Log in

No account? Create an account


Frank Davis

Banging on about the Smoking Ban

Previous Entry Share Next Entry
Richard White, author of Smoke Screens, replies point by point to Chris Snowdon (CATCH-1).

The Case for the Defence.

The points raised by Hill are all valid, but that doesn't necessarily mean the smoking studies are valid.

1. Strength: Hill gave the example of chimney sweeps and scrotal cancer which found a relative risk (RR) of 200 (ie. they were 200 times more likely to get this rare disease). Such a relative risk was so large that it required no epidemiological study. It was observable to the naked eye, as it were—as obvious as finding the association between mining and coughing, or being a woman and enjoying Sex in the City. The lung cancer-smoking link (from hereafter "the smoking theory" just to wind up any ASH supporters) is not quite as large as that—hardly any are—but it is generally in the region of 5 to 20, always greater than 2 to 3 and sometimes as high as 50. By any standard, this is a strong association.

'Association' is a linguist's nightmare, because it proves nothing. Any study can show that, for instance, air intake is 'associated' with lung cancer - or impotence, acne, the flu, bad breath, baldness etc etc, because we all breathe air and so any ailment we have will have a 100% association with breathing. It's only through common sense we know it's not actual causative (except in some cases of course, I am talking about 'everything'). Strength is only as valid as the study, and even if the most rigorous epidemiological study was conducted on smoking (which Doll's certainly weren't), it would prove nothing. First and foremost, any epidemiologist will admit epidemiology cannot identify causes or 'prove' something, only offer a link for further analysis. In this case, that was done in animal studies. To this day, scientists have not managed to induce lung cancer in any animal through tobacco smoke (excluding the F334 rats and A/J mice, specially bred to develop cancer). What the animal studies routinely do is embarrass researchers by having the animals outlive the non-smoking ones, and in the case of the F334 and A/Js, not only did they outlive the non-smoking ones, those exposed to smoke exceeded the total life expectancy of those breeds, and suffered less cancer than would be expected in them.

As a last point on strength and my point it is only as strong as it is valid, the crucial point is that smoking has never been singled out as a factor, it has always been examined just as lifestyle. It's unscientific to look at a group of smoking dock workers and compare them to non-smoking millionaires, for example. 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. Merely noticing they smoke is a moot point. Thus, it tends to rest on animal studies, which, as admitted in the Minnesota vs Tobacco 1997 court case, have all failed.

Doll's own work was hideously flawed. The hospital one looked only at inner-city patients for instance, and took no note of their lifestyles, diets and so forth. And it would be so easy to find a correlation of smoking with disease because smoking rates were so incredibly high. We also know that he not only found smokers were more likely to get lung cancer, but he also found that inhalers suffered less lung cancer than non-inhalers, with the same degree of statistical significance. Doll decided to omit the question in further research, which surely highlights his lack of objectivity. The real testament is surely that lung cancer increased as smoking rates decreased, and is now increasing more in non-smokers than smokers. Perhaps that is because the real reason(s) for lung cancer was overlooked when the smoking rates were so high?

2. Consistency: As Hill said: "Has it been repeatedly observed by different persons, in different places, circumstances and times?" Clearly the answer is yes. The smoking theory has been demonstrated again and again all over the world since the 1930s.

True enough, but that's not the end of the matter because, as mentioned above, smoking has yet to be analysed as a standalone factor. 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.

3. Specificity: In other words, does the disease only affect the exposed group? The fact that there is no malaria without mosquitoes supports the theory that mosquitoes spread malaria. Asbestosis is entirely specific to people who have been exposed to asbestos. Is there the same specificity with smoking and lung cancer? The answer is no. People developed lung cancer before smoking arrived in Europe and nonsmokers still get lung cancer in reasonably large numbers. Other factors are involved—other forms of smoke, radon and several other risk factors. But, as Hill said, people can get scrotal cancer without being chimney sweeps. He continued: "If other causes of death are raised 10, 20 or even 50% in smokers whereas cancer of the lung is raised 900 – 1000% we have specificity – a specificity in the magnitude of the association."

But it's only recently that smoking levels have decreased to a point that it can all be more accurately analysed. for some reason we always seem to just look at the 1930s onwards, but people have been smoking for millennia. Humans evolved in smoke-filled huts, by open-fires, tobacco-filled rooms. Tobacco has been used medicinally for thousands of years, and people have smoked for thousands of years. Only in the 1930s did we see a surge in lung cancer rates. To me, that's very non-specific of tobacco being a causative agent and we need to look at what else happened in that time - how about the introduction of diesel? The Great Fire? Smog? Testing of the atom bomb? Also indicative of it being innocent as a causative agent is the fact that the Semai people start smoking aged 2, and in a study conducted in the 1970s, of over 12,000 participants not a single case of lung cancer was found.

4. Temporality: In other words, cause and effect. Does smoking cause lung cancer or do smokers happen to be people who put themselves at risk of lung cancer more than nonsmokers. This is a valid question that less scrupulous epidemiologists fail to ask. We know today that smokers are more likely to be in lower socio-economic groups. This is a major confounding factor. The fact that lower socio-economic groups are also more likely to end up in prison and are more likely to have a baby die in the first 12 months of life does not prevent junk scientists claiming that secondhand smoke "causes" criminality or cot death. But these associations are very weak whereas the smoking theory is strong. If there was a more significant risk factor for lung cancer that it associated with smoking, but is not smoking, we need to hear what it is. The suggestions put forward—such as vehicle exhaust, asbestos exposure or pollution—are not specific enough to smokers to explain the statistical association between smoking and lung cancer.

Doll himself acknowledged that the consumption of vitamin E, through proper diet, could offset (or drastically lower) the risk of lung cancer from smoking. In fact, diet has consistently been shown to have a massive effect on the risk of lung cancer.

5. Biological gradient: Does the risk rise with the number of cigarettes smoked or the number of years of smoking. With a very good degree of consistency, studies have shown the answer to be yes.

Indeed they have, but again, smoking wasn't isolated. If people smoke through stress, as we know some do, how do we know the stress wasn't what caused the disease, which we know it can do? In such instances, smoking is a 'symptom', but not the problem. We're jumping the gun by assuming the visual factor is the causative agent.

6. Plausibility: Is it plausible that filling the lungs with smoke over a hundred times a day could damage them? I would say so. If not that, then what? Sometimes I hear smokers' rights people disputing the smoking theory while blaming car exhaust fumes. This seems to me to be inconsistent. Either breathing fumes, toxins and carcinogens into the lungs is dangerous or it is not. There is almost certainly a threshold below which the human body can filter and tolerate these fumes (which makes passive smoking and multiple chemical sensitivity less plausible as serious risks), but directly breathing smoke in must be well above that.

The quantities of the chemicals and toxins are tiny, less than we inhale in normal air. It's a plausible premise, yes, but one would assume that forcing an animal with smaller lungs than us, more susceptible to cancer than us, with a lower life expectancy than us, to smoke as much as most humans would quite adequately demonstrate the toxicity. The problem is, though, that it never has!

7. Coherence: Does it fit the overall pattern? Again, yes. The lung cancer rate rose first amongst men because they were the first to smoke and it rose later amongst women when they started to smoke. It is highest in regions and countries where people smoke and lowest where they do not. In Sweden, the use of snus has led to Europe's lowest smoking rate and also the lowest lung cancer rate. Is there a more plausible explanation for this than that smoking causes lung cancer?

I disagree entirely. Women in Europe began smoking somewhat later as a general rule (although there were plenty of female smokers prior to the 1930s, as shown in polls from the times), there is ample documentation of female pipe smokers going back hundreds of years. And, as said before, people have been smoking for millennia. We must overcome this hang-up that smoking is a recent activity. As for countries, that's entirely false. Actually the countries with the highest smoking rates tend to have the lowest lung cancer rates and vice versa. Greece, Japan, China and hungary demonstrate this, while America the opposite (low rate of smoking, comparatively high rate of lung cancer). I devoted a whole sub-chapter to World Data in my book, I can provide excerpts if required.

8. Experiment: This is the most difficult aspect of the smoking theory since lung cancer takes decades to develop and is therefore difficult to demonstrate in a laboratory experiment. Scientists have successfully made animals develop lung cancer by forcing them to smoke, and they have done the same by painting cigarette tar on mice. Does this prove the smoking theory? Not necessarily. The defence will say that the doses are unrealistically high. I have some sympathy with that view, but it certainly does not disprove the theory.

Already dealt with this above.
Tags: ,

Mark Wadsworth said

So I shall sign on as Mark Wadsworth and try again...

You are tilting at the wrong windmill. Smoking is bad for your physical health, there is no denying that.

But that is not the point. The point is that for a lot of people (me included) smoking is good for your mental health. So the choice is: a long miserable life or a shorter happy life. I chose the latter.

Of course there is no such thing as negative health impact of second hand smoking etc.

Re: Mark Wadsworth said

Mark, I deleted your original message (I couldn't edit it). I hope it reads correctly now.

Is smoking bad for your physical health? I've been smoking for 40 years, and have suffered no major health upsets during that time.

However these days I cough a lot more than I used to - something that I put down to the fact that since the smoking ban I've been so angry that I've actually smoked more.

I'm not particularly physically fit, but at my age I don't expect to be able to run a mile anyway. And wouldn't want to if I could.


Re: Mark Wadsworth said (Anonymous) Expand

To add to the Debate

I realize this is old but I think that might be a plus

Ann W.

* Bias in the Attribution of Lung Cancer as Cause of Death and Its Possible Consequences for Calculating Smoking-Related Risks
* Theodor D. Sterling, Wilfred L. Rosenbaum and James J. Weinkam
* Epidemiology
Vol. 3, No. 1 (Jan., 1992), pp. 11-16
(article consists of 6 pages)
* Published by: Lippincott Williams & Wilkins
* Stable URL: http://www.jstor.org/stable/3702931

Most published calculations of mortality risk, especially those for lung cancer associated with smoking, are based almost exclusively on the underlying cause as recorded on death certificates. Such risk calculations implicitly assume that the conditional probability of recording lung cancer as the underlying cause of death, given that it really is the underlying cause, is the same for all exposure groups. If these probabilities are not equal for all exposure groups, we call the resulting bias a cause of death attribution bias. We analyzed the 1986 National Mortality Followback Survey, a sample of 18,733 U.S. death certificates, and the 1954-1962 Dorn study, a follow-up study of approximately 250,000 holders of U.S. Veterans Life Insurance. Both data sets include information on the smoking habits of decedents and on the underlying and contributing causes of their deaths. We found that lung cancer as an underlying cause is recorded with a much smaller relative frequency if the decedent is known to be a never-smoker and with a much larger relative frequency when the decedent is known to be a smoker. On the other hand, lung cancer as a contributing cause is recorded with a much larger frequency if the decedent is known to be a never-smoker and with a much smaller frequency when the decedent is known to be a smoker. The reverse is true for cancers other than of the lung. There is no similar pattern related to smoking for other causes of death (specifically for myocardial infarction, other chronic ischemic heart disease, diabetes, or cerebrovascular disease). This pattern provides evidence of a possible bias because knowledge of a decedent's smoking status appears to influence the designation of lung cancer or some other cancer as the underlying cause or a contributing cause of death. This bias is especially strong when the choice of possible underlying causes of death is limited to one of a number of cancers. Insofar as calculations of lung cancer risk utilize exclusively recorded underlying causes, the observed attribution bias must result in an overestimate of the lung cancer mortality rate for smokers.


"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 smoke."

Can you clarify this please?

Ray Johnstone's The Scientific Scandal of AntiSmoking has a little about it:

Over the next decade the results of other similar trials appeared. It had been argued that if an improvement in one life-style factor, smoking, were of benefit, then an improvement in several - eg smoking, diet and exercise - should produce even clearer benefits. And so appeared the results of the whimsically acronymed Multiple Risk Factor Intervention Trial or MRFIT, with its 12,886 American subjects. Similarly, in Europe 60,881 subjects in four countries took part in the WHO Collaborative Trial. In Sweden the Goteborg study had 30,022 subjects. These were enormously expensive, wide-spread and time-consuming experiments. In all, there were 6 such trials with a total of over a hundred thousand subjects each engaged for an average of 7.4 years, a grand total of nearly 800,000 subject-years. The results of all were uniform, forthright and unequivocal: giving up smoking, even when fortified by improved diet and exercise, produced no increase in life expectancy. Nor was there any change in the death rate for heart disease or for cancer. A decade of expensive and protracted research had produced a quite unexpected result.

Re: Clarification (Anonymous) Expand
Really interesting stuff! I was unaware of the animal studies or of the studies above.

Great idea Frank! Looking forward to the responses.

Mr A

Hi Rich,
A question for you. You write that ''for some reason we always seem to just look at the 1930s onwards, but people have been smoking for millennia. Humans evolved in smoke-filled huts, by open-fires, tobacco-filled rooms.''

Some say that what we now identify as lung cancer was diagnosed as tuberculosis in those years. And tuberculosis was quite common in those years. What are your views on this?


Absolutely true. Here is an excerpt from Smoke Screens on this issue:

Indeed, we even know how diagnosis improved and why it was the 1930s specifically that showed more lung cancer cases: mass miniature radiography. This was developed in 1935 and started to be used in Britain in 1936 to screen for tuberculosis; lorries would arrive at school playgrounds or specific areas within a town, such as a car park, factory yard, or local public health clinic, for people to get screened. Naturally, the people most likely to get screened were those with a cough as that was the most obvious sign of tuberculosis. As one may expect, lung cancer and tuberculosis look entirely different on an x-ray, and the new diagnostic method allowed doctors to not only make a clear distinction between the diseases, but also find numerous new cases of lung cancer that would have previously been overlooked. The scale of this new diagnostic technique cannot be understated. School children had no choice but to be tested; a van would arrive and the pupils would be taken out by class to be x-rayed. For the rest of the population, posters were put up across the country saying where the van would be and when. The fear of tuberculosis was similar to the fear of cancer today; people were scared they would be stricken by the disease and would therefore endeavour to get checked. As previously mentioned, the most obvious symptom of tuberculosis is a dry cough, and the same is true for lung cancer. As such, it was very easy for misdiagnosis to occur prior to mass miniature radiography, and it is similarly clear to see why a sudden surge in lung cancer rates occurred in the 1930s. This decade saw not only a new diagnostic tool, but it being used with extreme efficiency. Prior to this time, diagnosis would have taken place through educated opinion and a doctor using his knowledge of the diseases to make a diagnostic decision. However, with tuberculosis and lung cancer having such similar symptoms, and the former being so prominent in people’s minds, it stands to reason that doctors would typically overlook lung cancer. With the advent of mass miniature radiography, such misdiagnosis would have been largely avoided. Furthermore, with the screening van or lorry being so prominent and easily accessible – a conscious decision by the authorities – an increased number of people would have been checked, either compulsorily or voluntarily through fear or increased education. An increase in numbers alone would account for higher cases of both diseases, but the newly-available tool allowed, for the first time ever, a solid way of differentiating victims of tuberculosis and lung cancer.

Below is a graph showing the respective figures for the diseases; you can see the linear pattern of cancer increasing as TB and influenza decreased

Year Tuberculosis Cancer Influenza, pneumonia
1970 2.6 162.8 30.9
1960 6.1 149.2 37.3
1950 22.5 139.8 31.3
1940 45.9 120.3 70.3
1930 71.1 97.4 102.5
1920 113.1 83.4 207.3
1910 153.8 76.2 155.9
1900 194.4 64.0 202.2

Re: Rampant Antismoking Signifies Grave Danger (p.31-33)

One critical problem is that the raw data (i.e., specific-cause mortality) used in studies of lung cancer is not particularly reliable. There is the issue of detection error which can be considerable. And, concerning lung cancer specifically, there is the issue of detection bias. 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.” There is a definite bias in the medical establishment to diagnose lung cancer in smokers and particularly in heavy smokers.

Unfortunately, there are few of these sorts of studies and they tend to be older studies. Antismokers never refer to these issues – for obvious reasons.

So, when we hear of RR’s of 10.0 or more for lung cancer in smokers compared to non-smokers, these are uncorrected for detection error and bias. Using two of the largest studies on lung cancer, the lung cancer rate amongst heavy smokers was 9-15% (average 12%) and for nonsmokers, ~1-2%. Using a correction of just 2% for detection bias (and it’s probably considerably more than that, given the absolutist antismoking stance of the medical establishment) would yield a lung-cancer rate of 10% among smokers and 3-4% among nonsmokers. This would result in an RR of around ~3.00 rather than ~12.0. The lung cancer rate amongst smokers above a baseline would be 7%. Again, I would suggest that the correction for bias should be even greater. (I would also suggest that there is an amount of detection bias concerning lung cancer diagnosis in nonsmokers, with a higher likelihood of LC diagnosed in nonsmokers known to have been exposed to SHS). A predictive strength of 7% does not justify an attribution of “cause”. It is simply far too low. It must be remembered that 90%+ of lifelong heavy smokers (above a baseline), DO NOT develop lung cancer.

As others have pointed out, the major, early studies made no attempt to account for potential confounders. For example, a number of the early lung cancer studies were on veteran groups with no attempt to account for other exposures in military training or on the battlefield. This applies to the “doctors’ study”, too, in that significant numbers may have served in the military. In the doctors’ study there was no information as to doctors’ area of medical service that could produce confounding, e.g., radiology. More recently identified confounders such as diet and industrial exposures are also important.

Another critical piece of information that regularly goes missing is overall cancer mortality – in proportional terms – between smokers/nonsmokers. Again from RASGD, the overall cancer-mortality rate, in proportional terms, for smokers and nonsmokers is roughly the same at about 33%. This tends to suggest that there is an amount of “migration” due to detection bias – particularly for lung cancer. It also dispels the myth that smokers are more prone to cancer generally, i.e., that smoking “causes” cancer. It also strongly suggests a “cancer-prone” group – about a third of the population is cancer prone reflecting some sort of abnormality/deficiency, e.g., genetic, hormonal.

Given confounders and unknowns in the circumstance, the most that can be said is that smoking is associated with an elevated risk of lung cancer. This, however, does not serve the antismoking cause. The antismoking slogan began as “Smoking may cause lung cancer”. The qualifier “may” was then removed to produce “Smoking causes lung cancer” for maximal inflammatory effect. Such statements are deceiving, not only in the causal attribution but in the absolutism. There are many smokers and nonsmokers that now believe that the vast majority of smokers WILL develop lung cancer or that they will develop fatal cancer far in excess of nonsmokers.


Hi Rich,
A question for you. You write that ''for some reason we always seem to just look at the 1930s onwards, but people have been smoking for millennia. Humans evolved in smoke-filled huts, by open-fires, tobacco-filled rooms.''

Some say that what we now identify as lung cancer was diagnosed as tuberculosis in those years. And tuberculosis was quite common in those years. What are your views on this?


Just read someplace where nicotine destroyed TB in all environments,I dont have it right at hand but maybe rose or frank does.........

Re: tb and nicotine

Here's something on it Harley http://www.data-yard.net/10c/nicotine.htm

But, that could be nicotine without the smoke. Certainly we can't deny that smoke can be harmful albeit nicotine can be beneficial. I believe my question remains valid: Did people suffer from lung cancer prior to the 30's but was mistakingly diagnosed as tuberculosis because we didn't know better?


Shocker: `Villain' Nicotine Slays Tb
A Ucf Researcher Said That Less Nicotine Than Is In A Single Cigarette Works.
May 22, 2001|By Robyn Suriano, Sentinel Staff WriterNicotine might be a surprising alternative someday for treating stubborn forms of tuberculosis, a University of Central Florida researcher said Monday.

The compound stopped the growth of tuberculosis in laboratory tests, even when used in small quantities, said Saleh Naser, an associate professor of microbiology and molecular biology at UCF.

Naser said nicotine worked better than about 10 other substances also tested. If it proves itself in further study, people might swallow capsules of nicotine or get intravenous doses to stave off their TB in the future


LOL Harley, we were posting at the same time. :-) See my reply to yours above.

Nicotine fix

"Tiny levels of nicotine kill the tuberculosis bacterium, researchers in Florida have discovered. They say it might be possible to use nicotine to treat the growing problem of drug-resistant forms of TB.

"The amount of nicotine needed to kill the bacteria is less than in one cigarette," says Saleh Naser of the University of Central Florida, who presented his results at a meeting of the American Society for Microbiology in Orlando on Monday.

Chance discovery

Naser made the discovery by chance. A colleague of his inserted a gene for a protein into tobacco plants, to see if it would kill the TB bacterium. But when Naser tested the antibactericidal properties of these plants, he found normal tobacco was just as effective at killing cells. Further studies showed nicotine was responsible for the effect.

Naser and his colleague George Ghobrial found that as little as 0.27 micrograms of nicotine per millilitre was enough to kill Mycobacterium tuberculosis. It was also effective against other strains of Mycobacteria.

Naser says that smoking doesn't work because the level of nicotine fluctuates so much. "The dosage is wrong," he says.

The advantage of nicotine, Naser claims, is that it should work against antibiotic-resistant bacteria. However, he doesn't yet understand how it destroys bacterial cells. His team now plans to test nicotine on TB bacteria growing in tissue cultures."

But this is old news, newly rediscovered.

"When Mr. Samuel Pepys on June 7, 1665, for the first time saw several houses marked with the ominous red cross, and the words "Lord, have mercy upon us" chalked upon the doors, he felt so ill at ease that he was obliged to buy some roll tobacco to smell and chew.

"Tobacco as a Prophylactic in Contagious Disease.
Allen (1835) stated that Diemerbroeck [De peste, 1646] has usually been quoted as authority for the anticontagious character of tobacco.

During the Great Plague in London in 1665, children were told to smoke in their school- rooms (Lancet 1: 1266-1267, 1902); and A Brief Abstract of the Virtues of the American Tobacco Plant (1783) records that buffers of the dead, in charge of dead-carts, at first used tobacco as a deodorizer, "little thinking that what they used for momentary relief would prove a constant preventive.

When the Plague was happily stayed, the virtues of tobacco began to be investigated, and it was found that those persons who plentifully used it, either in smoking or in snuffing, had most wonderfully escaped the dire contagion: for though they' visited the chambers of the sick, attended the funerals of cartloads at a time, they unexpectedly avoided the infection."
http://tobaccodocuments.org/ness/2445.html?zoom=750&ocr_position=above_foramatted&start_page=1 p9


(I would also suggest that there is an amount of detection bias concerning lung cancer diagnosis in nonsmokers, with a higher likelihood of LC diagnosed in nonsmokers known to have been exposed to SHS). A predictive strength of 7% does not justify an attribution of “cause”. It is simply far too low. It must be remembered that 90%+ of lifelong heavy smokers (above a baseline), DO NOT develop lung cancer.

Lung cancer in smokers may be different from lung cancer in nonsmokers: Vancouver study
By PAMELA FAYERMAN, Vancouver Sun November 9, 2010

Lung cancer in smokers has different genetic mutations and looks like a different disease than lung cancer in non-smokers, a team of B.C. Cancer Agency scientists has discovered.

Tumours of those who had never smoked actually had twice as many genetic abnormalities (DNA mutations) as those who were current or former smokers, according to the research presented Tuesday at a conference in Philadelphia of the American Association of Cancer Research. Using gene analysis technologies, the scientists compared tissue samples among comparison groups: 30 individuals who had never smoked and 53 who were either current smokers or former smokers.

Although doctors and scientists have suspected for some time that there were different biological mechanisms underlying lung cancers in smokers and non-smokers, the B.C. study is said to be the first to find whole regions of mutations.

Never-smokers account for up to 15 per cent of lung cancer cases and the research shows that while there were DNA mutations in both never-smokers and smokers, the never smoker tumours had far more alterations. For some unknown reason, never smokers who get lung cancer are more likely to be female.

Study co-author Kelsie Thu said while carcinogens (cancer-causing substances) in cigarettes trigger DNA mutations that lead to cancer cell growth, in non-smokers, it is now apparent there are other mechanisms causing tumour development. Study co-author Raj Chari said the challenge in non-smokers is detecting their cancers earlier since they tend to be diagnosed in the advanced, incurable stages because no one suspects they could possibly have lung cancer.

Frank I am with ya,I started smoking more after the bans went down. Iver at the club many have stated the same thing!

Damn it! The machine says that I cannot post my comments in one piece. I must obey! I will split this into two parts.


I have observed that our discussions so far have revolved around epidemiology. I thought that it may be worth while to consider the actual physical facts about what exactly lung cancer is. And so I googled 'lung cancer'. Wikipedia emerged, and so I clicked Wikipedia. I was confronted, in the first instance, by a message from James Wales, founder of Wikipedia, asking for donations to fund Wikipedia. Thereafter, came a detailed exposition of what lung cancer is.
I mention the message from James Wales only to illustrate the relative importance of:
a) His message,
b) The nature of lung cancer.
Since his message 'heads up' the article about lung cancer, is it not reasonable to believe that he sees his request for funds as more important than detailed information about lung cancer in the article?
At first glance, the above statement may seem to be silly, but I have a serious point, which is this: "To what extent do politicians regard 'the message' as more important than the CONTENT of the message?"
Thus, we have had today, THE SECRETARY OF STATE FOR HEALTH, the TOP MAN IN THE GOVERNMENT AS REGARDS HEALTH, saying that 80 000 people are killed each year by smoking. Sounds impressive, but without AGE RELATION SHIPS, the statistics are meaningless. As are phrases such as 'heart disease' when the reality is the heart stops beating because the body cannot any longer provide the 'energy' for the heart to continue to beat. The only real indication of DEATH is that the heart stops beating – thus all deaths occur because the heart stops beating and all deaths are CAUSED because the heart stops beating.


Going back to the Wikipedia article about lung cancer, it seems to be the case that there are five or more variations of lung cancer. That, in itself, indicates that that it is very difficult to decide what is the cause of the cancer. But we can go further. We can look at the following quote from Wiipedia:
"""English: Micrograph of squamous carcinoma, also squamous cell carcinoma. FNA specimen of a lung lesion. Pap stain. Clinicoradiological findings in the case suggested it was a lung primary, i.e. lung cancer.
The micrograph show a 3-dimensional cluster of cells with the nuclear changes of malignancy (variation in nuclear size, staining and shape), and features of squamous differentiation (moderate amount of cytoplasm, small/indistinct nucleoli, nucleus in the cell centre, keratinization)."""
It seems to me that this statement is not only in a foreign language. The language is alien - as in from another galaxy! For heaven's sake!, what does the word 'squamous' (as in 'squamous cell carcinoma') actually mean?
It seems to me to be true that we are falling into the trap. We are discussing ancient history, when the 'thinking' has advanced. And yet, it is almost certainly true that politicians are being fooled. Why? Because none of the studies indicate age.
The Office of Nat Stats recently issued information about deaths resulting from 'pulmonary diseases' (heart or blood circulation - whatever). But there was no age relationship quoted. The statement said that the 'age relationship' would be published in 2011. Erm...If the REASONS for deaths is so clear, why are the AGES of deaths so unclear?
It seems to me to be true that even the Office of Nat Stats has been got at. Surely, this cannot be true! Surely, no government can allow Health Zealots, no matter how worthy their intentions may be, to interfere with THE FACTS! And yet, we become suspicious about interference, and rightly so.
My really serious point in this post is that few of us understand the jargon of lung cancer. But is it possible that the 'cause' of lung cancer is just 'old age', and it is possible that smoking accelerates 'old age' as regards the lungs. By that, I mean that the repair mechanisms of the body become exhausted.
It is a decision that smokers make - whether to live longer, maybe, or die 'prematurely'. But if the 'prematurity' is minuscule, how much more minuscule must be the effect of passive smoking? And, in terms of ‘orders of magnitude’ (and I do actually mean ‘orders of magnitude’), how much more minuscule must the ‘danger’ be as regards children – or pet cats or dogs or mice?
The objective of the debate is to PROVE that smoking causes lung cancer, or to DISPROVE. It may not be possible to prove either. What is important, however, is to show that 'tobacco control' is nonsensical since no one really knows what the cause of lung cancer is or has any idea of age relationships.
In my opinion, 'age' is the critical thing.
But I may be wrong. It may be that if you tell people often enough that they are ill, they will become ill - but not necessarily for the reason that you promote.

"What the animal studies routinely do is embarrass researchers by having the animals outlive the non-smoking ones, and in the case of the F334 and A/Js, not only did they outlive the non-smoking ones, those exposed to smoke exceeded the total life expectancy of those breeds, and suffered less cancer than would be expected in them."

But how could that be?

Try this -

Nicotinic acid - 1941

"We find that the smoke from ordinary Ripple cigarettes contains the anti - pellagra vitamin or nicotinic acid in fairly substantial amounts. However, the quantity is probably too low for a man to rely upen this source alone for his nicotinic acid requirement. At least to do so he would find it necessary smoke an unreasonable number of cigarettes daily"

"Niacin was first discovered from the oxidation of nicotine to form nicotinic acid. When the properties of nicotinic acid were discovered, it was thought prudent to choose a name to dissociate it from nicotine, in order to avoid the perception that vitamins or niacin-rich food contains nicotine. The resulting name 'niacin' was derived from nicotinic acid + vitamin."

Niacin is also referred to as Vitamin B3 because it was the third of the B vitamins to be discovered. It has historically been referred to as "vitamin PP", a name derived from the term "pellagra-preventing factor".

Niacin and Niacinamide In Flue Cured Cigarette Smoke Condensate August 10 - 1960

Mapping the role of NAD metabolism in prevention and treatment of carcinogenesis
"The association of lower NAD with malignancy in skin supports
the hypothesis that niacin maybe an important preventive
factor in cancer."

"Niacin deficiency in humans, which leads to low NAD status, causes sun sensitivity in skin, indicative of deficiencies in responding to UV damage."

"Niacin deficient keratinocytes are more sensitive to photodamage, as both poly(ADP-ribose) polymerases and Sirtuins are inhibited by the unavailability of their substrate, NAD+, leading to unrepaired DNA damage upon photodamage and a subsequent increase in cell death.

Furthermore, the identification of the nicotinic acid receptor in human skin keratinocytes provides a further link to niacin's role as a potential skin cancer prevention agent and suggests the nicotinic acid receptor as a potential target for skin cancer prevention agents."

Niacin deficiency and cancer in women
"A new interest in the relationship between niacin and cancer has evolved from the discovery that the principal form of this vitamin, NAD, is consumed as a substrate in ADP-ribose transfer reactions. Poly(ADP-ribose) polymerase, an enzyme activated by DNA strand breaks, is the ADP-ribosyltransferase of greatest interest with regard to effects on the niacin status of cells since its Km for NAD is high, and its activity can deplete NAD.

Studies of the consequences of DNA damage in cultured mouse and human cells as a function of niacin status have supported the hypothesis that niacin may be a protective factor that limits carcinogenic events"

"Researchers at the New South Wales Cancer Institute painted healthy volunteers with a lotion containing vitamin B3 or nicotinamide.
They found those patients treated with the substance suffered no damage to their immunity when exposed to ultra violet light.

In another first, the study found men were twice as likely to suffer immune damage from the sun than women.

Scientists are not exactly sure how vitamin B3 boosts the skin's defences against cancer."
Tests so far have shown it is safe and effective as a topical treatment

Bombarding an animal with smoke thick with water soluble niacin might asphyxiate it I suppose, but is very unlikely to produce the result they were looking for.


Be careful when using the WP lung cancer page. At least one of the half dozen people who control the passive smoking page has, in the past, contributed. Take a look at the discussion and history pages to see if there have been any disputes. With the new discovery that lc among smokers and non-smokers may be different diseases, which would blow a hole in the passive smoking edifice, this is likely to become a bigger problem.