup of smokers develop LC? It is by addressing these issues and adding other antecedent factors that will provide a set of antecedents with much, much higher predictive strength for LC. Unless the role of other factors is understood, the role of smoking is not understood. (See also post by “Magnetic” Re:Ditto in CATCH-3)
Magnetic
Chris, Frank is right here (well, almost; the actual division should be 99.7% by 95.8% to get 1.04).
Your final sentence doesn’t follow from the numbers that you quoted. It should actually state:
….. The non-lung cancer patients were 13.5 times more likely to be non-smokers.
but equally true, would be this version:
….. The lung cancer patients were 1.04 times more likely to be smokers.
Of these two statements, the likeliest to achieve statistical confidence is the latter, since it is derived from much larger subsamples (27/2 vs 620/645), so Frank is correct again, ie the null hypothesis (that lung cancer is not strongly associated with smoking) would stand.
All of which is fairly meaningless in isolation, but it does demonstrate just how easy it is to misread statistics.
Brian Bond
“The geographical spread of lung cancer follows several decades behind the geographical spread of smoking. For the lung cancer epidemic to begin, you need to have a sizeable group of people who have been smoking for at least 20 years.”
Chris,
See Rose’s post, CATCH-1, 2010-11-28 02:47 pm (UTC)
Magnetic
“The geographical spread of lung cancer follows several decades behind the geographical spread of smoking. For the lung cancer epidemic to begin, you need to have a sizeable group of people who have been smoking for at least 20 years.”
Chris,
See Rose’s post, CATCH-1, 2010-11-28 02:47 pm (UTC)
Magnetic
Doctors
Royal Army Medical Corps
“Mustard gas, first used in 1917, delayed any effect for up to 12 hours, and then began to rot the body from both within and without and a very painful death took from four to five weeks. Lachrimatory gasses caused blindness.
Gas hung around in sunken roads for weeks, and it was possible to be overcome merely by removing a patient’s clothing, so it was not only during an attack that one could become gassed”
http://www.ramc-ww1.com/chain_of_evacuation.php
“Survival after a mustard gas exposure is common, but note that Mustard agents are strong carcinogens. If the immediate mustard attack does not kill you it is highly likely that you develop lung cancer later in life.
Survivors also commonly cope with chronic asthma and/or bronchitis as well. ”
http://www.shu.edu/academics/artscibiol3341aa/EnvToxWeb/Spring%202005/mustard%20agents/mustard%201.htm
link no longer works.
Mustard Gas exposure and carcinogenesis of the lung – Iran
RESULTS: A relatively early age of lung cancer onset (ranging from 28 to 73 with a mean of 48) in mustard gas victims, particularly those in the non-smoking population (mean age of 40.7), may be an indication of a unique etiology for these cancers.
Seven of the 20 patients developed lung cancer before the age of 40.”
http://lib.bioinfo.pl/pmid:19559099
Rose
Doctors
Royal Army Medical Corps
“Mustard gas, first used in 1917, delayed any effect for up to 12 hours, and then began to rot the body from both within and without and a very painful death took from four to five weeks. Lachrimatory gasses caused blindness.
Gas hung around in sunken roads for weeks, and it was possible to be overcome merely by removing a patient’s clothing, so it was not only during an attack that one could become gassed”
http://www.ramc-ww1.com/chain_of_evacuation.php
“Survival after a mustard gas exposure is common, but note that Mustard agents are strong carcinogens. If the immediate mustard attack does not kill you it is highly likely that you develop lung cancer later in life.
Survivors also commonly cope with chronic asthma and/or bronchitis as well. ”
http://www.shu.edu/academics/artscibiol3341aa/EnvToxWeb/Spring%202005/mustard%20agents/mustard%201.htm
link no longer works.
Mustard Gas exposure and carcinogenesis of the lung – Iran
RESULTS: A relatively early age of lung cancer onset (ranging from 28 to 73 with a mean of 48) in mustard gas victims, particularly those in the non-smoking population (mean age of 40.7), may be an indication of a unique etiology for these cancers.
Seven of the 20 patients developed lung cancer before the age of 40.”
http://lib.bioinfo.pl/pmid:19559099
Rose
“The geographical spread of lung cancer follows several decades behind the geographical spread of smoking. For the lung cancer epidemic to begin, you need to have a sizeable group of people who have been smoking for at least 20 years.”
Chris,
See Rose’s post, CATCH-1, 2010-11-28 02:47 pm (UTC)
Magnetic
Brian,
I divided by 98% because that was the percentage of smokers in the whole study, and that seemed to me to be the real base from which to calculate the variation.
Frank
The debate catch 4
I think that Frank makes a good point about there always having been ‘anti-smoking zealots’. His thought caused me to ask this question:
If the ‘science’ was settled by the early studies (including the big American ones which Chris quotes), why are we still having dozens and dozens of studies every year? If the science is settled, what are they looking for? Isaac Newton ‘settled’ the matter of gravity for 300 years -only when Einstein asked some questions about whether Newton’s laws applied in ALL circumstances (and the circumstances which Einstein was concerned with were rather obscure) did physicists start to investigate again – and they are still investigating.
Could it be that these researchers are, quietly and secretively, looking for CAUSALITY and are unable to find it? Dave Atherton, some months ago, mentioned the new research which indicated that ‘second-hand’ smokers (and non-smokers?) suffer a different form of lung cancer from smokers. Did the researchers just happen upon this difference by accident or where they looking for it? What were they looking for? Was it perhaps some definitive causality – such as some specific proteins in the genome which could be linked directly to tobacco smoke?
I must admit that I am way out of my depth here, but I think the questions are reasonable. Perhaps Dave Atherton could enlighten us.
I wish someone would enlighten us about these ‘relative risks’. I thought that I had got it right in my mind when I understood it as this:
Supposing that you find a group of people who (say for religious reasons) do not smoke at all. And supposing you find that 4 persons in 100 000 deaths die from lung cancer. You could then decide that the ‘risk’ of dying from lung cancer for non smokers is 1 (4 per 100 000 = 1). If you find a group who all smoke and you find that 16 people die per 100 000 deaths from lung cancer, then the risk quadruples, but that is the ‘absolute risk’ – the ‘relative risk’ is the difference between 4 and 16, expressed as a fraction of 4. IE, 12 divided by 4 = 3. So we see that to get a Relative risk of 3, we have to quadruple our original risk in non-smokers.
Be that as it may. The fact is that these ‘relative risks’ must be amusing for statisticians to play with, but I would much prefer THE NUMERICAL FACTS! The latest figures from the Office of National Statistics (for 2009) give lung cancer deaths as 30 000 out of a total of 500 000. But how many of this 30 000 were very old? According to the Office of Nat Stats, they cannot give us info about the ages of the people who died until Feb/Mar 2011. But, in the body of words in the report, they are quite able to talk about ‘age standardised’ figures.
“”Age-standardised, all age mortality rates for the 10 leading causes of death by sex in England and Wales, 2009, and comparison rates for 2004 ……….””
So they cannot give us the ages, but they can do the ‘age standardised’ calculations! I smell a rat.
The debate catch 4
I think that Frank makes a good point about there always having been ‘anti-smoking zealots’. His thought caused me to ask this question:
If the ‘science’ was settled by the early studies (including the big American ones which Chris quotes), why are we still having dozens and dozens of studies every year? If the science is settled, what are they looking for? Isaac Newton ‘settled’ the matter of gravity for 300 years -only when Einstein asked some questions about whether Newton’s laws applied in ALL circumstances (and the circumstances which Einstein was concerned with were rather obscure) did physicists start to investigate again – and they are still investigating.
Could it be that these researchers are, quietly and secretively, looking for CAUSALITY and are unable to find it? Dave Atherton, some months ago, mentioned the new research which indicated that ‘second-hand’ smokers (and non-smokers?) suffer a different form of lung cancer from smokers. Did the researchers just happen upon this difference by accident or where they looking for it? What were they looking for? Was it perhaps some definitive causality – such as some specific proteins in the genome which could be linked directly to tobacco smoke?
I must admit that I am way out of my depth here, but I think the questions are reasonable. Perhaps Dave Atherton could enlighten us.
I wish someone would enlighten us about these ‘relative risks’. I thought that I had got it right in my mind when I understood it as this:
Supposing that you find a group of people who (say for religious reasons) do not smoke at all. And supposing you find that 4 persons in 100 000 deaths die from lung cancer. You could then decide that the ‘risk’ of dying from lung cancer for non smokers is 1 (4 per 100 000 = 1). If you find a group who all smoke and you find that 16 people die per 100 000 deaths from lung cancer, then the risk quadruples, but that is the ‘absolute risk’ – the ‘relative risk’ is the difference between 4 and 16, expressed as a fraction of 4. IE, 12 divided by 4 = 3. So we see that to get a Relative risk of 3, we have to quadruple our original risk in non-smokers.
Be that as it may. The fact is that these ‘relative risks’ must be amusing for statisticians to play with, but I would much prefer THE NUMERICAL FACTS! The latest figures from the Office of National Statistics (for 2009) give lung cancer deaths as 30 000 out of a total of 500 000. But how many of this 30 000 were very old? According to the Office of Nat Stats, they cannot give us info about the ages of the people who died until Feb/Mar 2011. But, in the body of words in the report, they are quite able to talk about ‘age standardised’ figures.
“”Age-standardised, all age mortality rates for the 10 leading causes of death by sex in England and Wales, 2009, and comparison rates for 2004 ……….””
So they cannot give us the ages, but they can do the ‘age standardised’ calculations! I smell a rat.
Re: The debate catch 4
Junican,
Ignoring confounders such as age, your example produces a relative risk of 16/4 = 4.
RR = (Probability of LC amongst those exposed)/(Probability of those not exposed) – see Wikipedia for more info or try plugging the numbers into Medcalc:
http://www.medcalc.be/calc/relative_risk.php
Use a=16, b=99984, c=4, d=99996 (no commas)
(b=100,000-16, d=100,000-4)
Of course a RR of 4 is a 300% increase.
Tony
Re: The debate catch 4
Junican,
Ignoring confounders such as age, your example produces a relative risk of 16/4 = 4.
RR = (Probability of LC amongst those exposed)/(Probability of those not exposed) – see Wikipedia for more info or try plugging the numbers into Medcalc:
http://www.medcalc.be/calc/relative_risk.php
Use a=16, b=99984, c=4, d=99996 (no commas)
(b=100,000-16, d=100,000-4)
Of course a RR of 4 is a 300% increase.
Tony
The debate catch 4
I think that Frank makes a good point about there always having been ‘anti-smoking zealots’. His thought caused me to ask this question:
If the ‘science’ was settled by the early studies (including the big American ones which Chris quotes), why are we still having dozens and dozens of studies every year? If the science is settled, what are they looking for? Isaac Newton ‘settled’ the matter of gravity for 300 years -only when Einstein asked some questions about whether Newton’s laws applied in ALL circumstances (and the circumstances which Einstein was concerned with were rather obscure) did physicists start to investigate again – and they are still investigating.
Could it be that these researchers are, quietly and secretively, looking for CAUSALITY and are unable to find it? Dave Atherton, some months ago, mentioned the new research which indicated that ‘second-hand’ smokers (and non-smokers?) suffer a different form of lung cancer from smokers. Did the researchers just happen upon this difference by accident or where they looking for it? What were they looking for? Was it perhaps some definitive causality – such as some specific proteins in the genome which could be linked directly to tobacco smoke?
I must admit that I am way out of my depth here, but I think the questions are reasonable. Perhaps Dave Atherton could enlighten us.
I wish someone would enlighten us about these ‘relative risks’. I thought that I had got it right in my mind when I understood it as this:
Supposing that you find a group of people who (say for religious reasons) do not smoke at all. And supposing you find that 4 persons in 100 000 deaths die from lung cancer. You could then decide that the ‘risk’ of dying from lung cancer for non smokers is 1 (4 per 100 000 = 1). If you find a group who all smoke and you find that 16 people die per 100 000 deaths from lung cancer, then the risk quadruples, but that is the ‘absolute risk’ – the ‘relative risk’ is the difference between 4 and 16, expressed as a fraction of 4. IE, 12 divided by 4 = 3. So we see that to get a Relative risk of 3, we have to quadruple our original risk in non-smokers.
Be that as it may. The fact is that these ‘relative risks’ must be amusing for statisticians to play with, but I would much prefer THE NUMERICAL FACTS! The latest figures from the Office of National Statistics (for 2009) give lung cancer deaths as 30 000 out of a total of 500 000. But how many of this 30 000 were very old? According to the Office of Nat Stats, they cannot give us info about the ages of the people who died until Feb/Mar 2011. But, in the body of words in the report, they are quite able to talk about ‘age standardised’ figures.
“”Age-standardised, all age mortality rates for the 10 leading causes of death by sex in England and Wales, 2009, and comparison rates for 2004 ……….””
So they cannot give us the ages, but they can do the ‘age standardised’ calculations! I smell a rat.
I think that this could easily be settled with the right statistics, although I don’t have them.
We are all accustomed to seeing the graphs where smoking prevelance declines, then lung cancer rates decline (or in the case of women, flatten) some time later. However, both of these statistics relate to the population, overall.
I would like to see a graph of the rate of lung cancer in smokers over, say, the past 50 years. If the rate of lung cancer in smokers, only, has stayed relatively steady (should approximate a horizontal line), then smoking almost certainly is correlated with lung cancer.
If smoking was not causing lung cancer (and if this decline was related to something else), then there should be a decline in lung cancers within the smoking population which is approximately the same as the decline in the overall population.
Possible confounders: filters, light cigarettes, reduction in total number of “heavy” smokers.
I think that this could easily be settled with the right statistics, although I don’t have them.
We are all accustomed to seeing the graphs where smoking prevelance declines, then lung cancer rates decline (or in the case of women, flatten) some time later. However, both of these statistics relate to the population, overall.
I would like to see a graph of the rate of lung cancer in smokers over, say, the past 50 years. If the rate of lung cancer in smokers, only, has stayed relatively steady (should approximate a horizontal line), then smoking almost certainly is correlated with lung cancer.
If smoking was not causing lung cancer (and if this decline was related to something else), then there should be a decline in lung cancers within the smoking population which is approximately the same as the decline in the overall population.
Possible confounders: filters, light cigarettes, reduction in total number of “heavy” smokers.
As a starting point we should look:
1) Has the incidence of LC reduced to match the reduction in smoking?
2) Is the incidence of smokers remaining static as a percentage among LC sufferers?
After this we can start to refine things. But I’m finding it bloody difficult to get the answers to those 2 simple things.
As a starting point we should look:
1) Has the incidence of LC reduced to match the reduction in smoking?
2) Is the incidence of smokers remaining static as a percentage among LC sufferers?
After this we can start to refine things. But I’m finding it bloody difficult to get the answers to those 2 simple things.
I think that this could easily be settled with the right statistics, although I don’t have them.
We are all accustomed to seeing the graphs where smoking prevelance declines, then lung cancer rates decline (or in the case of women, flatten) some time later. However, both of these statistics relate to the population, overall.
I would like to see a graph of the rate of lung cancer in smokers over, say, the past 50 years. If the rate of lung cancer in smokers, only, has stayed relatively steady (should approximate a horizontal line), then smoking almost certainly is correlated with lung cancer.
If smoking was not causing lung cancer (and if this decline was related to something else), then there should be a decline in lung cancers within the smoking population which is approximately the same as the decline in the overall population.
Possible confounders: filters, light cigarettes, reduction in total number of “heavy” smokers.
Burden of Proof/Either-Or
I think I’m with Mr. Snowdon on this one.
His words:
“Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.”
I don’t think it’s a valid contradiction to say that this is a clumsy invocation of correlation in the absence of an explanation of causation. No one in this debate can be placed in the position of pretending to know all of the factors that might cause or contribute to lung cancer in any individual person, nonetheless wide swaths of people. Nor can anyone tell precisely why most heavy smokers don’t get lung cancer.
while I think it’s valid to point out that the anti-tobacco establishment has played a key role in sidelining the pursuit of any such hard science regarding lung cancer in favor of a moral/political agenda, only available evidence can be taken into consideration. Whether we like it or not, that evidence is statistical, epidemiological evidence. I think Mr. Snowdon shares in being critical of the problems that arise from an over-reliance on this kind of evidence.
However, I don’t think that he should be expected to fend off every objection to the “smoking-contributes-to-lung-cancer” hypothesis, thereby allowing any perceived failure of an adequate explanation from him to serve, by default, as a reason to say: “See that! He couldn’t explain it to my satisfaction! Therefore, no one knows if smoking plays a causative role in developing lung cancer!”
To do so shifts the burden of proof away from the person who is simply claiming to know what is factually true: lung cancer is much more prevalent in smokers than non-smokers. If the contention otherwise is that smoking does not play a causative role in lung cancer, then one isn’t necessarily being forced to “prove a negative”, but to deliver a viable alternative hypothesis that takes the heavy correlation into consideration.
Frankly, the “or” side of the “either/or” equation seems rather weak when it comes to “EITHER smoking has played a major role in lung cancer in most people (smokers) who have it OR coal dust, nuclear test pollution, general environmental pollution, stress, poverty, etc, etc, etc.
The proper burden of proof then lies on the “OR” side of the “Either/Or” equation. In other words, it simply isn’t enough to try and debunk the causative role of smoking in lung cancer. Rather, as Mr. Snowdon implied in the quote above, the burden of proof then lies with opponents of the “smoking-is-the-major-contributor-to-lung-cancer” hypothesis to provide a viable alternative hypothesis, rather than conjecture and speculation.
I certainly don’t mean to suggest that a possible alternative reason doesn’t exist, but I don’t think this interesting debate is going to be worth it in the end if the expectations are unreasonable. No one is going to be able to say “Eureka! It’s not the smoking after all– it’s that damn (insert reason here)! Unless, of course, someone has a good case to make, and each of those cases should be considered on their own merits.
I hope that made some sense.
-WS
Burden of Proof/Either-Or
I think I’m with Mr. Snowdon on this one.
His words:
“Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.”
I don’t think it’s a valid contradiction to say that this is a clumsy invocation of correlation in the absence of an explanation of causation. No one in this debate can be placed in the position of pretending to know all of the factors that might cause or contribute to lung cancer in any individual person, nonetheless wide swaths of people. Nor can anyone tell precisely why most heavy smokers don’t get lung cancer.
while I think it’s valid to point out that the anti-tobacco establishment has played a key role in sidelining the pursuit of any such hard science regarding lung cancer in favor of a moral/political agenda, only available evidence can be taken into consideration. Whether we like it or not, that evidence is statistical, epidemiological evidence. I think Mr. Snowdon shares in being critical of the problems that arise from an over-reliance on this kind of evidence.
However, I don’t think that he should be expected to fend off every objection to the “smoking-contributes-to-lung-cancer” hypothesis, thereby allowing any perceived failure of an adequate explanation from him to serve, by default, as a reason to say: “See that! He couldn’t explain it to my satisfaction! Therefore, no one knows if smoking plays a causative role in developing lung cancer!”
To do so shifts the burden of proof away from the person who is simply claiming to know what is factually true: lung cancer is much more prevalent in smokers than non-smokers. If the contention otherwise is that smoking does not play a causative role in lung cancer, then one isn’t necessarily being forced to “prove a negative”, but to deliver a viable alternative hypothesis that takes the heavy correlation into consideration.
Frankly, the “or” side of the “either/or” equation seems rather weak when it comes to “EITHER smoking has played a major role in lung cancer in most people (smokers) who have it OR coal dust, nuclear test pollution, general environmental pollution, stress, poverty, etc, etc, etc.
The proper burden of proof then lies on the “OR” side of the “Either/Or” equation. In other words, it simply isn’t enough to try and debunk the causative role of smoking in lung cancer. Rather, as Mr. Snowdon implied in the quote above, the burden of proof then lies with opponents of the “smoking-is-the-major-contributor-to-lung-cancer” hypothesis to provide a viable alternative hypothesis, rather than conjecture and speculation.
I certainly don’t mean to suggest that a possible alternative reason doesn’t exist, but I don’t think this interesting debate is going to be worth it in the end if the expectations are unreasonable. No one is going to be able to say “Eureka! It’s not the smoking after all– it’s that damn (insert reason here)! Unless, of course, someone has a good case to make, and each of those cases should be considered on their own merits.
I hope that made some sense.
-WS
Re: Burden of Proof/Either-Or
But Chris presented the case for the prosecution in the debate “Does Smoking Cause Lung Cancer”, so it is only right and proper for him (and others) to argue their corner.
I don’t think anyone has denies the strong statistical association between smoking and LC, so there is general acceptance that there is something that merits further (biological) investigation. Who would argue against this?
Surely any smoker wants to know, with a high degree of certainty, what the chances are of succumbing to a disease that was entirely due to smoking. But lung cancer doesn’t yet present any such certainty, so we need more research into why lung cancer is/was so predominant in smokers, not just bald assertions of “the debate is over” variety.
Chris is offering a very spirited set of arguments, and has done his research well, but he does have a tendency to fall back on rhetoric when responding to counter arguments. Eg:
…For the lung cancer epidemic to begin, you need to have a sizeable group of people who have been smoking for at least 20 years
Where is the a priori evidence for this, the physiological proof that lung cancer takes decades to develop in smokers? Furthermore, if it is indeed the case, what is happening within the smoker’s organs during that period that results in carcinogenesis in old age; and what research is being carried out into clinical interventions that could counteract this?
…“Recent decades have seen more smokers getting adenocarcinoma and … ‘light’ cigarettes allow (or require, even) the smoke to go deeper into the lungs. Old, unfiltered heavy cigarettes were not inhaled so deeply and so the tumour would form higher up the lung”
But this has got nothing to do with tumour position within the lungs. Adenocarcinoma and Squamous Cell Carcinoma are histologically different types of cancer. It was always easy to use this fact to ‘prove’ that smoking ’caused’ (squamous cell) lung cancer. The fact that the majority of smokers’ LCs are now also adenocarcinoma may be inconvenient for anti-tobacco, but it really does need a proper explanation.
My suspicion is that 50+ years ago smoking did make a strong biological contribution to the formation of lung tumours (maybe ’caused’, but more likely a more complex process involving other factors). Do remember that the vast majority of studies that still form the foundation of the causal hypothesis were carried out in the 1950s and 1960s, ie based on the peoples’ smoking habits in the 1940s/1950s and (if Chris is correct) back to the 20s and 30s. Chris cites the US Surgeon General’s report of 1964! Nobody is researching into whether smoking causes lung cancer any more. As AGW alarmists would say “the science is settled”. But is it?
There is little doubt (outside of anti-tobacco groupthink) that cigarettes have become immensely ‘safer’ since these studies were carried out. The use of filter tips, lower tar levels, changes in types of tobacco used and curing methods have resulted in huge reductions in measurable levels of known carcinogens. Also people are generally smoking much less than they did 50+ years ago. The 100 a day smoker is rare now – even 20 a day is deemed to be ‘heavy’ smoking. The improvements are such that the ‘safe’ level of smoking is round about 10 cigarettes per day (see Gio Batta Gori [*]).
So, given these changes, isn’t it feasible that there are actually very few new lung cancers that are ’caused’ by smoking (squamous cell) and since smokers now experience the same type (adenocarcinoma) as non-smokers (and seemingly at a similar rate), is smoking any longer the dominant factor in lung carcinogenesis?
You see, without new research we may be missing the fact that the battle against lung cancer is actually being won by making cigarettes safer, rather than by declaring war on smokers. If this is the case, then much blood is on the hands of the anti-tobacco lobby, who collectively forced the termination of all ‘safe cigarette’ development efforts, resulting in the unnecessary premature deaths of literally millions of smokers.
[*] I commend everyone to research the writings of Gio Gori.
Re: Burden of Proof/Either-Or
“I don’t think anyone has denies the strong statistical association between smoking and LC, so there is general acceptance that there is something that merits further (biological) investigation. Who would argue against this?”
No one who is being reasonable. I don’t think I did.
“Surely any smoker wants to know, with a high degree of certainty, what the chances are of succumbing to a disease that was entirely due to smoking. But lung cancer doesn’t yet present any such certainty, so we need more research into why lung cancer is/was so predominant in smokers, not just bald assertions of “the debate is over” variety.”
It certainly wasn’t my intent to imply that “the debate is over” (though I’m not sure if that was directed at my comments or simply the prevailing arrogance of tobacco control. No worries, either way.) Rather, my point is that absence of evidence is not evidence of absence. On one side you have a 10 fold statistical correlation, and on the other you have a hypotheis of, let’s say, HPV is the true culprit when it comes to lung cancer. I’m not suggesting that an alternative theory like the latter should be dismissed. To the contrary, I believe it should be investigated. Nonetheless, the burden of proof is then to prove the latter. There’s no need to re-establish the statistical correlation, because it seems to me that it’s a settled matter.
“But Chris presented the case for the prosecution in the debate “Does Smoking Cause Lung Cancer”, so it is only right and proper for him (and others) to argue their corner.”
Of course. But there shouldn’t be a false expectation that Chris, or anyone, is going to be able to bat down every proposed alternative hypothesis. Exploring these ideas is interesting and worthwhile, but nothing I’ve ever seen proposed amounts to better proof than the strong statistical correlation. Also, there shouldn’t be a false expectation that Chris or anyone is going to be able to “prove” that “smoking causes lung cancer” because, as Chris noted, epidemiology simply can not do that.
Otherwise, I fully agree that more emphasis should be given to inquiry regarding the specific, biological, causative mechanisms involved in lung cancer. Unfortunately, because public health is a collective, government enterprise, it emphasizes broad brush cure-alls like anti-smoking at the expense of seeking out (and providing access to) more useful and specific information.
-WS
Re: Burden of Proof/Either-Or
“I don’t think anyone has denies the strong statistical association between smoking and LC, so there is general acceptance that there is something that merits further (biological) investigation. Who would argue against this?”
No one who is being reasonable. I don’t think I did.
“Surely any smoker wants to know, with a high degree of certainty, what the chances are of succumbing to a disease that was entirely due to smoking. But lung cancer doesn’t yet present any such certainty, so we need more research into why lung cancer is/was so predominant in smokers, not just bald assertions of “the debate is over” variety.”
It certainly wasn’t my intent to imply that “the debate is over” (though I’m not sure if that was directed at my comments or simply the prevailing arrogance of tobacco control. No worries, either way.) Rather, my point is that absence of evidence is not evidence of absence. On one side you have a 10 fold statistical correlation, and on the other you have a hypotheis of, let’s say, HPV is the true culprit when it comes to lung cancer. I’m not suggesting that an alternative theory like the latter should be dismissed. To the contrary, I believe it should be investigated. Nonetheless, the burden of proof is then to prove the latter. There’s no need to re-establish the statistical correlation, because it seems to me that it’s a settled matter.
“But Chris presented the case for the prosecution in the debate “Does Smoking Cause Lung Cancer”, so it is only right and proper for him (and others) to argue their corner.”
Of course. But there shouldn’t be a false expectation that Chris, or anyone, is going to be able to bat down every proposed alternative hypothesis. Exploring these ideas is interesting and worthwhile, but nothing I’ve ever seen proposed amounts to better proof than the strong statistical correlation. Also, there shouldn’t be a false expectation that Chris or anyone is going to be able to “prove” that “smoking causes lung cancer” because, as Chris noted, epidemiology simply can not do that.
Otherwise, I fully agree that more emphasis should be given to inquiry regarding the specific, biological, causative mechanisms involved in lung cancer. Unfortunately, because public health is a collective, government enterprise, it emphasizes broad brush cure-alls like anti-smoking at the expense of seeking out (and providing access to) more useful and specific information.
-WS
Re: Burden of Proof/Either-Or
But Chris presented the case for the prosecution in the debate “Does Smoking Cause Lung Cancer”, so it is only right and proper for him (and others) to argue their corner.
I don’t think anyone has denies the strong statistical association between smoking and LC, so there is general acceptance that there is something that merits further (biological) investigation. Who would argue against this?
Surely any smoker wants to know, with a high degree of certainty, what the chances are of succumbing to a disease that was entirely due to smoking. But lung cancer doesn’t yet present any such certainty, so we need more research into why lung cancer is/was so predominant in smokers, not just bald assertions of “the debate is over” variety.
Chris is offering a very spirited set of arguments, and has done his research well, but he does have a tendency to fall back on rhetoric when responding to counter arguments. Eg:
…For the lung cancer epidemic to begin, you need to have a sizeable group of people who have been smoking for at least 20 years
Where is the a priori evidence for this, the physiological proof that lung cancer takes decades to develop in smokers? Furthermore, if it is indeed the case, what is happening within the smoker’s organs during that period that results in carcinogenesis in old age; and what research is being carried out into clinical interventions that could counteract this?
…“Recent decades have seen more smokers getting adenocarcinoma and … ‘light’ cigarettes allow (or require, even) the smoke to go deeper into the lungs. Old, unfiltered heavy cigarettes were not inhaled so deeply and so the tumour would form higher up the lung”
But this has got nothing to do with tumour position within the lungs. Adenocarcinoma and Squamous Cell Carcinoma are histologically different types of cancer. It was always easy to use this fact to ‘prove’ that smoking ’caused’ (squamous cell) lung cancer. The fact that the majority of smokers’ LCs are now also adenocarcinoma may be inconvenient for anti-tobacco, but it really does need a proper explanation.
My suspicion is that 50+ years ago smoking did make a strong biological contribution to the formation of lung tumours (maybe ’caused’, but more likely a more complex process involving other factors). Do remember that the vast majority of studies that still form the foundation of the causal hypothesis were carried out in the 1950s and 1960s, ie based on the peoples’ smoking habits in the 1940s/1950s and (if Chris is correct) back to the 20s and 30s. Chris cites the US Surgeon General’s report of 1964! Nobody is researching into whether smoking causes lung cancer any more. As AGW alarmists would say “the science is settled”. But is it?
There is little doubt (outside of anti-tobacco groupthink) that cigarettes have become immensely ‘safer’ since these studies were carried out. The use of filter tips, lower tar levels, changes in types of tobacco used and curing methods have resulted in huge reductions in measurable levels of known carcinogens. Also people are generally smoking much less than they did 50+ years ago. The 100 a day smoker is rare now – even 20 a day is deemed to be ‘heavy’ smoking. The improvements are such that the ‘safe’ level of smoking is round about 10 cigarettes per day (see Gio Batta Gori [*]).
So, given these changes, isn’t it feasible that there are actually very few new lung cancers that are ’caused’ by smoking (squamous cell) and since smokers now experience the same type (adenocarcinoma) as non-smokers (and seemingly at a similar rate), is smoking any longer the dominant factor in lung carcinogenesis?
You see, without new research we may be missing the fact that the battle against lung cancer is actually being won by making cigarettes safer, rather than by declaring war on smokers. If this is the case, then much blood is on the hands of the anti-tobacco lobby, who collectively forced the termination of all ‘safe cigarette’ development efforts, resulting in the unnecessary premature deaths of literally millions of smokers.
[*] I commend everyone to research the writings of Gio Gori.
Burden of Proof/Either-Or
I think I’m with Mr. Snowdon on this one.
His words:
“Since the obvious explanation for this strong, dose-sensitive association is that chronic smoking raises the risk of lung cancer significantly, any defence of smoking as the causative factor must provide an alternative. That alternative must be closely correlated with smoking itself and must have a correlation with lung cancer that is at least as strong as the correlations found for smoking and lung cancer.”
I don’t think it’s a valid contradiction to say that this is a clumsy invocation of correlation in the absence of an explanation of causation. No one in this debate can be placed in the position of pretending to know all of the factors that might cause or contribute to lung cancer in any individual person, nonetheless wide swaths of people. Nor can anyone tell precisely why most heavy smokers don’t get lung cancer.
while I think it’s valid to point out that the anti-tobacco establishment has played a key role in sidelining the pursuit of any such hard science regarding lung cancer in favor of a moral/political agenda, only available evidence can be taken into consideration. Whether we like it or not, that evidence is statistical, epidemiological evidence. I think Mr. Snowdon shares in being critical of the problems that arise from an over-reliance on this kind of evidence.
However, I don’t think that he should be expected to fend off every objection to the “smoking-contributes-to-lung-cancer” hypothesis, thereby allowing any perceived failure of an adequate explanation from him to serve, by default, as a reason to say: “See that! He couldn’t explain it to my satisfaction! Therefore, no one knows if smoking plays a causative role in developing lung cancer!”
To do so shifts the burden of proof away from the person who is simply claiming to know what is factually true: lung cancer is much more prevalent in smokers than non-smokers. If the contention otherwise is that smoking does not play a causative role in lung cancer, then one isn’t necessarily being forced to “prove a negative”, but to deliver a viable alternative hypothesis that takes the heavy correlation into consideration.
Frankly, the “or” side of the “either/or” equation seems rather weak when it comes to “EITHER smoking has played a major role in lung cancer in most people (smokers) who have it OR coal dust, nuclear test pollution, general environmental pollution, stress, poverty, etc, etc, etc.
The proper burden of proof then lies on the “OR” side of the “Either/Or” equation. In other words, it simply isn’t enough to try and debunk the causative role of smoking in lung cancer. Rather, as Mr. Snowdon implied in the quote above, the burden of proof then lies with opponents of the “smoking-is-the-major-contributor-to-lung-cancer” hypothesis to provide a viable alternative hypothesis, rather than conjecture and speculation.
I certainly don’t mean to suggest that a possible alternative reason doesn’t exist, but I don’t think this interesting debate is going to be worth it in the end if the expectations are unreasonable. No one is going to be able to say “Eureka! It’s not the smoking after all– it’s that damn (insert reason here)! Unless, of course, someone has a good case to make, and each of those cases should be considered on their own merits.
I hope that made some sense.
-WS
funny timing
just read this morning.
bear with the google-translation, you’ll get the picture.
“More get lung cancer despite fewer smokers”
http://translate.google.com/translate?js=n&prev=_t&hl=en&ie=UTF-8&layout=2&eotf=1&sl=da&tl=en&u=http%3A%2F%2Fwww.dr.dk%2FNyheder%2FUdland%2F2010%2F12%2F01%2F075617.htm%3Frss%3Dtrue&act=url
funny timing
just read this morning.
bear with the google-translation, you’ll get the picture.
“More get lung cancer despite fewer smokers”
http://translate.google.com/translate?js=n&prev=_t&hl=en&ie=UTF-8&layout=2&eotf=1&sl=da&tl=en&u=http%3A%2F%2Fwww.dr.dk%2FNyheder%2FUdland%2F2010%2F12%2F01%2F075617.htm%3Frss%3Dtrue&act=url
Re: funny timing
btw frank, are you monitoring/moderating this?
I would like to ‘invite’ some people over, but haven’t done so yet, because it would probably drag in some very nasty trolls.
Re: funny timing
Yes, I am monitoring. And I don’t particularly want any trolls.
Re: funny timing
K, I’ll wait then.
Re: funny timing
K, I’ll wait then.
Re: funny timing
Yes, I am monitoring. And I don’t particularly want any trolls.
Re: funny timing
btw frank, are you monitoring/moderating this?
I would like to ‘invite’ some people over, but haven’t done so yet, because it would probably drag in some very nasty trolls.
funny timing
just read this morning.
bear with the google-translation, you’ll get the picture.
“More get lung cancer despite fewer smokers”
http://translate.google.com/translate?js=n&prev=_t&hl=en&ie=UTF-8&layout=2&eotf=1&sl=da&tl=en&u=http%3A%2F%2Fwww.dr.dk%2FNyheder%2FUdland%2F2010%2F12%2F01%2F075617.htm%3Frss%3Dtrue&act=url
Re: funny timing
btw frank, are you monitoring/moderating this?
I would like to ‘invite’ some people over, but haven’t done so yet, because it would probably drag in some very nasty trolls.
Re: funny timing
Yes, I am monitoring. And I don’t particularly want any trolls.
Chuckles
WS, Your comment above suggests that there MUST be a CAUSE for cancer, and it must be rooted in the foul and lascivious pleasures we wallow in, or at least in the filthy modern practices we indulge in regarding energy, food, transport and similar.
Most cancers are diseases of the aged, if the heart attacks and strokes don’t get you the cancer will. Or to translate, if the plumbing or the wiring don’t go faulty with age, the maintenance and repair schedule will eventually go haywire?
Chuckles
WS, Your comment above suggests that there MUST be a CAUSE for cancer, and it must be rooted in the foul and lascivious pleasures we wallow in, or at least in the filthy modern practices we indulge in regarding energy, food, transport and similar.
Most cancers are diseases of the aged, if the heart attacks and strokes don’t get you the cancer will. Or to translate, if the plumbing or the wiring don’t go faulty with age, the maintenance and repair schedule will eventually go haywire?
Re: Chuckles
Chuckles, regarding your first paragraph, I don’t see how I implied in any way that a moral equation should be inserted. You should know me better than that, anyway, from our many previous shared threads/discussions.
Other than that, effects have causes and vice versa. I don’t think that simply chalking the matters being discussed up to aging is going to be entirely sufficient.
-WS
Re: Chuckles
Chuckles, regarding your first paragraph, I don’t see how I implied in any way that a moral equation should be inserted. You should know me better than that, anyway, from our many previous shared threads/discussions.
Other than that, effects have causes and vice versa. I don’t think that simply chalking the matters being discussed up to aging is going to be entirely sufficient.
-WS
Chuckles
WS, Your comment above suggests that there MUST be a CAUSE for cancer, and it must be rooted in the foul and lascivious pleasures we wallow in, or at least in the filthy modern practices we indulge in regarding energy, food, transport and similar.
Most cancers are diseases of the aged, if the heart attacks and strokes don’t get you the cancer will. Or to translate, if the plumbing or the wiring don’t go faulty with age, the maintenance and repair schedule will eventually go haywire?
What is being compared here is relative and absolute risk. The former is used by epidemiologists to argue for a causal connection between smoking and lung cancer. This is understandable: you want to compare the number of incidences of a disease (lung cancer) where certain conditions apply (smoking) against the number of incidences where the same conditions do not apply, and use that as evidence for a causal link. Bradford Hill, to be fair to him, was aware of this:
‘I would reject the argument sometimes advanced that what matters is the absolute difference between the death rates of our various groups and not the ratio of one to the other. That depends upon what we want to know. If we want to know how many extra deaths from cancer of the lung will take place through smoking (i.e. presuming causation), then obviously we must use the absolute differences between the death rates – 0.07 per 1,000 per year in nonsmoking doctors, 0.57 in those smoking 1–14 and 2.27 for 25 or more daily. But it does not follow here, or in more specifically occupational problems, that this best measure of the effect upon mortality is also the best measure in relation to etiology. In this respect the ratios of 8, 20 and 32 to 1 are far more informative. It does not, of course, follow that the differences revealed by ratios are of any practical importance. Maybe they are, maybe they are not; but that is another point altogether. We may recall John Snow’s classic analysis of the opening weeks of the cholera epidemic of 1854. The death rate that he recorded in the customers supplied with the grossly polluted water of the Southwark and Vauxhall Company was in truth quite low – 71 deaths in each 10,000 houses. What stands out vividly is the fact that the small rate is 14 times the figure of 5 deaths per 10,000 houses supplied with the sewage free water of the Lambeth Company.’
It might be possible, then, to argue for a causal connection between smoking and lung cancer (by means of the high relative risk), but then to go on to say that actually it doesn’t cause it all that often (by means of the low absolute risk). Both statements can be true – smoking can be a cause of lung cancer, but it’s no where near as harmful as we have been led to believe. Questions concerning causation and those concerning harmfulness are thus quite separate, and there is a danger that the two can become entwined.
DW
Frank
In that case, the statement would have been:
…The lung cancer patients were 1.017 times more likely than the general population to be smokers.
whereas Chris’s original position was based on a comparison of the effect group (lung cancer patients) against the control group (non-lung cancer).
This is actually a good example of how the Odds Ratio (RR) differs from Relative Risk in epidemiological calculations, the 1.04 is numerically similar to the OR calculation, whereas your 1.017 is equivalent to RR (not the exact calculations, but mathematically equivalent). It demonstrates that an OR will always be larger than the RR calculated from the same data. This is worth remembering when looking at epi studies; OR and RR are not the same.
Sorry if I seem to be nit-picking, but I have a long professional history in this area, which results in arguably more despair in myself than in others, because I see people who really should know better (epidemiologists) abusing my discipline (statistics) in order to influence the gullible and thick (politicians).
Good debate though – I am currently quite agnostic on the main topic, but as someone who actually did some work for Richard Doll in the early part of my career, that is quite some movement of position.
Brian Bond
As a starting point we should look:
1) Has the incidence of LC reduced to match the reduction in smoking?
2) Is the incidence of smokers remaining static as a percentage among LC sufferers?
After this we can start to refine things. But I’m finding it bloody difficult to get the answers to those 2 simple things.
I think it very important to the discussion of the early studies to put them in the context of the time.
Right from the start there is an urban-rural divide.
“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
1953
“Bessy Braddock, Labour MP for Liverpool Exchange, favoured an environmental explanation, and therefore found the urban–rural divide a barrier to acceptance of the smoking–lung cancer connection.
‘In view of the fact that cigarette and pipe smoking goes on all over the country, it is folly to say that it is the main cause of lung cancer.’
Click to access 0-19-926030-3.pdf
So the problem is in the cities.
POLLUTED CITY AIR IS CANCER SUSPECT; Fumes From Engines Found to Contain Several Chemicals That Produce the Disease
LUNG DEATHS RISING FAST
Easing of Traffic Congestion and Better Maintenance of Motors Held Important – New York Times 1953
“Studies indicating that the polluted air over large cities may be the major factor in the alarming increase in deaths from lung cancer in the last twenty years were reported yesterday to the American Cancer Society
http://legacy.library.ucsf.edu/action/document/page?tid=nvi43c00
Medicine: Death in the Smoke
Monday, May. 11, 1959
“It does not take “a London particular” to send cough-racked Britons to their beds —or their graves. The tight little island’s air is tightly packed with pollutant particles, boosting the bronchitis and chest-disease rate to the world’s highest. Last week Dr. Horace Joules (rhymes with rules), of London’s Central Middlesex Hospital, painted a Dickensian picture of what a medical nightmare the past winter had been in the city which some Englishmen still call “the Smoke.”
“We are a great community hospital of 800 beds,” said Dr. Joules, “but during February and March we ceased to be a general hospital. We had to suspend all admissions except emergency cases of chest and heart disease.* In those two months we admitted 616 such cases, and 196 died. The hospital really was an annex of the mortuary. If there had been a few days of smog, there would have been a holocaust in London.”
Echoed Edgware General Hospital’s Dr. Hugh J. Trenchard: “It is time to panic.”
*The two are closely related because failing hearts may be fatally threatened by breathing difficulties.”
http://www.time.com/time/magazine/article/0,9171,865848,00.html
Historic smog death toll rises
“Maureen Scholes, a nurse at the Royal London Hospital at the time, recalls being unable to see from one end of the ward to the other because of the pollution.
“You couldn’t see along the corridor that you walked in when you came on duty.
“You couldn’t see actually from one end of the ward to the other and it’s not that enormous a length.”
http://news.bbc.co.uk/1/hi/health/2545747.stm
Toxicologic and Epidemiologic Clues from the Characterization of the 1952 London Smog Fine Particulate Matter in Archival Autopsy Lung Tissues
Click to access 6114.pdf
Boston December 30th 1959
Lung Cancer Cause
“A man who has devoted his scientific career to a study of the causes of cancer warns that air pollution is a more important factor than cigarette smoking in the increase of lung cancer.
He is Dr, Wilhelm C Hueper, chief of the environmental section of the National Cancer Institute at Bethesda, and he makes the significant observation that the upsurge in lung cancer first was noted between 1900 and 1920, several years before the practice of cigarette smoking was widespread.
Boston, having one of the most serious air pollution in the entire United States, cannot fail to be impressed – and disturbed – by Dr Hueper’s findings.
http://legacy.library.ucsf.edu/action/document/page;jsessionid=431567CE1BD9A55DA749F6EE58FC5DD1?tid=jsv02a00
Rose
I think it very important to the discussion of the early studies to put them in the context of the time.
Right from the start there is an urban-rural divide.
“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
1953
“Bessy Braddock, Labour MP for Liverpool Exchange, favoured an environmental explanation, and therefore found the urban–rural divide a barrier to acceptance of the smoking–lung cancer connection.
‘In view of the fact that cigarette and pipe smoking goes on all over the country, it is folly to say that it is the main cause of lung cancer.’
Click to access 0-19-926030-3.pdf
So the problem is in the cities.
POLLUTED CITY AIR IS CANCER SUSPECT; Fumes From Engines Found to Contain Several Chemicals That Produce the Disease
LUNG DEATHS RISING FAST
Easing of Traffic Congestion and Better Maintenance of Motors Held Important – New York Times 1953
“Studies indicating that the polluted air over large cities may be the major factor in the alarming increase in deaths from lung cancer in the last twenty years were reported yesterday to the American Cancer Society
http://legacy.library.ucsf.edu/action/document/page?tid=nvi43c00
Medicine: Death in the Smoke
Monday, May. 11, 1959
“It does not take “a London particular” to send cough-racked Britons to their beds —or their graves. The tight little island’s air is tightly packed with pollutant particles, boosting the bronchitis and chest-disease rate to the world’s highest. Last week Dr. Horace Joules (rhymes with rules), of London’s Central Middlesex Hospital, painted a Dickensian picture of what a medical nightmare the past winter had been in the city which some Englishmen still call “the Smoke.”
“We are a great community hospital of 800 beds,” said Dr. Joules, “but during February and March we ceased to be a general hospital. We had to suspend all admissions except emergency cases of chest and heart disease.* In those two months we admitted 616 such cases, and 196 died. The hospital really was an annex of the mortuary. If there had been a few days of smog, there would have been a holocaust in London.”
Echoed Edgware General Hospital’s Dr. Hugh J. Trenchard: “It is time to panic.”
*The two are closely related because failing hearts may be fatally threatened by breathing difficulties.”
http://www.time.com/time/magazine/article/0,9171,865848,00.html
Historic smog death toll rises
“Maureen Scholes, a nurse at the Royal London Hospital at the time, recalls being unable to see from one end of the ward to the other because of the pollution.
“You couldn’t see along the corridor that you walked in when you came on duty.
“You couldn’t see actually from one end of the ward to the other and it’s not that enormous a length.”
http://news.bbc.co.uk/1/hi/health/2545747.stm
Toxicologic and Epidemiologic Clues from the Characterization of the 1952 London Smog Fine Particulate Matter in Archival Autopsy Lung Tissues
Click to access 6114.pdf
Boston December 30th 1959
Lung Cancer Cause
“A man who has devoted his scientific career to a study of the causes of cancer warns that air pollution is a more important factor than cigarette smoking in the increase of lung cancer.
He is Dr, Wilhelm C Hueper, chief of the environmental section of the National Cancer Institute at Bethesda, and he makes the significant observation that the upsurge in lung cancer first was noted between 1900 and 1920, several years before the practice of cigarette smoking was widespread.
Boston, having one of the most serious air pollution in the entire United States, cannot fail to be impressed – and disturbed – by Dr Hueper’s findings.
http://legacy.library.ucsf.edu/action/document/page;jsessionid=431567CE1BD9A55DA749F6EE58FC5DD1?tid=jsv02a00
Rose
I think it very important to the discussion of the early studies to put them in the context of the time.
Right from the start there is an urban-rural divide.
“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
1953
“Bessy Braddock, Labour MP for Liverpool Exchange, favoured an environmental explanation, and therefore found the urban–rural divide a barrier to acceptance of the smoking–lung cancer connection.
‘In view of the fact that cigarette and pipe smoking goes on all over the country, it is folly to say that it is the main cause of lung cancer.’
Click to access 0-19-926030-3.pdf
So the problem is in the cities.
POLLUTED CITY AIR IS CANCER SUSPECT; Fumes From Engines Found to Contain Several Chemicals That Produce the Disease
LUNG DEATHS RISING FAST
Easing of Traffic Congestion and Better Maintenance of Motors Held Important – New York Times 1953
“Studies indicating that the polluted air over large cities may be the major factor in the alarming increase in deaths from lung cancer in the last twenty years were reported yesterday to the American Cancer Society
http://legacy.library.ucsf.edu/action/document/page?tid=nvi43c00
Medicine: Death in the Smoke
Monday, May. 11, 1959
“It does not take “a London particular” to send cough-racked Britons to their beds —or their graves. The tight little island’s air is tightly packed with pollutant particles, boosting the bronchitis and chest-disease rate to the world’s highest. Last week Dr. Horace Joules (rhymes with rules), of London’s Central Middlesex Hospital, painted a Dickensian picture of what a medical nightmare the past winter had been in the city which some Englishmen still call “the Smoke.”
“We are a great community hospital of 800 beds,” said Dr. Joules, “but during February and March we ceased to be a general hospital. We had to suspend all admissions except emergency cases of chest and heart disease.* In those two months we admitted 616 such cases, and 196 died. The hospital really was an annex of the mortuary. If there had been a few days of smog, there would have been a holocaust in London.”
Echoed Edgware General Hospital’s Dr. Hugh J. Trenchard: “It is time to panic.”
*The two are closely related because failing hearts may be fatally threatened by breathing difficulties.”
http://www.time.com/time/magazine/article/0,9171,865848,00.html
Historic smog death toll rises
“Maureen Scholes, a nurse at the Royal London Hospital at the time, recalls being unable to see from one end of the ward to the other because of the pollution.
“You couldn’t see along the corridor that you walked in when you came on duty.
“You couldn’t see actually from one end of the ward to the other and it’s not that enormous a length.”
http://news.bbc.co.uk/1/hi/health/2545747.stm
Toxicologic and Epidemiologic Clues from the Characterization of the 1952 London Smog Fine Particulate Matter in Archival Autopsy Lung Tissues
Click to access 6114.pdf
Boston December 30th 1959
Lung Cancer Cause
“A man who has devoted his scientific career to a study of the causes of cancer warns that air pollution is a more important factor than cigarette smoking in the increase of lung cancer.
He is Dr, Wilhelm C Hueper, chief of the environmental section of the National Cancer Institute at Bethesda, and he makes the significant observation that the upsurge in lung cancer first was noted between 1900 and 1920, several years before the practice of cigarette smoking was widespread.
Boston, having one of the most serious air pollution in the entire United States, cannot fail to be impressed – and disturbed – by Dr Hueper’s findings.
http://legacy.library.ucsf.edu/action/document/page;jsessionid=431567CE1BD9A55DA749F6EE58FC5DD1?tid=jsv02a00
Rose
The trouble is this whole branch of “science” is based on guesswork. Someone above said it would be helpful if we had the actual stats for the number of smokers who got lung cancer etc etc. Trouble is we don’t even know how many smokers there are! The DoH says 21%. That recent EU report says 28%. Hey that’s only a difference of a few MILLION people, right? Then there is the small matter of at least a third of tobacco being illegally imported. Does that mean there are even more smokers than that? Then what about 60 a day smokers or ten a day smokers? Are they just “smokers” or is there a difference between them? What about social smokers? If asked, how many people who smoke every time they go out would say they were non-smokers? Would the honesty of their responses be distorted by years of denormalisation? For example, I went to a dinner party the other day and there were only 2 smokers there, out of about 20 people. By the end of the night there were 8 or 9 people outside cadging our fags. Are they smokers? The fact that one couple spent much of the evening avoiding each other as they thought their partner didn’t know they were social smokers (yes both of them!) indicates that if asked by a pollster they would probably say they were non-smokers.
When we don’t even know how many people smoke how can any reasonable guesstimate be done on smoking rates and lung cancer rates?
Mr A
The trouble is this whole branch of “science” is based on guesswork. Someone above said it would be helpful if we had the actual stats for the number of smokers who got lung cancer etc etc. Trouble is we don’t even know how many smokers there are! The DoH says 21%. That recent EU report says 28%. Hey that’s only a difference of a few MILLION people, right? Then there is the small matter of at least a third of tobacco being illegally imported. Does that mean there are even more smokers than that? Then what about 60 a day smokers or ten a day smokers? Are they just “smokers” or is there a difference between them? What about social smokers? If asked, how many people who smoke every time they go out would say they were non-smokers? Would the honesty of their responses be distorted by years of denormalisation? For example, I went to a dinner party the other day and there were only 2 smokers there, out of about 20 people. By the end of the night there were 8 or 9 people outside cadging our fags. Are they smokers? The fact that one couple spent much of the evening avoiding each other as they thought their partner didn’t know they were social smokers (yes both of them!) indicates that if asked by a pollster they would probably say they were non-smokers.
When we don’t even know how many people smoke how can any reasonable guesstimate be done on smoking rates and lung cancer rates?
Mr A
You must have a starting point. Have the rates of LC declined in ratio to the number of smokers and, whatever the total, have the LC rates of smokers remained static as a percentage. They’re simple questions and bloody difficult to find the answers. That, by itself, is deeply suspicious.
If Chris or anyone can answer this for us, it will certainly help not just this debate, but the whole smoking question.
You must have a starting point. Have the rates of LC declined in ratio to the number of smokers and, whatever the total, have the LC rates of smokers remained static as a percentage. They’re simple questions and bloody difficult to find the answers. That, by itself, is deeply suspicious.
If Chris or anyone can answer this for us, it will certainly help not just this debate, but the whole smoking question.
The trouble is this whole branch of “science” is based on guesswork. Someone above said it would be helpful if we had the actual stats for the number of smokers who got lung cancer etc etc. Trouble is we don’t even know how many smokers there are! The DoH says 21%. That recent EU report says 28%. Hey that’s only a difference of a few MILLION people, right? Then there is the small matter of at least a third of tobacco being illegally imported. Does that mean there are even more smokers than that? Then what about 60 a day smokers or ten a day smokers? Are they just “smokers” or is there a difference between them? What about social smokers? If asked, how many people who smoke every time they go out would say they were non-smokers? Would the honesty of their responses be distorted by years of denormalisation? For example, I went to a dinner party the other day and there were only 2 smokers there, out of about 20 people. By the end of the night there were 8 or 9 people outside cadging our fags. Are they smokers? The fact that one couple spent much of the evening avoiding each other as they thought their partner didn’t know they were social smokers (yes both of them!) indicates that if asked by a pollster they would probably say they were non-smokers.
When we don’t even know how many people smoke how can any reasonable guesstimate be done on smoking rates and lung cancer rates?
Mr A
You must have a starting point. Have the rates of LC declined in ratio to the number of smokers and, whatever the total, have the LC rates of smokers remained static as a percentage. They’re simple questions and bloody difficult to find the answers. That, by itself, is deeply suspicious.
If Chris or anyone can answer this for us, it will certainly help not just this debate, but the whole smoking question.
Junican, your explanation of relative risk is correct. What is more important is absolute excess risk, which for obvious reasons is never quoted by the authors of health scare papers. For example, lc among smokeless air breathing non smokers runs at about 5 per 1000. The claimed relative risk for spending 5 hours a day in a smoky atmosphere is 1.2. This gives an extra 1 case per 1000, or an absolute excess risk of 0.001; comparable with the claimed risk for bowel cancer from alcohol or bacon sanwiches. In fact, sitting in a smoke free pub drinking a glass of wine poses a greater carcinogen risk than sitting in a smoky pub drinking mineral water.
I agree with your point about deaths. Lansley mentions a figure of 80,000 deaths a year from smoking. Putting aside the problem of attributing this number of deaths to smoking, the important information is by how long these lifetimes were cut short, on average, by the act of smoking (NOT by being a smoker, who typically drinks more alcohol, has a poorer diet and takes less exercise). A useful contribution to this is the life expectancy calculator on the website of David Spiegelhalter, Professor of the public understanding of science at Cambridge. Using actuarial life tables and a study carried out by a Cambridge epidemiologist, smoking, alcohol, diet and exercise are, perhaps surprisingly to many, given equal weight and a 53 yr old smoker (me) will lose on average just 3 years of future life expectancy if he leads an otherwise healthy life.
Regarding your query about “age adjusted”: age adjustment is a method used so that useful comparisons can be made between groups with different age distributions. For example, without age adjustment, the lung cancer rate for a country from which everybody emigrated when they reached 60 would be miniscule compared to a similar country where they did not. Here are a couple of links.
http://seer.cancer.gov/seerstat/tutorials/aarates/definition.html
http://www.dhss.mo.gov/CDP_MICA/AARate.html
On the debate, I’m with Chris. The snus/low smoking among Swedish males/low lung cancer nails it for me. One point that has come up more than once is that former smokers have a higher incidence of lc than current smokers. This is because they are older. The median age for lc is 71. The reduction in risk from quitting does not compensate for the increase in risk for a former smoker getting older.
Thanks for the interesting debate, JB.
Junican, your explanation of relative risk is correct. What is more important is absolute excess risk, which for obvious reasons is never quoted by the authors of health scare papers. For example, lc among smokeless air breathing non smokers runs at about 5 per 1000. The claimed relative risk for spending 5 hours a day in a smoky atmosphere is 1.2. This gives an extra 1 case per 1000, or an absolute excess risk of 0.001; comparable with the claimed risk for bowel cancer from alcohol or bacon sanwiches. In fact, sitting in a smoke free pub drinking a glass of wine poses a greater carcinogen risk than sitting in a smoky pub drinking mineral water.
I agree with your point about deaths. Lansley mentions a figure of 80,000 deaths a year from smoking. Putting aside the problem of attributing this number of deaths to smoking, the important information is by how long these lifetimes were cut short, on average, by the act of smoking (NOT by being a smoker, who typically drinks more alcohol, has a poorer diet and takes less exercise). A useful contribution to this is the life expectancy calculator on the website of David Spiegelhalter, Professor of the public understanding of science at Cambridge. Using actuarial life tables and a study carried out by a Cambridge epidemiologist, smoking, alcohol, diet and exercise are, perhaps surprisingly to many, given equal weight and a 53 yr old smoker (me) will lose on average just 3 years of future life expectancy if he leads an otherwise healthy life.
Regarding your query about “age adjusted”: age adjustment is a method used so that useful comparisons can be made between groups with different age distributions. For example, without age adjustment, the lung cancer rate for a country from which everybody emigrated when they reached 60 would be miniscule compared to a similar country where they did not. Here are a couple of links.
http://seer.cancer.gov/seerstat/tutorials/aarates/definition.html
http://www.dhss.mo.gov/CDP_MICA/AARate.html
On the debate, I’m with Chris. The snus/low smoking among Swedish males/low lung cancer nails it for me. One point that has come up more than once is that former smokers have a higher incidence of lc than current smokers. This is because they are older. The median age for lc is 71. The reduction in risk from quitting does not compensate for the increase in risk for a former smoker getting older.
Thanks for the interesting debate, JB.
JB,
I nitpicked Junican’s arithmetic on relative risk in a reply to his post and stand by what I said. However I very much agree that absolute risk is the key issue both for active and especially for ‘passive’ smoking.
I also take your point about ex-smokers being older which makes direct comparison of rates difficult.
On the whole I am more aligned with Frank and Rich on the central question. Sweden’s example is all very well but what about the high smoking low lung cancer Japanese?
Tony
JB,
I nitpicked Junican’s arithmetic on relative risk in a reply to his post and stand by what I said. However I very much agree that absolute risk is the key issue both for active and especially for ‘passive’ smoking.
I also take your point about ex-smokers being older which makes direct comparison of rates difficult.
On the whole I am more aligned with Frank and Rich on the central question. Sweden’s example is all very well but what about the high smoking low lung cancer Japanese?
Tony
RR and Age Adj
Thanks for that JB – very helpful.
RR and Age Adj
Thanks for that JB – very helpful.
Junican, your explanation of relative risk is correct. What is more important is absolute excess risk, which for obvious reasons is never quoted by the authors of health scare papers. For example, lc among smokeless air breathing non smokers runs at about 5 per 1000. The claimed relative risk for spending 5 hours a day in a smoky atmosphere is 1.2. This gives an extra 1 case per 1000, or an absolute excess risk of 0.001; comparable with the claimed risk for bowel cancer from alcohol or bacon sanwiches. In fact, sitting in a smoke free pub drinking a glass of wine poses a greater carcinogen risk than sitting in a smoky pub drinking mineral water.
I agree with your point about deaths. Lansley mentions a figure of 80,000 deaths a year from smoking. Putting aside the problem of attributing this number of deaths to smoking, the important information is by how long these lifetimes were cut short, on average, by the act of smoking (NOT by being a smoker, who typically drinks more alcohol, has a poorer diet and takes less exercise). A useful contribution to this is the life expectancy calculator on the website of David Spiegelhalter, Professor of the public understanding of science at Cambridge. Using actuarial life tables and a study carried out by a Cambridge epidemiologist, smoking, alcohol, diet and exercise are, perhaps surprisingly to many, given equal weight and a 53 yr old smoker (me) will lose on average just 3 years of future life expectancy if he leads an otherwise healthy life.
Regarding your query about “age adjusted”: age adjustment is a method used so that useful comparisons can be made between groups with different age distributions. For example, without age adjustment, the lung cancer rate for a country from which everybody emigrated when they reached 60 would be miniscule compared to a similar country where they did not. Here are a couple of links.
http://seer.cancer.gov/seerstat/tutorials/aarates/definition.html
http://www.dhss.mo.gov/CDP_MICA/AARate.html
On the debate, I’m with Chris. The snus/low smoking among Swedish males/low lung cancer nails it for me. One point that has come up more than once is that former smokers have a higher incidence of lc than current smokers. This is because they are older. The median age for lc is 71. The reduction in risk from quitting does not compensate for the increase in risk for a former smoker getting older.
Thanks for the interesting debate, JB.
Secret plot to play down risks of air pollution
Professor Berridge said that the readiness of supposedly independent scientists to emphasise smoking over air pollution represented a wider shift away from the concept of health related to an individual’s environment and workplace towards one focused on that individual’s responsibility for his or her health as epitomised by smoking.”
http://www.independent.co.uk/news/uk/politics/secret-plot-to-play-down-risks-of-air-pollution-610356.html
By strange coincidence, at the same time that oil money was training such notable persons as Godber and Doll in Public Health –
1945-1946
Rockefeller Foundation offers fellowships for training “hand-picked” students in Public Health Department.
Introduction of lectures on sociology and social medicine.
http://www.lshtm.ac.uk/library/archives/history/chronology/
Medical Research Council
Rockefeller Medical Fellowships
1932
Click to access brmedj07385-0032a.pdf
“The new School of Hygiene & Tropical Medicine was opened in its present building in Keppel Street, a gift from the Rockefeller Foundation.
At that time, the term ‘hygiene’ was not restricted to its current meaning of ‘cleanliness’ or ‘sanitary science’, but was used in the wider sense of the establishment and maintenance of health – now more usually described as ‘public health'”
http://www.lshtm.ac.uk/prospectus/introduction.html
Firms ‘knew of leaded petrol dangers in 20s’
“Jamie Kitman, a New York lawyer and US editor of the magazine which did the research, discovered the consequences of leaded petrol were clearly identified by public health officials and scientists 75 years ago, and well known to the company’s executives. The potential consequences were denied and then endlessly debated by its inventors.
General Motors, duPont and Standard Oil were making billions of dollars worldwide from selling the lead formula which they had patented while paying for and controlling the research into the health effects for more than 40 years. The research always favoured the industry’s pro-lead views or was suppressed, Mr Kitman found.”
http://www.guardian.co.uk/environment/2000/jul/13/uknews/print
Science: Tetraethyl Lead
Monday, Nov. 10, 1924
“The Standard Oil Co. of New Jersey has a plant at Bayway, N. J. There last week a man suddenly became raving mad. He was taken to a hospital in Manhattan where he soon died. Others became affected. Within a few days, five men, all raving mad and confined in straight-jackets, died. In all there were 45 men—three shifts of 15 each—working together on the same job. All were placed under medical observation and care. Only ten of them were unaffected. The others all showed symptoms of the disease: headaches, nervousness, insomnia, lowered blood pressure. Such was the toll of the first major onslaught of the newest “occupational disease.” For some time experiments have been going forward in an effort to improve gasoline as an automobile fuel.”
http://www.time.com/time/magazine/article/0,9171,728055,00.html
So there could have been just the slightest hint of a conflict of interest.
Pollution ’causes cancer deaths’
“One in ten deaths from lung cancer in the UK may be linked to air pollution, an expert has said.
The finding adds to growing concerns that the threat to public health posed by air pollution may have been overlooked as many scientists chose to focus on smoking instead”
http://news.bbc.co.uk/1/hi/health/2557617.stm
City traffic fumes ‘can cause heart attacks’
“People living in big cities are “breathing in an oil spill” every day because of air pollution that can have significant effects on cardiovascular health, scientists said today.”
http://www.timesonline.co.uk/tol/news/science/article3389896.ece
Rose
Secret plot to play down risks of air pollution
Professor Berridge said that the readiness of supposedly independent scientists to emphasise smoking over air pollution represented a wider shift away from the concept of health related to an individual’s environment and workplace towards one focused on that individual’s responsibility for his or her health as epitomised by smoking.”
http://www.independent.co.uk/news/uk/politics/secret-plot-to-play-down-risks-of-air-pollution-610356.html
By strange coincidence, at the same time that oil money was training such notable persons as Godber and Doll in Public Health –
1945-1946
Rockefeller Foundation offers fellowships for training “hand-picked” students in Public Health Department.
Introduction of lectures on sociology and social medicine.
http://www.lshtm.ac.uk/library/archives/history/chronology/
Medical Research Council
Rockefeller Medical Fellowships
1932
Click to access brmedj07385-0032a.pdf
“The new School of Hygiene & Tropical Medicine was opened in its present building in Keppel Street, a gift from the Rockefeller Foundation.
At that time, the term ‘hygiene’ was not restricted to its current meaning of ‘cleanliness’ or ‘sanitary science’, but was used in the wider sense of the establishment and maintenance of health – now more usually described as ‘public health'”
http://www.lshtm.ac.uk/prospectus/introduction.html
Firms ‘knew of leaded petrol dangers in 20s’
“Jamie Kitman, a New York lawyer and US editor of the magazine which did the research, discovered the consequences of leaded petrol were clearly identified by public health officials and scientists 75 years ago, and well known to the company’s executives. The potential consequences were denied and then endlessly debated by its inventors.
General Motors, duPont and Standard Oil were making billions of dollars worldwide from selling the lead formula which they had patented while paying for and controlling the research into the health effects for more than 40 years. The research always favoured the industry’s pro-lead views or was suppressed, Mr Kitman found.”
http://www.guardian.co.uk/environment/2000/jul/13/uknews/print
Science: Tetraethyl Lead
Monday, Nov. 10, 1924
“The Standard Oil Co. of New Jersey has a plant at Bayway, N. J. There last week a man suddenly became raving mad. He was taken to a hospital in Manhattan where he soon died. Others became affected. Within a few days, five men, all raving mad and confined in straight-jackets, died. In all there were 45 men—three shifts of 15 each—working together on the same job. All were placed under medical observation and care. Only ten of them were unaffected. The others all showed symptoms of the disease: headaches, nervousness, insomnia, lowered blood pressure. Such was the toll of the first major onslaught of the newest “occupational disease.” For some time experiments have been going forward in an effort to improve gasoline as an automobile fuel.”
http://www.time.com/time/magazine/article/0,9171,728055,00.html
So there could have been just the slightest hint of a conflict of interest.
Pollution ’causes cancer deaths’
“One in ten deaths from lung cancer in the UK may be linked to air pollution, an expert has said.
The finding adds to growing concerns that the threat to public health posed by air pollution may have been overlooked as many scientists chose to focus on smoking instead”
http://news.bbc.co.uk/1/hi/health/2557617.stm
City traffic fumes ‘can cause heart attacks’
“People living in big cities are “breathing in an oil spill” every day because of air pollution that can have significant effects on cardiovascular health, scientists said today.”
http://www.timesonline.co.uk/tol/news/science/article3389896.ece
Rose
Secret plot to play down risks of air pollution
Professor Berridge said that the readiness of supposedly independent scientists to emphasise smoking over air pollution represented a wider shift away from the concept of health related to an individual’s environment and workplace towards one focused on that individual’s responsibility for his or her health as epitomised by smoking.”
http://www.independent.co.uk/news/uk/politics/secret-plot-to-play-down-risks-of-air-pollution-610356.html
By strange coincidence, at the same time that oil money was training such notable persons as Godber and Doll in Public Health –
1945-1946
Rockefeller Foundation offers fellowships for training “hand-picked” students in Public Health Department.
Introduction of lectures on sociology and social medicine.
http://www.lshtm.ac.uk/library/archives/history/chronology/
Medical Research Council
Rockefeller Medical Fellowships
1932
Click to access brmedj07385-0032a.pdf
“The new School of Hygiene & Tropical Medicine was opened in its present building in Keppel Street, a gift from the Rockefeller Foundation.
At that time, the term ‘hygiene’ was not restricted to its current meaning of ‘cleanliness’ or ‘sanitary science’, but was used in the wider sense of the establishment and maintenance of health – now more usually described as ‘public health'”
http://www.lshtm.ac.uk/prospectus/introduction.html
Firms ‘knew of leaded petrol dangers in 20s’
“Jamie Kitman, a New York lawyer and US editor of the magazine which did the research, discovered the consequences of leaded petrol were clearly identified by public health officials and scientists 75 years ago, and well known to the company’s executives. The potential consequences were denied and then endlessly debated by its inventors.
General Motors, duPont and Standard Oil were making billions of dollars worldwide from selling the lead formula which they had patented while paying for and controlling the research into the health effects for more than 40 years. The research always favoured the industry’s pro-lead views or was suppressed, Mr Kitman found.”
http://www.guardian.co.uk/environment/2000/jul/13/uknews/print
Science: Tetraethyl Lead
Monday, Nov. 10, 1924
“The Standard Oil Co. of New Jersey has a plant at Bayway, N. J. There last week a man suddenly became raving mad. He was taken to a hospital in Manhattan where he soon died. Others became affected. Within a few days, five men, all raving mad and confined in straight-jackets, died. In all there were 45 men—three shifts of 15 each—working together on the same job. All were placed under medical observation and care. Only ten of them were unaffected. The others all showed symptoms of the disease: headaches, nervousness, insomnia, lowered blood pressure. Such was the toll of the first major onslaught of the newest “occupational disease.” For some time experiments have been going forward in an effort to improve gasoline as an automobile fuel.”
http://www.time.com/time/magazine/article/0,9171,728055,00.html
So there could have been just the slightest hint of a conflict of interest.
Pollution ’causes cancer deaths’
“One in ten deaths from lung cancer in the UK may be linked to air pollution, an expert has said.
The finding adds to growing concerns that the threat to public health posed by air pollution may have been overlooked as many scientists chose to focus on smoking instead”
http://news.bbc.co.uk/1/hi/health/2557617.stm
City traffic fumes ‘can cause heart attacks’
“People living in big cities are “breathing in an oil spill” every day because of air pollution that can have significant effects on cardiovascular health, scientists said today.”
http://www.timesonline.co.uk/tol/news/science/article3389896.ece
Rose
Benzopyrene
Apparently in the days before the Clean Air Acts, city air was thick with it.
Testimony of Dr Hueper 1957
“They manipulated the evidence. Anyone who introduces a corrective factor in his calculations to make the evidence fit a preconceived idea, I do not feel that this is valid scientific evidence.
“Do you feel, in view of what you said, that the application of a corrective factor means a predetermined manipulation in this case?
A.In this case I could not say, no.
Q I want to get clear on that.You asked me to read on. I will do that. This appears on Page 435 of your May, 1957 article and reads;
“However, even this estimate is heavily biased by the arbitrary assumption that the benzpyrene content present allegedly in cigarette smoke was about 12 times as effective in eliciting cancers as benzpyrene demonstrated in atmospheric air.
Only when such a “corrective” coefficient is applied was it possible to obtain proportional correlations between the total exposure to benzpyrene from both cigarette smoking and air pollutants and the relative incidence rates of lung cancer found in the industrialized metropolitan Liverpool area, an intermediary urban-rural region, and the rural area of North Wales”
A That is right.
Q That was your statement.
A I would like to have that on the record too.
Q All right. It is in Doctor”
http://tobaccodocuments.org/rjr/503243231-3367.html?zoom=750&ocr_position=above_foramatted&start_page=91
According to Kitty Little
“Benzpyrene has never been shown to cause a lung cancer. This is most probably because it is oxidized before the necessary over-proliferation of cells is reached.
There seems to have been a peculiar reluctance to publish data on the oxidizing characteristics of 3:4 benzpyrene, although after the first draft of these notes was written, a peculiar statement appeared, unsupported by evidence, suggesting that it was an oxidation product that was the carcinogenic agent.”
http://legacy.library.ucsf.edu/action/document/page;jsessionid=1A622975CD35D2F66C01526368B52B33?tid=yth67a99&page=17
Which could be good news for those of us who are lovers of hot buttered toast and scorched red peppers.
Rose
Benzopyrene
Apparently in the days before the Clean Air Acts, city air was thick with it.
Testimony of Dr Hueper 1957
“They manipulated the evidence. Anyone who introduces a corrective factor in his calculations to make the evidence fit a preconceived idea, I do not feel that this is valid scientific evidence.
“Do you feel, in view of what you said, that the application of a corrective factor means a predetermined manipulation in this case?
A.In this case I could not say, no.
Q I want to get clear on that.You asked me to read on. I will do that. This appears on Page 435 of your May, 1957 article and reads;
“However, even this estimate is heavily biased by the arbitrary assumption that the benzpyrene content present allegedly in cigarette smoke was about 12 times as effective in eliciting cancers as benzpyrene demonstrated in atmospheric air.
Only when such a “corrective” coefficient is applied was it possible to obtain proportional correlations between the total exposure to benzpyrene from both cigarette smoking and air pollutants and the relative incidence rates of lung cancer found in the industrialized metropolitan Liverpool area, an intermediary urban-rural region, and the rural area of North Wales”
A That is right.
Q That was your statement.
A I would like to have that on the record too.
Q All right. It is in Doctor”
http://tobaccodocuments.org/rjr/503243231-3367.html?zoom=750&ocr_position=above_foramatted&start_page=91
According to Kitty Little
“Benzpyrene has never been shown to cause a lung cancer. This is most probably because it is oxidized before the necessary over-proliferation of cells is reached.
There seems to have been a peculiar reluctance to publish data on the oxidizing characteristics of 3:4 benzpyrene, although after the first draft of these notes was written, a peculiar statement appeared, unsupported by evidence, suggesting that it was an oxidation product that was the carcinogenic agent.”
http://legacy.library.ucsf.edu/action/document/page;jsessionid=1A622975CD35D2F66C01526368B52B33?tid=yth67a99&page=17
Which could be good news for those of us who are lovers of hot buttered toast and scorched red peppers.
Rose
Benzopyrene
Apparently in the days before the Clean Air Acts, city air was thick with it.
Testimony of Dr Hueper 1957
“They manipulated the evidence. Anyone who introduces a corrective factor in his calculations to make the evidence fit a preconceived idea, I do not feel that this is valid scientific evidence.
“Do you feel, in view of what you said, that the application of a corrective factor means a predetermined manipulation in this case?
A.In this case I could not say, no.
Q I want to get clear on that.You asked me to read on. I will do that. This appears on Page 435 of your May, 1957 article and reads;
“However, even this estimate is heavily biased by the arbitrary assumption that the benzpyrene content present allegedly in cigarette smoke was about 12 times as effective in eliciting cancers as benzpyrene demonstrated in atmospheric air.
Only when such a “corrective” coefficient is applied was it possible to obtain proportional correlations between the total exposure to benzpyrene from both cigarette smoking and air pollutants and the relative incidence rates of lung cancer found in the industrialized metropolitan Liverpool area, an intermediary urban-rural region, and the rural area of North Wales”
A That is right.
Q That was your statement.
A I would like to have that on the record too.
Q All right. It is in Doctor”
http://tobaccodocuments.org/rjr/503243231-3367.html?zoom=750&ocr_position=above_foramatted&start_page=91
According to Kitty Little
“Benzpyrene has never been shown to cause a lung cancer. This is most probably because it is oxidized before the necessary over-proliferation of cells is reached.
There seems to have been a peculiar reluctance to publish data on the oxidizing characteristics of 3:4 benzpyrene, although after the first draft of these notes was written, a peculiar statement appeared, unsupported by evidence, suggesting that it was an oxidation product that was the carcinogenic agent.”
http://legacy.library.ucsf.edu/action/document/page;jsessionid=1A622975CD35D2F66C01526368B52B33?tid=yth67a99&page=17
Which could be good news for those of us who are lovers of hot buttered toast and scorched red peppers.
Rose
Re: Burden of Proof/Either-Or
But Chris presented the case for the prosecution in the debate “Does Smoking Cause Lung Cancer”, so it is only right and proper for him (and others) to argue their corner.
I don’t think anyone has denies the strong statistical association between smoking and LC, so there is general acceptance that there is something that merits further (biological) investigation. Who would argue against this?
Surely any smoker wants to know, with a high degree of certainty, what the chances are of succumbing to a disease that was entirely due to smoking. But lung cancer doesn’t yet present any such certainty, so we need more research into why lung cancer is/was so predominant in smokers, not just bald assertions of “the debate is over” variety.
Chris is offering a very spirited set of arguments, and has done his research well, but he does have a tendency to fall back on rhetoric when responding to counter arguments. Eg:
…For the lung cancer epidemic to begin, you need to have a sizeable group of people who have been smoking for at least 20 years
Where is the a priori evidence for this, the physiological proof that lung cancer takes decades to develop in smokers? Furthermore, if it is indeed the case, what is happening within the smoker’s organs during that period that results in carcinogenesis in old age; and what research is being carried out into clinical interventions that could counteract this?
…“Recent decades have seen more smokers getting adenocarcinoma and … ‘light’ cigarettes allow (or require, even) the smoke to go deeper into the lungs. Old, unfiltered heavy cigarettes were not inhaled so deeply and so the tumour would form higher up the lung”
But this has got nothing to do with tumour position within the lungs. Adenocarcinoma and Squamous Cell Carcinoma are histologically different types of cancer. It was always easy to use this fact to ‘prove’ that smoking ’caused’ (squamous cell) lung cancer. The fact that the majority of smokers’ LCs are now also adenocarcinoma may be inconvenient for anti-tobacco, but it really does need a proper explanation.
My suspicion is that 50+ years ago smoking did make a strong biological contribution to the formation of lung tumours (maybe ’caused’, but more likely a more complex process involving other factors). Do remember that the vast majority of studies that still form the foundation of the causal hypothesis were carried out in the 1950s and 1960s, ie based on the peoples’ smoking habits in the 1940s/1950s and (if Chris is correct) back to the 20s and 30s. Chris cites the US Surgeon General’s report of 1964! Nobody is researching into whether smoking causes lung cancer any more. As AGW alarmists would say “the science is settled”. But is it?
There is little doubt (outside of anti-tobacco groupthink) that cigarettes have become immensely ‘safer’ since these studies were carried out. The use of filter tips, lower tar levels, changes in types of tobacco used and curing methods have resulted in huge reductions in measurable levels of known carcinogens. Also people are generally smoking much less than they did 50+ years ago. The 100 a day smoker is rare now – even 20 a day is deemed to be ‘heavy’ smoking. The improvements are such that the ‘safe’ level of smoking is round about 10 cigarettes per day (see Gio Batta Gori [*]).
So, given these changes, isn’t it feasible that there are actually very few new lung cancers that are ’caused’ by smoking (squamous cell) and since smokers now experience the same type (adenocarcinoma) as non-smokers (and seemingly at a similar rate), is smoking any longer the dominant factor in lung carcinogenesis?
You see, without new research we may be missing the fact that the battle against lung cancer is actually being won by making cigarettes safer, rather than by declaring war on smokers. If this is the case, then much blood is on the hands of the anti-tobacco lobby, who collectively forced the termination of all ‘safe cigarette’ development efforts, resulting in the unnecessary premature deaths of literally millions of smokers.
[*] I commend everyone to research the writings of Gio Gori.
A question, out of interest, for Chris, WS and JB.
Given the limitations of statistical information and given that the observed correlation (LC and smoking) is atypical of the smokers group, impartial investigators are very wary of the language they use, careful to not overstate/exaggerate the observed correlation.
Considering the official evidence (hopefully corrected for detection bias), if you were responsible for summarizing this information into a statement or few statements, how would you present this information to the public or those that smoke?
For example:
“Smoking is a known risk factor for LC”
“Smoking may cause LC”
“Smoking causes LC”
“Smoking may be a contributing factor to LC for some smokers”
Etc.
Etc.
Magnetic
A question, out of interest, for Chris, WS and JB.
Given the limitations of statistical information and given that the observed correlation (LC and smoking) is atypical of the smokers group, impartial investigators are very wary of the language they use, careful to not overstate/exaggerate the observed correlation.
Considering the official evidence (hopefully corrected for detection bias), if you were responsible for summarizing this information into a statement or few statements, how would you present this information to the public or those that smoke?
For example:
“Smoking is a known risk factor for LC”
“Smoking may cause LC”
“Smoking causes LC”
“Smoking may be a contributing factor to LC for some smokers”
Etc.
Etc.
Magnetic
Smokers stand a possible risk of LC at 8 per 10,000
while non-smokers stand a comparable risk of 6 per 10,000
from all known possibilities anyone may come into contact with
in a given environment.
Smokers stand a possible risk of LC at 8 per 10,000
while non-smokers stand a comparable risk of 6 per 10,000
from all known possibilities anyone may come into contact with
in a given environment.
Magnetic,
Obviously, people tend not to be very precise in the way they use language. There are many examples of this, especially in special interest driven campaigns (ex: “drinking and driving kills”, “poverty causes crime”, or one of my favorites from a couple of years ago: “driving an SUV promotes terrorism”.)
Personally, when I’m trying to articulate the point in question during a conversation on the topic, I usually say something like: “A lifelong smoker is ten times more likely to develop lung cancer than a non-smoker, but only about 10% of such smokers ever get lung cancer.” Even that doesn’t take all of the points into consideration, and it would never fit on a bumper sticker.
Short and sweet: “Longterm smoking dramatically increases one’s risk for lung cancer”. I’m hardly willing to defend it from criticism though.
-WS
Magnetic,
Obviously, people tend not to be very precise in the way they use language. There are many examples of this, especially in special interest driven campaigns (ex: “drinking and driving kills”, “poverty causes crime”, or one of my favorites from a couple of years ago: “driving an SUV promotes terrorism”.)
Personally, when I’m trying to articulate the point in question during a conversation on the topic, I usually say something like: “A lifelong smoker is ten times more likely to develop lung cancer than a non-smoker, but only about 10% of such smokers ever get lung cancer.” Even that doesn’t take all of the points into consideration, and it would never fit on a bumper sticker.
Short and sweet: “Longterm smoking dramatically increases one’s risk for lung cancer”. I’m hardly willing to defend it from criticism though.
-WS
A question, out of interest, for Chris, WS and JB.
Given the limitations of statistical information and given that the observed correlation (LC and smoking) is atypical of the smokers group, impartial investigators are very wary of the language they use, careful to not overstate/exaggerate the observed correlation.
Considering the official evidence (hopefully corrected for detection bias), if you were responsible for summarizing this information into a statement or few statements, how would you present this information to the public or those that smoke?
For example:
“Smoking is a known risk factor for LC”
“Smoking may cause LC”
“Smoking causes LC”
“Smoking may be a contributing factor to LC for some smokers”
Etc.
Etc.
Magnetic
Magnetic, I don’t know what is the accepted precise meaning of “causes”. That’s a question for a logician. For my personal practical purposes, I take “very large relative risk” and effect following cause to equate with “causes”. Small RR can be the result of confounding and biases. X a risk factor for Y just means an association. For example, eating your own veg make keep you healthy because of the exercise from digging, rather than better veg, but eating your own veg would be a risk factor for good health.
JB
Magnetic, I don’t know what is the accepted precise meaning of “causes”. That’s a question for a logician. For my personal practical purposes, I take “very large relative risk” and effect following cause to equate with “causes”. Small RR can be the result of confounding and biases. X a risk factor for Y just means an association. For example, eating your own veg make keep you healthy because of the exercise from digging, rather than better veg, but eating your own veg would be a risk factor for good health.
JB
Magnetic, I don’t know what is the accepted precise meaning of “causes”. That’s a question for a logician. For my personal practical purposes, I take “very large relative risk” and effect following cause to equate with “causes”. Small RR can be the result of confounding and biases. X a risk factor for Y just means an association. For example, eating your own veg make keep you healthy because of the exercise from digging, rather than better veg, but eating your own veg would be a risk factor for good health.
JB
If there existed a gang of nutters who killed everyone who wore a red hat, would wearing a red hat be the cause of death? I don’t know.
JB
If there existed a gang of nutters who killed everyone who wore a red hat, would wearing a red hat be the cause of death? I don’t know.
JB
Nah. It’d just be a risk factor.
Nah. It’d just be a risk factor.
If there existed a gang of nutters who killed everyone who wore a red hat, would wearing a red hat be the cause of death? I don’t know.
JB
Smokers stand a possible risk of LC at 8 per 10,000
while non-smokers stand a comparable risk of 6 per 10,000
from all known possibilities anyone may come into contact with
in a given environment.
It works just as well for tea, if you can do without the visual effect.
“Highest level of tea consumption in the UK was reached in 1957 when 255 million kg were retained for domestic use.”
http://www.historyofceylontea.com/Tea_Feature/tea_features_marketing.html
Society for Risk Analysis 1995
Dietary Contributions to Nicotine Body Burden
“Using the available data for nicotine in 10 brands of brewed tea (2 instant and 8 leaves) tea nicotine concentration is modeled as a lognormal distribution (with a mean of 68.9 ng of nicotine per gram of brewed tea and a standard deviation of 75 ng/g).”
http://www.riskworld.com/abstract/1995/SRAam95/ab5aa174.htm
The Other Prohibition :The cigarette crisis in post-war Germany
“Very popular were tea leaves rolled in toilette paper. These surrogates had neither the effect of nicotine nor the smell or taste of tobacco. They were smoked anyway. At least there was some warm smoke and the action of smoking.”
http://www.mega.nu:8080/ampp/drugtext/hess1.htm
SMOKING LAGS LOSE THEIR TEABAGS
“TEABAGS have been banned at a non-smoking jail after lags used them in cigarettes instead of brewing up.
Inmates at the Isle of Man Prison now have to make do with tea granules after dozens were caught puffing away on teabags in their cells.”
http://www.dailystar.co.uk/news/view/115266/Smoking-lags-lose-their-teabags/
Rose
It works just as well for tea, if you can do without the visual effect.
“Highest level of tea consumption in the UK was reached in 1957 when 255 million kg were retained for domestic use.”
http://www.historyofceylontea.com/Tea_Feature/tea_features_marketing.html
Society for Risk Analysis 1995
Dietary Contributions to Nicotine Body Burden
“Using the available data for nicotine in 10 brands of brewed tea (2 instant and 8 leaves) tea nicotine concentration is modeled as a lognormal distribution (with a mean of 68.9 ng of nicotine per gram of brewed tea and a standard deviation of 75 ng/g).”
http://www.riskworld.com/abstract/1995/SRAam95/ab5aa174.htm
The Other Prohibition :The cigarette crisis in post-war Germany
“Very popular were tea leaves rolled in toilette paper. These surrogates had neither the effect of nicotine nor the smell or taste of tobacco. They were smoked anyway. At least there was some warm smoke and the action of smoking.”
http://www.mega.nu:8080/ampp/drugtext/hess1.htm
SMOKING LAGS LOSE THEIR TEABAGS
“TEABAGS have been banned at a non-smoking jail after lags used them in cigarettes instead of brewing up.
Inmates at the Isle of Man Prison now have to make do with tea granules after dozens were caught puffing away on teabags in their cells.”
http://www.dailystar.co.uk/news/view/115266/Smoking-lags-lose-their-teabags/
Rose
It works just as well for tea, if you can do without the visual effect.
“Highest level of tea consumption in the UK was reached in 1957 when 255 million kg were retained for domestic use.”
http://www.historyofceylontea.com/Tea_Feature/tea_features_marketing.html
Society for Risk Analysis 1995
Dietary Contributions to Nicotine Body Burden
“Using the available data for nicotine in 10 brands of brewed tea (2 instant and 8 leaves) tea nicotine concentration is modeled as a lognormal distribution (with a mean of 68.9 ng of nicotine per gram of brewed tea and a standard deviation of 75 ng/g).”
http://www.riskworld.com/abstract/1995/SRAam95/ab5aa174.htm
The Other Prohibition :The cigarette crisis in post-war Germany
“Very popular were tea leaves rolled in toilette paper. These surrogates had neither the effect of nicotine nor the smell or taste of tobacco. They were smoked anyway. At least there was some warm smoke and the action of smoking.”
http://www.mega.nu:8080/ampp/drugtext/hess1.htm
SMOKING LAGS LOSE THEIR TEABAGS
“TEABAGS have been banned at a non-smoking jail after lags used them in cigarettes instead of brewing up.
Inmates at the Isle of Man Prison now have to make do with tea granules after dozens were caught puffing away on teabags in their cells.”
http://www.dailystar.co.uk/news/view/115266/Smoking-lags-lose-their-teabags/
Rose
Re: funny timing
K, I’ll wait then.
Nah. It’d just be a risk factor.
Doctors
Royal Army Medical Corps
“Mustard gas, first used in 1917, delayed any effect for up to 12 hours, and then began to rot the body from both within and without and a very painful death took from four to five weeks. Lachrimatory gasses caused blindness.
Gas hung around in sunken roads for weeks, and it was possible to be overcome merely by removing a patient’s clothing, so it was not only during an attack that one could become gassed”
http://www.ramc-ww1.com/chain_of_evacuation.php
“Survival after a mustard gas exposure is common, but note that Mustard agents are strong carcinogens. If the immediate mustard attack does not kill you it is highly likely that you develop lung cancer later in life.
Survivors also commonly cope with chronic asthma and/or bronchitis as well. ”
http://www.shu.edu/academics/artscibiol3341aa/EnvToxWeb/Spring%202005/mustard%20agents/mustard%201.htm
link no longer works.
Mustard Gas exposure and carcinogenesis of the lung – Iran
RESULTS: A relatively early age of lung cancer onset (ranging from 28 to 73 with a mean of 48) in mustard gas victims, particularly those in the non-smoking population (mean age of 40.7), may be an indication of a unique etiology for these cancers.
Seven of the 20 patients developed lung cancer before the age of 40.”
http://lib.bioinfo.pl/pmid:19559099
Rose
Re: The debate catch 4
Junican,
Ignoring confounders such as age, your example produces a relative risk of 16/4 = 4.
RR = (Probability of LC amongst those exposed)/(Probability of those not exposed) – see Wikipedia for more info or try plugging the numbers into Medcalc:
http://www.medcalc.be/calc/relative_risk.php
Use a=16, b=99984, c=4, d=99996 (no commas)
(b=100,000-16, d=100,000-4)
Of course a RR of 4 is a 300% increase.
Tony
JB,
I nitpicked Junican’s arithmetic on relative risk in a reply to his post and stand by what I said. However I very much agree that absolute risk is the key issue both for active and especially for ‘passive’ smoking.
I also take your point about ex-smokers being older which makes direct comparison of rates difficult.
On the whole I am more aligned with Frank and Rich on the central question. Sweden’s example is all very well but what about the high smoking low lung cancer Japanese?
Tony
MRFIT
Chris said:
[Rich] MRFIT was primarily a study into cholesterol and heart disease. I’m not aware that they stratified the results to show smoking and lung cancer but I’m happy to be corrected on it.
I’m afraid I can’t agree here. It seems they had some surprising results relating to smoking cessation and lung cancer as described here:
Abstract:
http://www.ncbi.nlm.nih.gov/pubmed/9099400
Full paper:
http://tobaccodocuments.org/pm/2060549906-9917.html
The trial ‘enrolled 12,866 men (including 8194 cigarette smokers) ‘.The intervention group had a higher rate of quitting compared to the control group but had a 17% higher rate of lung cancer (not statistically significant).
I’m not sure about MONICA though.
Tony
MRFIT
Chris said:
[Rich] MRFIT was primarily a study into cholesterol and heart disease. I’m not aware that they stratified the results to show smoking and lung cancer but I’m happy to be corrected on it.
I’m afraid I can’t agree here. It seems they had some surprising results relating to smoking cessation and lung cancer as described here:
Abstract:
http://www.ncbi.nlm.nih.gov/pubmed/9099400
Full paper:
http://tobaccodocuments.org/pm/2060549906-9917.html
The trial ‘enrolled 12,866 men (including 8194 cigarette smokers) ‘.The intervention group had a higher rate of quitting compared to the control group but had a 17% higher rate of lung cancer (not statistically significant).
I’m not sure about MONICA though.
Tony
Re: MRFIT
P.S.
I think Rich overstated the results of the MRFIT study when he said (CATCH-2):
Plus, in ‘interference’ studies like MRFIT and MONICA, those who continued smoking had less incidence of cancer, heart disease and overall mortality than the group who continued to [not] smoke.
I don’t think the authors actually found anything that strong. All they found was a lack of improvement despite the success in persuading intervention subjects to quit.
The whole remit of anti-smoking is in intervening to persuade people to quit. So what should have happened at this point was an abject apology from them and an end to their gravy train. Too many vested interests by that point to let a little thing like science get in the way though.
Tony
Re: MRFIT
Tony, apologies if you think i overstated anything, although I do disagree I did. An excerpt from my book on MRFIT follows:
In the 1970s a study was conducted to see the effects of smoking cessation along with other known healthy behaviours. To give credit to the researchers, they avoided the self-selection problem that skews results of epidemiological studies and the participants were chosen at random. The study group was called the Multiple Risk Factor Intervention Trial (MRFIT) Research Group.
The study consisted of 12,866 ‘high risk’ men, aged thirty-five to fifty-seven, who were randomly assigned to one of two groups. Group one was a special intervention (SI) program in which there was drug-care treatment for hypertension, counselling to help stop smoking, and dietary advice to lower blood cholesterol – this group will be known as the SI group. Group two, the control group, were left to their own devices regarding their lifestyle choices.
The MRFIT Research Group released its first report in 1982, with an average follow-up time of seven years. The results showed no statistically significant difference between the mortality in the SI group and the control group in spite of the SI group having adopted healthier lifestyles.
In 1990 the MRFIT released another report of ten and a half years worth of research with the same two groups. In this report, the SI group had a statistically significant reduction in coronary heart disease, however this was attributed to reduction in hypertension rather than smoking, as M. O. Kjelsberg, in the journal Circulation in 1990 stated:
Two factors appear to have contributed to this more favourable mortality trend for the SI Group: (1) a change in the diuretic protocol for SI men about 5 years after randomization, which involved replacement of [one blood pressure lowering drug with another]; and (2) a favourable effect of intervention on nonfatal cardiovascular events during the trial years. In addition, delay until the full impact of beneficial effects on mortality end points from smoking cessation and cholesterol lowering could have contributed.
In other words, the initial drugs were having, at best, no effect or, at worst, were killing the participants. By switching the drugs the participants had lower rates of CHD. The study found no evidence that smoking had any effect on CHD. Interestingly, there were more deaths from ischemic heart disease in the SI group than the control group, with the SI group having ninety-six deaths compared to eighty-six in the control group, and the SI group also had sixty-six deaths from cancer of the respiratory and intrathoracic organs compared to fifty-five in the control group.
The health establishment tried to explain away the discrepancies of the study, with one group of writers saying that the higher incidence of lung cancer in the SI group involved smokers or ex-smokers, and there were no primary lung cancer deaths among those who had never smoked. What must have slipped their mind was the fact that all the participants were chosen because they were deemed to be at high risk – there were no ‘never smokers’ in the group.
Re: MRFIT
Hi Rich,
Thanks for your reply. Is it just me or has your reply and several others elsewhere been hidden from the mainline comments and only appears as a link? Something amiss with livejournal perhaps?
Anyway I agree with what you wrote in your book but thought you overstated the case slightly in CATCH-2.
Looking at the full text of the paper, on page 3 (or page 127 of the journal) the authors conclude that:
“(ii) in the SI group, the rate of death from lung cancer for smokers who achieved sustained cessation was lower than the rate for those who continued to smoke, whereas in the UC group, the rate of death from lung cancer for smokers who sustained cessation was equivalent to or higher than the rate for those who continued to smoke;”
Tony
Re: MRFIT
So at best, we can average it out and find no difference in the real world. At least, that’s my opinion.
As for the links, don’t know how it usually works, but it appears it’s to minimise ‘clutter’ on the page.
Re: MRFIT
So at best, we can average it out and find no difference in the real world. At least, that’s my opinion.
As for the links, don’t know how it usually works, but it appears it’s to minimise ‘clutter’ on the page.
Re: MRFIT
Hi Rich,
Thanks for your reply. Is it just me or has your reply and several others elsewhere been hidden from the mainline comments and only appears as a link? Something amiss with livejournal perhaps?
Anyway I agree with what you wrote in your book but thought you overstated the case slightly in CATCH-2.
Looking at the full text of the paper, on page 3 (or page 127 of the journal) the authors conclude that:
“(ii) in the SI group, the rate of death from lung cancer for smokers who achieved sustained cessation was lower than the rate for those who continued to smoke, whereas in the UC group, the rate of death from lung cancer for smokers who sustained cessation was equivalent to or higher than the rate for those who continued to smoke;”
Tony
Re: MRFIT
Tony, apologies if you think i overstated anything, although I do disagree I did. An excerpt from my book on MRFIT follows:
In the 1970s a study was conducted to see the effects of smoking cessation along with other known healthy behaviours. To give credit to the researchers, they avoided the self-selection problem that skews results of epidemiological studies and the participants were chosen at random. The study group was called the Multiple Risk Factor Intervention Trial (MRFIT) Research Group.
The study consisted of 12,866 ‘high risk’ men, aged thirty-five to fifty-seven, who were randomly assigned to one of two groups. Group one was a special intervention (SI) program in which there was drug-care treatment for hypertension, counselling to help stop smoking, and dietary advice to lower blood cholesterol – this group will be known as the SI group. Group two, the control group, were left to their own devices regarding their lifestyle choices.
The MRFIT Research Group released its first report in 1982, with an average follow-up time of seven years. The results showed no statistically significant difference between the mortality in the SI group and the control group in spite of the SI group having adopted healthier lifestyles.
In 1990 the MRFIT released another report of ten and a half years worth of research with the same two groups. In this report, the SI group had a statistically significant reduction in coronary heart disease, however this was attributed to reduction in hypertension rather than smoking, as M. O. Kjelsberg, in the journal Circulation in 1990 stated:
Two factors appear to have contributed to this more favourable mortality trend for the SI Group: (1) a change in the diuretic protocol for SI men about 5 years after randomization, which involved replacement of [one blood pressure lowering drug with another]; and (2) a favourable effect of intervention on nonfatal cardiovascular events during the trial years. In addition, delay until the full impact of beneficial effects on mortality end points from smoking cessation and cholesterol lowering could have contributed.
In other words, the initial drugs were having, at best, no effect or, at worst, were killing the participants. By switching the drugs the participants had lower rates of CHD. The study found no evidence that smoking had any effect on CHD. Interestingly, there were more deaths from ischemic heart disease in the SI group than the control group, with the SI group having ninety-six deaths compared to eighty-six in the control group, and the SI group also had sixty-six deaths from cancer of the respiratory and intrathoracic organs compared to fifty-five in the control group.
The health establishment tried to explain away the discrepancies of the study, with one group of writers saying that the higher incidence of lung cancer in the SI group involved smokers or ex-smokers, and there were no primary lung cancer deaths among those who had never smoked. What must have slipped their mind was the fact that all the participants were chosen because they were deemed to be at high risk – there were no ‘never smokers’ in the group.
Re: MRFIT
P.S.
I think Rich overstated the results of the MRFIT study when he said (CATCH-2):
Plus, in ‘interference’ studies like MRFIT and MONICA, those who continued smoking had less incidence of cancer, heart disease and overall mortality than the group who continued to [not] smoke.
I don’t think the authors actually found anything that strong. All they found was a lack of improvement despite the success in persuading intervention subjects to quit.
The whole remit of anti-smoking is in intervening to persuade people to quit. So what should have happened at this point was an abject apology from them and an end to their gravy train. Too many vested interests by that point to let a little thing like science get in the way though.
Tony
MRFIT
Chris said:
[Rich] MRFIT was primarily a study into cholesterol and heart disease. I’m not aware that they stratified the results to show smoking and lung cancer but I’m happy to be corrected on it.
I’m afraid I can’t agree here. It seems they had some surprising results relating to smoking cessation and lung cancer as described here:
Abstract:
http://www.ncbi.nlm.nih.gov/pubmed/9099400
Full paper:
http://tobaccodocuments.org/pm/2060549906-9917.html
The trial ‘enrolled 12,866 men (including 8194 cigarette smokers) ‘.The intervention group had a higher rate of quitting compared to the control group but had a 17% higher rate of lung cancer (not statistically significant).
I’m not sure about MONICA though.
Tony
Re: MRFIT
P.S.
I think Rich overstated the results of the MRFIT study when he said (CATCH-2):
Plus, in ‘interference’ studies like MRFIT and MONICA, those who continued smoking had less incidence of cancer, heart disease and overall mortality than the group who continued to [not] smoke.
I don’t think the authors actually found anything that strong. All they found was a lack of improvement despite the success in persuading intervention subjects to quit.
The whole remit of anti-smoking is in intervening to persuade people to quit. So what should have happened at this point was an abject apology from them and an end to their gravy train. Too many vested interests by that point to let a little thing like science get in the way though.
Tony
RR and Age Adj
Thanks for that JB – very helpful.
question for Chris
Chris in your reply to Anon (which was me) you stated “Recent decades have seen more smokers getting adenocarcinoma and the reason you give in your comment is the most common explanation, ie. ‘light’ cigarettes allow (or require, even) the smoke to go deeper into the lungs. Old, unfiltered heavy cigarettes were not inhaled so deeply and so the tumour would form higher up the lung.”
In the Toronto study “Lung cancer risk in never-smokers: a population-based case-control study of epidemiologic risk factors” it states that 49% of the non smokers had adenocarcinoma whereas only 28% of the ever smoked did.
The actually number was 76/156 for non smokers and 80/289 for ever smoked. (It would have been interesting to see how the ever smoked broke down between current and former and remember the defination of ever smoked is more then 100 cigarettes in a life time ).
If as you state is true, that smokers are now getting adenocarcinoma from inhaling deeper, then why are there so many non smokers with adenocarcinoma? And for that matter, why is it assumed that the adenocarcinoma in ever smoked must be from smoking and not the same reason as non smokers?
question for Chris
Chris in your reply to Anon (which was me) you stated “Recent decades have seen more smokers getting adenocarcinoma and the reason you give in your comment is the most common explanation, ie. ‘light’ cigarettes allow (or require, even) the smoke to go deeper into the lungs. Old, unfiltered heavy cigarettes were not inhaled so deeply and so the tumour would form higher up the lung.”
In the Toronto study “Lung cancer risk in never-smokers: a population-based case-control study of epidemiologic risk factors” it states that 49% of the non smokers had adenocarcinoma whereas only 28% of the ever smoked did.
The actually number was 76/156 for non smokers and 80/289 for ever smoked. (It would have been interesting to see how the ever smoked broke down between current and former and remember the defination of ever smoked is more then 100 cigarettes in a life time ).
If as you state is true, that smokers are now getting adenocarcinoma from inhaling deeper, then why are there so many non smokers with adenocarcinoma? And for that matter, why is it assumed that the adenocarcinoma in ever smoked must be from smoking and not the same reason as non smokers?
Re: question for Chris
Can you give me the link for the study? It’s not clear if it was prospective or case-control.
Re: question for Chris
Can you give me the link for the study? It’s not clear if it was prospective or case-control.
question for Chris
Chris in your reply to Anon (which was me) you stated “Recent decades have seen more smokers getting adenocarcinoma and the reason you give in your comment is the most common explanation, ie. ‘light’ cigarettes allow (or require, even) the smoke to go deeper into the lungs. Old, unfiltered heavy cigarettes were not inhaled so deeply and so the tumour would form higher up the lung.”
In the Toronto study “Lung cancer risk in never-smokers: a population-based case-control study of epidemiologic risk factors” it states that 49% of the non smokers had adenocarcinoma whereas only 28% of the ever smoked did.
The actually number was 76/156 for non smokers and 80/289 for ever smoked. (It would have been interesting to see how the ever smoked broke down between current and former and remember the defination of ever smoked is more then 100 cigarettes in a life time ).
If as you state is true, that smokers are now getting adenocarcinoma from inhaling deeper, then why are there so many non smokers with adenocarcinoma? And for that matter, why is it assumed that the adenocarcinoma in ever smoked must be from smoking and not the same reason as non smokers?
Re: MRFIT
Tony, apologies if you think i overstated anything, although I do disagree I did. An excerpt from my book on MRFIT follows:
In the 1970s a study was conducted to see the effects of smoking cessation along with other known healthy behaviours. To give credit to the researchers, they avoided the self-selection problem that skews results of epidemiological studies and the participants were chosen at random. The study group was called the Multiple Risk Factor Intervention Trial (MRFIT) Research Group.
The study consisted of 12,866 ‘high risk’ men, aged thirty-five to fifty-seven, who were randomly assigned to one of two groups. Group one was a special intervention (SI) program in which there was drug-care treatment for hypertension, counselling to help stop smoking, and dietary advice to lower blood cholesterol – this group will be known as the SI group. Group two, the control group, were left to their own devices regarding their lifestyle choices.
The MRFIT Research Group released its first report in 1982, with an average follow-up time of seven years. The results showed no statistically significant difference between the mortality in the SI group and the control group in spite of the SI group having adopted healthier lifestyles.
In 1990 the MRFIT released another report of ten and a half years worth of research with the same two groups. In this report, the SI group had a statistically significant reduction in coronary heart disease, however this was attributed to reduction in hypertension rather than smoking, as M. O. Kjelsberg, in the journal Circulation in 1990 stated:
Two factors appear to have contributed to this more favourable mortality trend for the SI Group: (1) a change in the diuretic protocol for SI men about 5 years after randomization, which involved replacement of [one blood pressure lowering drug with another]; and (2) a favourable effect of intervention on nonfatal cardiovascular events during the trial years. In addition, delay until the full impact of beneficial effects on mortality end points from smoking cessation and cholesterol lowering could have contributed.
In other words, the initial drugs were having, at best, no effect or, at worst, were killing the participants. By switching the drugs the participants had lower rates of CHD. The study found no evidence that smoking had any effect on CHD. Interestingly, there were more deaths from ischemic heart disease in the SI group than the control group, with the SI group having ninety-six deaths compared to eighty-six in the control group, and the SI group also had sixty-six deaths from cancer of the respiratory and intrathoracic organs compared to fifty-five in the control group.
The health establishment tried to explain away the discrepancies of the study, with one group of writers saying that the higher incidence of lung cancer in the SI group involved smokers or ex-smokers, and there were no primary lung cancer deaths among those who had never smoked. What must have slipped their mind was the fact that all the participants were chosen because they were deemed to be at high risk – there were no ‘never smokers’ in the group.
Re: Chuckles
Chuckles, regarding your first paragraph, I don’t see how I implied in any way that a moral equation should be inserted. You should know me better than that, anyway, from our many previous shared threads/discussions.
Other than that, effects have causes and vice versa. I don’t think that simply chalking the matters being discussed up to aging is going to be entirely sufficient.
-WS
Re: Burden of Proof/Either-Or
“I don’t think anyone has denies the strong statistical association between smoking and LC, so there is general acceptance that there is something that merits further (biological) investigation. Who would argue against this?”
No one who is being reasonable. I don’t think I did.
“Surely any smoker wants to know, with a high degree of certainty, what the chances are of succumbing to a disease that was entirely due to smoking. But lung cancer doesn’t yet present any such certainty, so we need more research into why lung cancer is/was so predominant in smokers, not just bald assertions of “the debate is over” variety.”
It certainly wasn’t my intent to imply that “the debate is over” (though I’m not sure if that was directed at my comments or simply the prevailing arrogance of tobacco control. No worries, either way.) Rather, my point is that absence of evidence is not evidence of absence. On one side you have a 10 fold statistical correlation, and on the other you have a hypotheis of, let’s say, HPV is the true culprit when it comes to lung cancer. I’m not suggesting that an alternative theory like the latter should be dismissed. To the contrary, I believe it should be investigated. Nonetheless, the burden of proof is then to prove the latter. There’s no need to re-establish the statistical correlation, because it seems to me that it’s a settled matter.
“But Chris presented the case for the prosecution in the debate “Does Smoking Cause Lung Cancer”, so it is only right and proper for him (and others) to argue their corner.”
Of course. But there shouldn’t be a false expectation that Chris, or anyone, is going to be able to bat down every proposed alternative hypothesis. Exploring these ideas is interesting and worthwhile, but nothing I’ve ever seen proposed amounts to better proof than the strong statistical correlation. Also, there shouldn’t be a false expectation that Chris or anyone is going to be able to “prove” that “smoking causes lung cancer” because, as Chris noted, epidemiology simply can not do that.
Otherwise, I fully agree that more emphasis should be given to inquiry regarding the specific, biological, causative mechanisms involved in lung cancer. Unfortunately, because public health is a collective, government enterprise, it emphasizes broad brush cure-alls like anti-smoking at the expense of seeking out (and providing access to) more useful and specific information.
-WS
Magnetic,
Obviously, people tend not to be very precise in the way they use language. There are many examples of this, especially in special interest driven campaigns (ex: “drinking and driving kills”, “poverty causes crime”, or one of my favorites from a couple of years ago: “driving an SUV promotes terrorism”.)
Personally, when I’m trying to articulate the point in question during a conversation on the topic, I usually say something like: “A lifelong smoker is ten times more likely to develop lung cancer than a non-smoker, but only about 10% of such smokers ever get lung cancer.” Even that doesn’t take all of the points into consideration, and it would never fit on a bumper sticker.
Short and sweet: “Longterm smoking dramatically increases one’s risk for lung cancer”. I’m hardly willing to defend it from criticism though.
-WS
The smoking/lung cancer theory
Since I’m neither an epidemiologist nor a statistician, I feel I may be out of my league in this debate. But, since there is such a plethora of expertise available here, It may be an excellent time to ask a few questions.
First, most of these older studies focused on smoking as the major cause of LC while ignoring all other risk factors. But, if this same procedure were to be applied to other possible risk factors, aging for example, then similar very high risks could be attributed to the aging process.
For example, StatCan mortality data show that LC death rates are 9 times higher among those 70 to 74 than those between 50 and 54. And someone between 80 and 84 is 13 times more likely to die of LC than those 50 to 54. And, although the smoking/LC studies explain this disparity, by claiming a dose response relationship among smokers, with LC risk increasing with the amount smoked and duration of smoking, that doesn’t explain the age disparity among the roughly 20% of LC cases which are not attributed to smoking.
Question. Has this age differential ever been explained in the non-smokers who develop lung cancer?
Question. Has anyone ever established LC rates among non-smokers independent of these smoking/LC studies?
The increase in the incidence of LC is generally believed to have begun around 1900, and first became noticeable after 1930. But, in 1900, average life expectancy at birth was only 47(for males) and, the percentage of the population over the age of 65 was quite small at roughly 5%. By 1944, (my birth year) average life expectancy at birth was 64, and the percentage of the population over the age of 65, the age at which the majority (roughly 72% in Canada) of LC cases occur, had also increased significantly.
Question: Is it possible that the apparent increase in LC cases since 1900 could have been the result of improvements in medical science which led to significant increases in life expectancy and the proportion of the population living well past 65? Has anyone bothered to find out?
If these studies, conducted mainly in the fifties and sixties, were intended to find the cause(s) of cancer, why was the comparison limited to smokers and non-smokers. Wouldn’t the more appropriate study have been to investigate what was different between the non-smokers and smokers who developed LC and those who didn’t?
Question. Since the studies of the LC/smoking link concentrated on the different rates of LC among smokers and non-smokers, isn’t this, in itself, indicative of bias, intentional or not?
Question. Has anyone ever bothered to do a study which showed why some smokers (roughly 1 in 10) develop lung cancer, while the other 90% do not? And, if not, why not? Wouldn’t a failure to do a follow-up study also suggest bias in favour of the smoking/LC theory?
And, finally, Health Canada SAM data claims that almost 80% of LC deaths are attributable to smoking. But, looking closely, it can be seen that those smoking related deaths are among both smokers and former smokers who comprise roughly 70% of the population over the age of 15.
Question. Why aren’t the extremely high risk factors apparently found in these studies reflected in actual mortality data.
The Old Rambler
The smoking/lung cancer theory
Since I’m neither an epidemiologist nor a statistician, I feel I may be out of my league in this debate. But, since there is such a plethora of expertise available here, It may be an excellent time to ask a few questions.
First, most of these older studies focused on smoking as the major cause of LC while ignoring all other risk factors. But, if this same procedure were to be applied to other possible risk factors, aging for example, then similar very high risks could be attributed to the aging process.
For example, StatCan mortality data show that LC death rates are 9 times higher among those 70 to 74 than those between 50 and 54. And someone between 80 and 84 is 13 times more likely to die of LC than those 50 to 54. And, although the smoking/LC studies explain this disparity, by claiming a dose response relationship among smokers, with LC risk increasing with the amount smoked and duration of smoking, that doesn’t explain the age disparity among the roughly 20% of LC cases which are not attributed to smoking.
Question. Has this age differential ever been explained in the non-smokers who develop lung cancer?
Question. Has anyone ever established LC rates among non-smokers independent of these smoking/LC studies?
The increase in the incidence of LC is generally believed to have begun around 1900, and first became noticeable after 1930. But, in 1900, average life expectancy at birth was only 47(for males) and, the percentage of the population over the age of 65 was quite small at roughly 5%. By 1944, (my birth year) average life expectancy at birth was 64, and the percentage of the population over the age of 65, the age at which the majority (roughly 72% in Canada) of LC cases occur, had also increased significantly.
Question: Is it possible that the apparent increase in LC cases since 1900 could have been the result of improvements in medical science which led to significant increases in life expectancy and the proportion of the population living well past 65? Has anyone bothered to find out?
If these studies, conducted mainly in the fifties and sixties, were intended to find the cause(s) of cancer, why was the comparison limited to smokers and non-smokers. Wouldn’t the more appropriate study have been to investigate what was different between the non-smokers and smokers who developed LC and those who didn’t?
Question. Since the studies of the LC/smoking link concentrated on the different rates of LC among smokers and non-smokers, isn’t this, in itself, indicative of bias, intentional or not?
Question. Has anyone ever bothered to do a study which showed why some smokers (roughly 1 in 10) develop lung cancer, while the other 90% do not? And, if not, why not? Wouldn’t a failure to do a follow-up study also suggest bias in favour of the smoking/LC theory?
And, finally, Health Canada SAM data claims that almost 80% of LC deaths are attributable to smoking. But, looking closely, it can be seen that those smoking related deaths are among both smokers and former smokers who comprise roughly 70% of the population over the age of 15.
Question. Why aren’t the extremely high risk factors apparently found in these studies reflected in actual mortality data.
The Old Rambler
The smoking/lung cancer theory
Since I’m neither an epidemiologist nor a statistician, I feel I may be out of my league in this debate. But, since there is such a plethora of expertise available here, It may be an excellent time to ask a few questions.
First, most of these older studies focused on smoking as the major cause of LC while ignoring all other risk factors. But, if this same procedure were to be applied to other possible risk factors, aging for example, then similar very high risks could be attributed to the aging process.
For example, StatCan mortality data show that LC death rates are 9 times higher among those 70 to 74 than those between 50 and 54. And someone between 80 and 84 is 13 times more likely to die of LC than those 50 to 54. And, although the smoking/LC studies explain this disparity, by claiming a dose response relationship among smokers, with LC risk increasing with the amount smoked and duration of smoking, that doesn’t explain the age disparity among the roughly 20% of LC cases which are not attributed to smoking.
Question. Has this age differential ever been explained in the non-smokers who develop lung cancer?
Question. Has anyone ever established LC rates among non-smokers independent of these smoking/LC studies?
The increase in the incidence of LC is generally believed to have begun around 1900, and first became noticeable after 1930. But, in 1900, average life expectancy at birth was only 47(for males) and, the percentage of the population over the age of 65 was quite small at roughly 5%. By 1944, (my birth year) average life expectancy at birth was 64, and the percentage of the population over the age of 65, the age at which the majority (roughly 72% in Canada) of LC cases occur, had also increased significantly.
Question: Is it possible that the apparent increase in LC cases since 1900 could have been the result of improvements in medical science which led to significant increases in life expectancy and the proportion of the population living well past 65? Has anyone bothered to find out?
If these studies, conducted mainly in the fifties and sixties, were intended to find the cause(s) of cancer, why was the comparison limited to smokers and non-smokers. Wouldn’t the more appropriate study have been to investigate what was different between the non-smokers and smokers who developed LC and those who didn’t?
Question. Since the studies of the LC/smoking link concentrated on the different rates of LC among smokers and non-smokers, isn’t this, in itself, indicative of bias, intentional or not?
Question. Has anyone ever bothered to do a study which showed why some smokers (roughly 1 in 10) develop lung cancer, while the other 90% do not? And, if not, why not? Wouldn’t a failure to do a follow-up study also suggest bias in favour of the smoking/LC theory?
And, finally, Health Canada SAM data claims that almost 80% of LC deaths are attributable to smoking. But, looking closely, it can be seen that those smoking related deaths are among both smokers and former smokers who comprise roughly 70% of the population over the age of 15.
Question. Why aren’t the extremely high risk factors apparently found in these studies reflected in actual mortality data.
The Old Rambler
Re: Smoking prevalence in 1947
This estimate has male smoking prevelence in 1950
at ~83% (Females 40%) for ages 35-59 in the UK.
Click to access beijing_peto.pdf
Re: Smoking prevalence in 1947
This estimate has male smoking prevelence in 1950
at ~83% (Females 40%) for ages 35-59 in the UK.
Click to access beijing_peto.pdf
Re: Smoking prevalence in 1947
This estimate has male smoking prevelence in 1950
at ~83% (Females 40%) for ages 35-59 in the UK.
Click to access beijing_peto.pdf
Re: question for Chris
Can you give me the link for the study? It’s not clear if it was prospective or case-control.
Re: MRFIT
Hi Rich,
Thanks for your reply. Is it just me or has your reply and several others elsewhere been hidden from the mainline comments and only appears as a link? Something amiss with livejournal perhaps?
Anyway I agree with what you wrote in your book but thought you overstated the case slightly in CATCH-2.
Looking at the full text of the paper, on page 3 (or page 127 of the journal) the authors conclude that:
“(ii) in the SI group, the rate of death from lung cancer for smokers who achieved sustained cessation was lower than the rate for those who continued to smoke, whereas in the UC group, the rate of death from lung cancer for smokers who sustained cessation was equivalent to or higher than the rate for those who continued to smoke;”
Tony
Re: MRFIT
So at best, we can average it out and find no difference in the real world. At least, that’s my opinion.
As for the links, don’t know how it usually works, but it appears it’s to minimise ‘clutter’ on the page.
As mentioned elsewhere in 2012:
… Chris Snowdon’s words in the paragraph “Animal Studies” above, about the Auerbach-Hammond beagle experiment are not the whole truth – even though that was what The American Cancer Society said in their press conference about the study in February 1970.
However later developments in the 70’s and 80’s show that the beagle-study’s findings were eventually rejected by everyone in the smoking / health field, even by the Surgeon General.
A deposition from 2001 casts light over the controversy surrounding the Auerbach-Hammond beagle study. Please see pages 3411 to 3439:
Title: Deposition of JAMES D. MOLD, Ph.D., October 4, 2001, In Re: TOBACCO LITIGATION (MEDICAL MONITORING CASES) [BLANKENSHIP]
Date: 2001 October 04
https://www.industrydocumentslibrary.ucsf.edu/tobacco/docs/#id=yfll0001