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.
‘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?
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.
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.
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.
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.
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!
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.
Already dealt with this above.