Reif

Controversy with Reif

In his later career as a smoking sceptic, Burch increasingly found himself engaging with opponents who would have been unworthy of his attention in the days before he was branded a scientific heretic. One such was Arnold Reif of Boston City Hospital and Boston University School of Medicine. (“Arnold Reif who hailed from Yorkshire. We met some years ago and bear no rancour although his anti-smoking attitude appears to border on fanaticism”.) Reif’s paper Effect of Cigarette Smoking on Susceptibility to Lung Cancer purported to rebut “Fisher’s fallacy” and “Burch’s extension of Fisher’s views”, together with a restatement of orthodoxy on smoking and cancer. He was concerned that “Medical scientists who debate Tobacco Industry executives on radio or TV (as I have done) should be aware of the the scientific fallacies they are likely to encounter and prepared to rebut them definitively.”

Since the paper criticised Burch extensively by name, it might be thought that he was entitled to defend himself in the journal Oncology which printed it. Burch had no such expectation.

If they can publish Reif’s essay without shame it is unlikely that they will look with favour on mine. Although my effort was almost certainly wasted, the writing afforded me some amusement mixed up with a sense of shame at attacking so pathetic an opponent. Bully! However, to be bracketed with Fisher – even an evil Fisher whose logic can be faulted – is flattery indeed!” (to Hickey, 4 September 1981).

(“Bully”: probably “Oh what a bully I am” rather than “Bully for me”.)

He was right. “My suspicions about Oncology have been duly confirmed. Needless to say the referees made no attempt to fault my arguments; my paper contained ‘no novelty’ and my ideas ‘had been widely reported elsewhere’.” (to Hickey, 20 October 1981).

Hickey suggested publication in the Journal of Chronic Disease, now co-edited by Alvan Feinstein, but Burch intended another paper for that outlet and sent his reply to Reif to Medical Hypotheses, where it appeared in 1982.

Burch did not bother to consider Reif’s theory of smoking and cancer (a variant of Doll’s view of cigarette smoking as a promoter of lung cancer), but concentrates on the issue of causation. Reif’s list of 12 facts supposedly disproving the constitutional hypothesis and Burch’s refutation of the refutation deserve quotation in full. The rest of the paper discusses the possible genetic basis of the correlation. Reif raises the familiar objection that cancer genes doubling as smoke genes must be implausibly coordinated, and that Burch assumes the truth of his autoaggressive theory. Burch answers these points and considers evidence for the genetic theory: some of this is new, for instance a report by Brian Henderson on mainland China and a study of Mormons by James Enstrom.

Burch sent his reply to Reif to Marvin Kastenbaum, a statistician at the Tobacco Institute and apparently that organisation’s Burch-watcher (see his report on Lee’s examination of Burch and on the Royal Statistical Society address). Whether they had other contact is unknown.

What follows is quotation from Burch’s paper and includes Burch’s quotations from Reif.

Reif’s claim

1 Smokers who quit have a far lower chance of dying of lung cancer than those who continue to smoke.

Reif’s evidence

Demonstrated in numerous studies: prospectively for British physicians, US citizens and veterans, Canadian veterans and Japanese men; and retrospectively for cancer patients. lf smoking had no effect on lung cancer rates, neither should quitting.

Burch’s response

Quitters and continuing smokers are both self-selected. Quitters differ in many respects from continuing smokers before they give up smoking. The person who is not constitutionally predisposed to habituated smoking (and therefore less likely to be predisposed to lung cancer) tends to quit.

Reif’s claim

2 A straight-line relationship exists between the number of cigarettes smoked daily and lung cancer incidence.

Reif’s evidence

Demonstrated in numerous studies. If the habit-cancer linkage theory applied, the genetic likelihood of developing lung cancer would have to be linked not only with whether, but how much one smoked.

Burch’s response

Armitage argued that this linear relationship presents theoretical difficulties for one causal interpretation. Doll and Peto have since proposed a quadratic relationship. In constitutional terms, light smokers tend to be ‘social’ smokers, tend to quit readily and are less likely to be predisposed to lung cancer than heavy smokers.

Reif’s claim

3 Ways of smoking that reduce the amount of tar inhaled also reduce the risk of lung cancer.

Reif’s evidence

For the habit-cancer linkage theory to apply to these data the ability to tolerate low tar and nicotine intake would have to be linked to a lesser tendency to develop lung cancer.

Burch’s response

As with 1, the phenomenon of self-selection does not allow simple interpretation. Secular trends in whole populations do not correlate with ‘constant tar’ cigarette consumption. Also see 5.

Reif’s claim

4 The lung cancer rates for pipe and cigar smokers are much lower than for cigarette smokers.

Reif’s evidence

To explain these data by the habit-cancer linkage theory, the tendency to smoke in a particular manner would have to be linked to the tendency to develop lung cancer.

Burch’s response

The evidence from twins and studies of morphology show that pipe and cigar smokers tend to differ constitutionally from one another and from cigarette- and non-smokers. This fact, combined with the experimental evidence that shows condensates from cigars to be much more carcinogenic than those from cigarettes, greatly embarrasses the causal hypothesis; it presents no problem for the constitutional view.

Reif’s claim

5 Increase in exposure. whether through deeper inhalation or by starting to smoke earlier in life, increases lung cancer risk.

Reif’s evidence

For the habit-cancer linkage theory to explain these facts the genetic traits that accounted for these behavioral characteristics would have to be linked to the tendency to develop lung cancer.

Burch’s response

When the level of smoking is controlled then for medium and heavy smokers the risk of lung cancer in inhalers is paradoxically lower than in non-inhalers. Fisher regarded this as a ‘fair knock out’ for the theory that smoke in the lung causes lung cancer. In constitutional terms, the ‘early’ smoker tends to be genetically predisposed to ‘habituated’ rather than ‘social’ smoking.

Reif’s claim

6 Women are fast catching up with men in the development of lung cancer, after a lag of about 30 years behind men in taking up smoking.

Reif’s evidence

The data on the amount smoked by women and the time relationship of tobacco smoking and lung cancer incidence relative to men accords precisely with the cause-and-effect relationship, and argues strongly against the habit-cancer linkage theory.

Burch’s response

Quantitative analysis of long-term secular trends and of recent trends in sex- and age-specific mortality does not support causal theories and shows no sign of the 30-year lag. Unfortunately errors of death certification and detection bias (see text) prohibit definitive conclusions.

Reif’s claim

7 Subgroups of a population forbidden to smoke by their religious sect have drastically lower rates of lung cancer.

Reif’s evidence

For the habit-cancer linkage theory to accord with these facts, only those genetically fated not to smoke would join these sects, and ignores the point that most Utah Mormons were born into their sect.

Burch’s response

Membership of such sects is either through self-selection or through birth (with inheritance) from self-selected parents.

Reif’s claim

8 In most occupations that pose a high risk of lung cancer, the large excess lung cancer mortality of smokers as compared to nonsmokers is maintained.

Reif’s evidence

To explain the dramatic smoker/non-smoker differential for asbestos workers or uranium miners by the habit-cancer linkage theory would require not only the tendency to smoke, but the tendency to work in a particular industry to be linked to the tendency to develop lung cancer.

Burch’s response

The constitutional hypothesis does not exclude effects resulting from extrinsic carcinogens such as asbestos and ionizing radiation. Nevertheless, we should not assume that the choice of occupation never involves genetic factors.

Reif’s claim

9 Compared to the powerful effects of cigarette smoking, air pollution is not a major factor in lung cancer incidence.

Reif’s evidence

Air pollution has only a mild (if any) effect on lung cancer incidence. At worst, it may be equivalent to smoking perhaps 1-2 cigarettes/day.

Burch’s response

No problem for constitutionalists. Differences between urban and rural populations present some interesting paradoxes for thoroughgoing causationists.

Reif’s claim

10 The latest findings on lung cancer in monozygotic twins support a causal relationship between smoking and lung cancer.

Reif’s evidence

Only a few cases of lung cancer have been substantiated in twins whose smoking habits are known. These scant data are discussed in the text.

Burch’s response

Numbers are too small to distinguish between rival interpretations but as they stand they agree with the constitutional hypothesis. However, twins studies present awkward problems of interpretation.

Reif’s claim

11 Animal experimentation with chemical carcinogens supports the dose-response relationship found in man.

Reif’s evidence

We now have a vast store of information on chemical carcinogenesis with tobacco tar, which supports the data on dose-response in man.

Burch’s response

Which relationship? See 2. Furthermore, condensates of cigar smoke, are, paradoxically, much more carcinogenic for animals than are those of cigarette smoke.

Reif’s claim

12 Dogs exposed to cigarette smoke have developed lung cancer.

Reif’s evidence

The much higher lung cancer incidence in cigarette than in pipe smokers is attributed to proximity between the source of smoke and the lung. This has only been achieved by training dogs to smoke through a tracheotomy tube.

Burch’s response

The design of the experiments has been severely criticized. In view of species differences, only the direct evidence for man is strictly relevant to smoking and lung cancer in man.

Sources

A Half-life of Burch