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.