It is not the fault of the anti-smoking industry, the witch-finders of modern times, if everyone does not know what ETS is: Environmental Tobacco Smoke.
The chemical composition of ETS consists of sidestream smoke generated by a burning cigarette, and mainstream smoke exhaled by the smoker. The major contribution to ETS is from the sidestream smoke.
“Some years ago, I made a prediction...I said that the anti-smoking movement had a big problem...even if smoking really were so harmful to smokers as was claimed, the natural response would be to call it a matter of individual choice...The only solution to this problem, I said, would be for it to find – and this was my term – an ’innocent bystander’...The ideological function of this search for innocent bystanders has been crucial...”
Thus Peter Berger, Professor of Sociology at Boston University. [1] Or, as Mr Des Wilson, of PAT (Parents Against Tobacco), said in an article in the Times of the 9th January, 1990:
“The problem with the obvious alternative [to health education, which he admits is not entirely effective] – much tougher controls – is that it tends to be opposed even by non-smokers who believe that in a free society people should be able to choose whether to smoke or not.
The campaign being launched today by 100 well-known parents to protect children from smoking could represent the most effective approach yet, for it circumvents the ’free to choose’ obstacle.”
And therefore leads, one presumes, to the possibility of imposing Mr Wilson’s wished-for “much tougher controls”.
Interesting that Mr Wilson sees freedom of choice as an obstacle. There is another aspect of the question to be considered: epidemiologists. A little thought will show that these are people who study epidemics, and until about 1950 there was a very wide field for them to practise on. Tuberculosis, smallpox, plague, typhus, cholera and the rest of the terrible list were widespread. Partly because of immunization programmes and anti-biotics, and perhaps equally because of improved standards of public cleanliness with water, sewage and housing, these ancient curses have withdrawn within the borders of countries whose governments cannot or will not use the counter-measures available; and since these governments do not encourage the work of epidemiologists, there is, as Skrabanek has remarked: “an epidemic of epidemiologists who are short of diseases suitable for their investigations”. [2]
(This may be one reason why the great AIDS myth was so sedulously spread. I am sure that the epidemiologists did not set out to deceive anyone, but the chance of getting their teeth into anything as dramatic, tragic, and likely to keep them employed for a long time could not be missed). It is very understandable that when the World Health Organization dubbed the widespread custom of smoking an “epidemic”, [3] there were many people eager to agree. Jobs for the boys, indeed, for many years to come.
The World Health Organization (WHO) is a part of the United Nations Organization that has not escaped the criticisms levelled at that body, and has attracted others peculiar to itself. B.J. Cutler, foreign affairs columnist for Scripps Howard News Service, says: [4]
“It suffers from the same maladies as other international agencies: a bloated bureaucracy, too many conferences, and a plethora of programs that detract from what should be its focus – meeting the health needs of the world’s poorest people”.
“Once a year WHO’s bureaucrats and delegates...meet in Geneva and once a year, America’s leading expert on WHO mismanagement issues a damning paper timed to coincide with the conclave.
“In his list of horrors, Mr Dietrich points out that each posh WHO assembly costs $2,5 million...more than twice as much as the organization spends annually to fight malaria in Africa.
“Two-thirds of its staff are in comfy offices in European or US cities. It gives twice as much per head to extremely wealthy countries like Saudi Arabia and Singapore as to the world’s poorest, Ethiopia, which got a total of 5 cents per person in 1989. Out of its 1990-91 budget of $1,4 billion, it can find only $500,000 to fight the leading child killers in South East Asia, respiratory infections. This amounts to less than one penny per child”.
It sets up conferences in agreeable places like Geneva and Perth, Australia, on smoking, in which extreme hostility towards smokers is displayed and conspiracy theories voiced, and the gaiety of nations somewhat enhanced; though the remarks of Professor Stanton Glantz, described as a “leading activist”, at one of these “posh assemblies”, the 1990 conference, perhaps go a little further than simple humour and have uncomfortable reminiscences of earlier “activists”, (see under):
“The main thing the science has done on the issue of ETS, in addition to help people like me to pay mortgages, is it has legitimized the concerns that people have that they don’t like cigarette smoke [his grammar, not mine]. And that is a strong emotional force that needs to be harnessed and used. We’re on a roll, and the bastards are on the run.” [5]
However, the movement ran into the difficulty described by Professor Berger: the activists were told to mind their own business.
The assault then switched to the nuisance that smokers were to others. The smokers were able to retort that a lot of people were nuisances to others: people who played loud music, did not use deodorants, did use powerful toilet waters, after-shave and hair lotions not of the highest quality, drank a lot of beer or cheap wine, did not wash themselves or their clothes much, and ate garlic, sometimes all at once.
You can’t say: “Please put out your garlic,” or “kindly take your armpits into the garden.” The smoker has to suffer in silence; let the others endure his smoke (which does at least mask some of the other horrors). So, as Professor Berger says, a victim became necessary, and one was duly found: “the passive smoker”. The first of these unfortunates seems to have been a mouse.
E. Lorenz et al. found no evidence of harm done to mice exposed to cigarette smoke for up to 693 hours [6], but this was in 1943, before the great smoking witch-hunt had got under weigh (except, of course, in Nazi Germany).
Once it had got going, the evidence started to come in, from Britain [7], France [8], the US [9]; but the epithet itself appears to have first been used in 1963, when an article by H. Otto in the Frankfurter Zeitschrift fuer Pathologie was entitled “Experimentelle Untersuchungen an Maeusen mit passiver Zigarettenrauchbeatmung” (Experimental investigations on mice through passive inhalation of cigarette smoke). [10] So there is our passive smoking (passiver Zigarettenrauchbeatmung) for apparently the first time.
There is a curious appropriateness in the fact that it is in German that it first appears, since the Nazi campaign against smoking was of peculiar intensity. Adolf Hitler himself refused to let anyone smoke in his presence, and gave 100,000 German marks of his own money to the first Institute for the Struggle against Tobacco [Institut fuer die Bekaempfung des Tabakwesens] in 1942 [11]; and one Bonne, in 1934, is on record as having said that alcohol, nicotine and syphilis were the three causes of degeneracy of Hitlerian German youth: for those afflicted the remedy he suggested was sterilization. [12]
Many German scientists working in the second half of the century, however sincerely anti-National Socialism, must have spent at least some of their youth listening to this sort of thing.
It was at the Third World Conference on Smoking and Health set up by WHO in New York in 1975 that the subject of passive smoking was first discussed. C.F. Tate cited one patient who: “became so tight with wheezing and asthma that she could not get her breath” while working in an area where smoking was allowed.
From this one case, the speaker went on to draw a heart-rending picture of approximately 34 million others for whom the problem is real and extremely serious. [13] He did not quote any medical facts to support any of this, though he did cite information about carbon monoxide made by a researcher, A.F. Aronow, whose conclusions on passive smoking have been questioned by two American government agencies. [14] Anyhow, this conflicts with the fact that tobacco smoke has not been proven to be an allergen. [15] However, the passive smoking scare had taken off, and the evidence began to come in. It is worth while having a brief look at the various surveys that have been carried out:
On this subject, the best known and most often quoted study is that of Hirayama, reported in the British Medical Journal in 1981. [16] He made use of a test devised by N. Mantel, who replied with an analysis of Hirayama’s work that expressed doubts about its ambiguities and omissions, and also about the fact that Hirayama had mistaken an X for X2. [17] He pointed out that Hirayama had made mistakes of up to 1,000% in another set of figures. [18]
Hirayama replied that prominent statisticians [anonymous] had confirmed the validity of his test. As J.R. Johnstone remarks: “In any other area of science – or indeed intellectual discourse generally – this would be enough to negate Hirayama’s contribution.” [19]
However, far from being negated, Hirayama’s contribution has been widely used and extravagantly praised. In that WHO conference in Perth, Australia, during which Professor Glantz made his feelings plain, the preliminary literature spoke of Dr Hirayama’s work in areas such as passive smoking having attracted “considerable international attention”. Not a word about X2. [20] And no less a personage than Glantz himself, of the poor grammar and ferocious opinions, paid tribute to Hirayama at this same “posh conference”. In 1983 Hirayama published an update of his study. [21] It said he had been right all along. Nevertheless, at the 1983 Workshop on Atmospheric Tobacco Smoke [22], criticisms of the Hirayama study were summarized thus:
“[the] study has been criticized in detail by other researchers from the point of view of questionnaire reliability, absence of histological diagnosis, statistical treatment [X 2?], grouping of smoking habits among husbands and confounding factors such as air pollution from heating and/or cooking.”
Another study that is often quoted is that by Trichopolous et al. in Greece. [23] In this it appeared that non-smoking wives of heavy smokers were more likely to get lung cancer than women who actually smoked themselves (Hirayama found a similar anomaly). These authors too published an update in which they found they’d been right before, but to their credit, they acknowledged that their study was criticized, by themselves and others, for several reasons, and conceded that “doubt must remain about the histological evidence and hospital differences...” [24] This, in the atmosphere surrounding most scientific dispute, is so very creditable that it is possible to wish that one could believe them about their main conclusions. But it is not easy to in the face of this, their own admission, and comments such as those by Heller, [25] who found the 1983 paper even less convincing than the 1981 report. So these are the two studies that are most often quoted as proof of the relationship between passive smoking and lung cancer.
The National Health and Medical Research Council of Australia (NHMRC) [26], and the Surgeon-General of the USA [27] have concluded from them that the evidence is “strongly suggestive”, even “compelling”.
They have done this by ignoring anything that does not fit in (which means any of the corrections subsequently published); as Johnstone says: [28]
“The answer may lie in a quite uncritical evaluation of the evidence...This avoidance of published corrections leads to a quite natural sense of security in acceptance of erroneous published conclusions.”
With this natural sense of security, then, we can see why Garfinkel et al.’s report in 1985, [29] was used as it was. The NHMRC’s Report states that this study (of 134 women) shows: “[a] positive association in non-smoking females: statistically significant”. But Garfinkel summarises the result, in fact, by saying: “In conclusion, we found an elevated risk of lung cancer, ranging from 13 to 31 percent, in women exposed to the smoke of others, although the increase was not statistically significant [emphasis added]”.
There was a small sub-set of women whose husbands smoked more than 20 cigarettes a day who were significantly more likely to develop lung cancer, but it must be remembered that when a statistician uses the word “significant” he does not do it as you and I do. We mean it as something of importance, something that matters; he means only that there is a result: it may matter or not.
The extent to which this result may matter is shown by the fact that there was another sub-set of women who had been exposed to passive smoking for 1-2 hours a day for the last 25 years, who, it seems, were significantly LESS likely to develop lung cancer.
You can go through Garfinkel’s close-packed pages and find other contradictions of this type: figures that show that passive smoking is dangerous and others that show it, apparently, is a benefit. Even Hirayama and Trichopolous appear to show that smoking wives of smokers have a lower rate of lung cancer than nonsmoking wives of smokers, which doesn’t make sense in their terms.
In fact, in a report published in 1981 [30] Garfinkel et al. stated, of a study on 94,000 men and 375,000 women, that non-smoking wives of smoking husbands had no statistically significant increased risk of lung cancer compared with wives of nonsmoking husbands. Correa et al., in a study of 30 lung cancer patients, showed that non-smokers married to heavy smokers doubled their risk of lung cancer, at least among the 22 women studied. [31]
However, the NHMRC Report seized on the Correa study, describing it as showing: “Positive association in both males and females statistically significant”. As shown in the Correa report, it was significant only for females.
Kabat and Wynder, in 1984, studied 134 cases, and reported no result in most cases: more male patients than controls were exposed to tobacco smoke at work, and the researchers said that the difference is just statistically significant (emphasis added), but admitted that this could be because of information bias. [32] Humble et al., (1987) in a study in New Mexico of 609 cases and 781 controls, found no results with smokers or ex-smokers married to smokers, but they found that nonsmokers (who had never smoked), married to smokers had about a two-fold increased risk of lung cancer. [33] This parallels the results found by Hirayama and Trichopolous mentioned above, and if you think about it it is very curious. Can it mean that smoking actually protects from cancer?
Surely it is extraordinary that in the three studies that have had the most positive results there has also been this shattering revelation.
The consequences of any wide-spread recognition of this would be so awful (think of all the anti-smokers out of work) that it is best to hasten on to the other studies (and only after this to consideration of the very strange fact mentioned by Burch about the Multiple Risk Factor Intervention Trial (MRFIT) in the USA, and the Whitehall study, described below).
There is one more that seemed to show a relationship between passive smoking and lung cancer: Repace and Lowrey (1984). This deals with 25 deaths from lung cancer among Californian Seventh Day Adventists, who are forbidden to smoke on religious grounds, compared with figures from the rest of the population. [34]
This has been so satisfactorily torn to pieces by Arundel et al. [35] that there is really no more to be said about it. It was shown that the evidence they presented to support the plausibility of their estimated risk for non-smokers from ETS exposure is “unstable and inaccurate”. The evidence they presented “is based on several errors and unrealistic assumptions”.
“The lung cancer risk estimates derived from the SDA [Seventh Day Adventist] study are based on very few observed deaths and are unstable. The apparent differences in lung cancer mortality between SDA and non-SDA never smokers may be due to a variety of factors other than ETS exposure. A number of assumptions and calculations are made that are clearly incorrect.”
Their linear model, we are told, “over-estimates the average nonsmoker’s exposure to ETS and the average current smoker’s lung cancer risk”. Obviously, if these are pushed up at will the result you want can be obtained...
The best available analyses, say Arundel and his colleagues, by Koo et al. in Hongkong and Garfinkel et al. in the USA, find no statistically significant increase in risk.
“...an association between lung cancer among non-smokers and the spouse’s smoking habit may be caused by confounding, not by ETS exposure”, says Arundel.
And “confounding could occur either from life-style factors and occupational exposures associated with active smoking or by unreported active smoking by self-reported non-smokers”.
A correspondent in The Lancet [1957 2: p. 1226], draws attention to this possibility in a way we can all recognize:
“Yesterday the morning post brought...an innocent looking letter from the MRC [Medical Research Council]...: ’Dear
Doctor: In 1951 you stated that you smoked an average of 3 cigarettes a day...’
’Why you hypocritical old...’
’How could I,’ he began brokenly, ’how could I say such a thing?’
“My husband is a heavy smoker, except when Giving Up Smoking. This happens three or four times a year...Clearly the questionnaire had caught him while he was Giving Up Smoking, or, more accurately, Tapering Off.
There it is: 3 cigarettes a day, all tabulated, analysed, with confidence limits and the rest of it. It makes you think. I mean, statistical methods are so reliable these days. Isn’t it appalling that they have to depend on people?”
Let us never forget that they do depend on people. So, to summarize the position:
Relative risk, or risk ratio, is a relationship of the rate of development of a disease among people exposed to some variable in the population studied, divided by the rate of the same disease in those not exposed; it is most frequently expressed as a “risk ratio”. If the disease rate is exactly the same in both groups, the risk ratio is 1.0. If it is lower, then the chance of contracting the disease is less.
If it is less than 1.0, then it is called negative; over that, positive. A risk ratio is commonly called “weak” when it is in the range of 1 to 3. A “strong” risk ratio would be in the range of 5 to 20. So you can see that in the studies listed below six show a weak risk ratio for lung cancer cases exposed to ETS, of 2.55 or less, but nine show a risk ratio below 1.0 – in fact, using the same criteria as the anti-smokers, we would be obliged to say that ETS protects against lung cancer.
Of course in both cases the risk ratio is too weak to make such a judgement, but that doesn’t stop the anti-smokers from making use of those that appear to support their argument.
There are one or two other points worth noticing: the small number of cases involved in some of the studies is one; also the curious difference between the rates in the sexes when both male and female have been studied?
Cohort Studies:
Garfinkel 1981 88 F 1.17
Gillis 1984 6 F 1.00
4 M 0.25
Hirayama 1984 163 F 1.45
1984b 7 - 2.28
Certain of those that produced positive results (Hirayama, Trichopoulos) have been very severely criticized (this is not true of any of those that produced negative results); one (Kabat & Wynder) stressed that the result they obtained was just significant, and could be the effect of bias; Garfinkel et al. had some results that were either not significant or directly confusing; and Correa et al. dealt with very few cases. Note that wherever there were more than a hundred cases, the result was either exceptionally weak (three of 1.65 or less), or showing less risk (two of less than 1.0).
The New Mexican study (Humble et al.) seems to have escaped criticism, to deal with a reasonable number of subjects, to have produced definite results, and to show a clear positive effect, but it is one of those that also seems to show that smoking protects from
lung cancer... [36] The report on the study also quotes Hirayama and Trichopolous without reservation, and says that its results agree with those of another study, by Dalager, 1986, who found a negative result, and Correa, whose results were as stated above; it also says that Garfinkel found an increased risk, which Garfinkel himself said was not statistically significant.
The study complicated the question by also taking into consideration the possibility of exposure to asbestos. Now the Report of the Royal Commission on Matters of Health and Safety Arising from the Use
of Asbestos in Ontario [37] says: “asbestos in building air will almost never pose a health hazard to building occupants”.
Even the World Health Organization, always one for a good scare, has admitted: “the risks...attributable to asbestos cannot be quantified reliably and are probably undetectably low”. [38] And it has admitted that there is not enough evidence to link passive smoking and lung cancer.
To Part Two Of This Pamphlet
Case Control Studies:
No. of cases Sex Risk ratio
Chan and Fung 34 F 0.75
Trichopoulos 1983 38 F 2.13
Correa 1983 14 F 2.07
2 M 1.97
Kabat & 13 F 0.79
Wynder 1984 5 M 1.00
Butler 1984 33 F 0.80
5 M 0.51
Garfinkel 1985 92 F 1.12
Wu 1986 29 F 1.20
Akiba 73 F 1.52
3 M 2.10
Lee 1986 22 F 1.03
8 M 1.31
Brownson 1987 19 F 1.68
Gao 1987 189 F 1.19
Humble 1987 14 F 1.78
Koo 1987 51 F 1.55
Lam 1987 115 F 1.65
Pershagen 1987 33 F 1.20
Geng 1988 34 F 2.16
Inoue &
Hirayama 1988 18 F 2.55
Katada 1988 17 F ‐ ‐
Lam & 1988 37 F 2.01
Cheng
Shimizu 1988 90 F 1.10
He 1990 45 F 0.74
Janerich 1990 129 F 0.93
Kabat 1990 13 M 1.20
35 F 0.90
Kalandidi 1990 91 F 2.11
Sobue 1990 64 F 0.94
Svensson 1990 17 F 1.20
Wu-Williams 1990 205 F 0.7
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