Best just to look at the various studies:
Hirayama (again) (1981, 1984): In 1981 he reported that “husbands’ smoking habits seemed to have no effect on their non-smoking wives’ risk of developing ischemic heart disease”. When the husband was a non-smoker, the relative risk was 1.0. If the husband was an ex-smoker, or smoked fewer than 20 a day, the relative risk was .97. If he smoked more than 20 a day, the relative risk was 1.03. In 1984 Hirayama reported a greater risk. For women married to non-smokers the relative risk was 1.0, with ex-smokers or those who smoked up to 20 a day, it was 1.10, and with those who smoked over 20, it was 1.31. Hirayama’s study has several major methodological problems, it is said. [39]
There is the potential misclassification of smokers and non-smokers (see the letter in The Lancet quoted above). A disproportionate number of women of “lower socio-economic status” were included. There was misclassification of “dose-response”. Ex-smoking husbands were lumped in with current cigarette smokers of up to 20 a day. This is surely eccentric, even for Hirayama. No attempt was made to estimate ETS exposure outside the home.
The study was based on an agricultural population, which is not typical of Japan in general, and the areas seemed to have been chosen because they were easier to collect material in. There was no control for other risk factors. Garland (1985): reported an increased relative risk for women married to smokers or ex-smokers, of 14.9. This he later corrected to 2.7. Another difficulty was that out of 695 women studied there were only 19 deaths, and there was a further problem here in that 15 of these were of women whose husbands had given up smoking when the survey started (can their husbands have turned so tetchy that the wives were nagged to death?) [40] Gillis (1989) found that the death rate was higher among those exposed to ETS, though only slightly. Again there were problems with the methodology: misclassification of subjects as non-smokers when they may be ex-smokers or current smokers (see The Lancet letter again); a sample size that was too small, and few results that were statistically significant. There were confusingly similar relative risks for active and passive smokers, says Dr Lawrence M. Wexler, Director of the Epidemiology Consulting Group and Adjunct Professor of Community and Preventive Medicine, New York. [41]
In all this welter of research, studies, reports, and general verbiage, there is one overwhelming fact. Svendsen (1987) reported on the results of the MRFIT trial. This dealt with 12,866 men considered to be at increased risk of heart disease. They were divided into two groups: one was treated with drugs for high blood pressure, encouraged to stop smoking and to eat less fat and cholesterol. The other was left alone.
At the end of seven years the mortality rates were 41.2 per 1,000 in the intervention group (doing the healthy things), and 40.4 per 1,000 in the other. Neither death rates from heart disease or any other cause were significantly different in the two groups, it was stated, except that there were 60 deaths from cancer other than in the lung in the intervention group, as against 48 in the other. [42]
Here must be mentioned the Whitehall study on the effects of reducing smoking. In this study, begun in 1968, 1,445 British civil servants who smoked were divided into two groups, one of which was advised to give up smoking, the other (the control group) was not.
After a year smoking in the first group (the intervention group) was down by 75%, and over the next ten years the difference in the smoking rate between the two groups continued to be marked, though it diminished somewhat.
After ten years, 17.2% of the intervention group was dead, against 17.5% of the control group (“statistically insignificant”).
There was no statistically significant change in deaths from heart disease, lung cancer or any other cause, except for cancer other than in the lung, where the death rate was 3.9% (28 deaths) in the intervention group, against 1.7% (12 deaths) in the control group. [43]
Burch, combining the results of the MRFIT study and the Whitehall study on the effects of giving up smoking, stated that in the two studies the death rate in cancer elsewhere than in the lungs rose significantly in the intervention group, (those doing healthy things like giving up smoking...) [43] All this is so extraordinary that one might think that great emphasis would be placed on research to establish just why it happened.
Consider this together with the odd fact mentioned above (that Hirayama and Trichopolous found that smoking wives of smokers have a lower lung cancer rate than non-smoking wives, and that Humble found no results with smokers or ex-smokers married to smokers, but two-fold increased risk with those who had never smoked), and of course Garfinkel’s finding that women exposed to passive smoking for twenty-five years were significantly less likely to develop lung cancer).
Then ask why research has not been carried out on a large scale to discover what lies behind this. Surely if cancers other than of the lung can be prevented by smoking we should all be told about it? Surely, it is of extreme importance that the facts on this matter should be established without doubt.
Think only of the suffering that could be avoided if this were true.
Of course, as the Whitehall and MRFIT studies, and all the other studies on the effects of a healthy lifestyle, as well as common sense through the ages, have shown, people must die of something, but cancer is one of the more unpleasant (and expensive) ways of doing so. So what has been done to investigate this all-important matter? The answer is: nothing much. Sir Ronald Fisher was slammed for amusing himself and his audiences by seizing on the fact reported in various surveys that inhalers had a lower cancer rate than non-inhalers. [44] And Burch tells us: [45]
“Stallones risked the creation of many personal enemies (emphasis added)” when he merely pointed out that changes in lifestyle had no effect: what would have had happened to him if he had observed that it might be argued that smoking did have at least one benefit, even if this was only the opportunity to die of something less painful and disgusting than cancer?
All this is plainly a matter of the highest importance, and it is most sincerely to be hoped that some responsible authority will take the matter up, and some small part of the huge funds that have gone into anti-smoking propaganda will be diverted into investigation of this vital question. Perhaps it’s a job for the World Health Organization?
Svendsen, in the report already mentioned [42] found a higher death rate from heart disease among husbands whose wives smoked; or rather, one husband whose wife smoked, since only one case was involved. [46] Again, we are told of methodological problems: information on smoking habits was collected only at the start of the 12 year period, so that no changes in smoking habits were reported; no information was collected on diet, exercise, blood pressure, etc.; and no ETS exposure outside the home was measured. Lee (1986), was one of the very few studies that attempted to examine ETS exposure outside as well as in the home. The original questionnaire was administered in ten hospital regions in England between 1977 and 1982. 200 cases and 200 matched controls were collected for each sex and age grouping (35-44, 45-54, 55-64, 65-74), to examine the possible link between ETS exposure and heart disease. It showed none. [47] Aronow (1978) described an examination of the possible relationship between exposure to ETS and angina brought on by exertion in both a well-ventilated and an unventilated room. [48]
This involved ten men, eight non-smokers and two smokers, exercising on a bicycle ergometer until they had an attack of angina. It showed a relationship between ETS and angina, at least, one supposes, in those subjects who were silly enough to go on until they actually had symptoms. Most angina sufferers would stop as soon as they decently could, claiming the attack was starting. Criticisms of the study do not put this point quite so baldly, but they do include a reference to the Hawthorne effect (subjects tend to produce symptoms suggested to them), and the extremely small number of smokers involved. [49] The criticisms also include the accusation that the senior investigator had submitted falsified data to the Food and Drug Administration. [50] Even the highly dramatic US Surgeon General, in the 1986 report, could find no more to say than that “further studies...are needed...” [51]
The National Research Council of Australia, in 1986, said: “no statistically significant effects of ETS exposure on heart rate or blood pressure were found in healthy men, women and school-aged children during resting conditions. During exercise there is no difference...”
“With respect to chronic cardiovascular morbidity and mortality [deaths from heart disease], although biologically plausible, there is no evidence of statistically significant effects due to ETS exposure, apart from the study by Hirayama in Japan.” [52] Amazing how Hirayama keeps on turning up. Perhaps he’s learnt to count. Schievelbein and Richter (1984) found that under real-life conditions people exposed to ETS inhaled only about .02 to .01 of the amount of particulate matter taken up by active smokers, and that nicotine concentration in ETS exposed people is within a range that is barely distinguishable from the background level, so exposure to ETS “is not likely to have an effect on the development and progression” of heart disease. [53] Or anything else, one would think, but don’t forget the Hawthorne effect.
It is axiomatic that as contraception becomes an aim in itself, abortion the new morality, and crimes against children mount, sentimentality about them grows correspondingly. So it was inevitable that the effects, or reputed effects, of passive smoking on children would soon be made use of.
P. Cameron, in 1967, published a paper entitled “The Presence of Pets and Smoking as Correlates of Perceived Disease”, thereby succeeding in attacking two human pleasures at once. This was based on a telephone survey of 1,000 homes in Denver. [54] The chief problem with telephone surveys, as anyone who has ever done them knows well, is that some people will agree to almost any statement you make, and answer yes or no at random, in order to get you off the telephone. So perhaps the results of the survey (an association between parental smoking and childhood respiratory problems), need not be taken entirely seriously.
However, this survey was followed by at least twenty-four others showing some sort of relationship between parental (usually maternal) smoking and various kinds of respiratory disease in the children. This was in young children under five. [55]
Another 26 studies concerned children of school-age. These were much more varied in their results, and it would not be unfair to say that for every positive result, or most of them, there was a negative one. There was an odd result or two: for example, boys seemed more at risk than girls. In 1988 Rubin and Darmus evaluated 30 studies dealing with ETS exposure and child health. They noted the existence of a few well-designed studies, we are told, but they stated that most had significant flaws in their design. [56]
There does seem to be a relationship between parental smoking and respiratory disease or symptoms in young children, though this decreases markedly as children grow older. “Among the possibilities to be considered”, we are told “are ETS, socio-economic factors and effects of maternal smoking during pregnancy and/or lactation”. [57]
It is reasonable to assume that a sensible mother would not smoke while pregnant, and certainly not when the baby was suckling or taking its bottle. It can also be said with confidence that children inherit or catch diseases from their parents, and those unfortunates handicapped by chronic complaints such as bronchitis or asthma are less likely to be able to compete successfully in the jobs’ market and thus more likely to be “socioeconomically disadvantaged”.
This is, of course, to recognise and respect those who do overcome their disabilities; nevertheless it must be acknowledged that there are those whose health problems are simply too much for them, combined perhaps with other factors. Their children are likely to be disadvantaged, whether the parents smoke or not.
A study in Hamilton, Ontario, in 1986, showed that “parental smoking, which is inversely related to family income, is positively correlated with several socio-economically related variables that can adversely influence respiratory health such as poorer outdoor air quality, increased parental coughing, higher gas stove usage, frequent change of address, and lower per capita living space.” [58]
An earlier study, in 1974, demonstrated how socioeconomic status “might confound the effect presumed to be caused by parental smoking...while parental smoking was associated with increased respiratory illness in infants, it also was associated with increased hospitalizations of infants due to injury and poisonings.” [59] The US Surgeon General’s 1979 Report noted this and stated that this suggests parental neglect rather than an effect specifically associated with parental smoking. [60]
More charitably, it could be said that parents dogged by ill health and poverty, and the problems that go with them, are less likely to be able to give their children the care they might well wish to.
Camacho et al., in a study of 1,331 children in two different residential areas, one industrial and the other rural, showed a significant association between respiratory disease and residence in the industrial area, and a strong association between the mothers’ and children’s respiratory symptoms, but no association between the mothers’ smoking habits and the children’s respiratory symptoms. [61]
In a five-year follow-up survey (important because the length of time during which the subjects are studied has a direct bearing on the reliability of the result, and many of the other studies mentioned, like the telephone survey by Cameron described above, seem to have been very much one-off affairs), Kerrebijn et al. found that “smoking and non-smoking parents have about the same proportion of children with respiratory symptoms. The number of cigarettes smoked by the parents has no influence...” [62] Taylor & Wadsworth, in 1987, found that the hospital admission rates of children with smoking mothers were not significantly different from those of children with non-smoking mothers. [63]
In general, the studies confirmed the view that it is unwise to smoke heavily in close contact with very young children, especially in a very small, unventilated room or a car, a thing that no one with any sense would do anyhow. It is sometimes said that smoking mothers have smaller babies, and C.R. Lowe, in 1959, ina survey of 2,042 pregnant women, found that the average weight of babies whose mothers smoked throughout pregnancy was 170 grams less, which was “sufficient to lower significantly the incidence of surgical induction of labour among smokers.” [64] Since surgical induction of labour is a nuisance to all concerned, and can’t be particularly good for the baby, the lesson to be drawn from this is equivocal. There is also a curious fact that doesn’t seem to have attracted any attention, but since it is based upon actual measurements that can be checked it might merit consideration:
A study of 922 former Harvard students (reported in Smoking and Health, Report of the Advisory Committee to the Surgeon General of the US Public Health Service, No. 1103), showed that:
“Smokers were consistently greater than non-smokers in height, weight, and in the dimensions of the head, face, shoulders, chest, hip, leg and hand. In addition, in eight out of ten bodily indices or proportions the smoker types showed mean deviations from the non-smoker that were all in the same direction and indicative of the same trend”. How can indirect smoking stunt a child when actual smoking plainly does not stop you from being bigger? P.N. Lee, in Environmental Tobacco Smoke and Mortality, states:
“There are particular problems...in the evaluation of any association between parental smoking, and e.g. childhood cancer, due to the difficulty of distinguishing possible genetic and transplacentally mediated effects from possible effects of ETS on the child”. [p.3.]
On eleven studies that asked about exposure to ETS in childhood the conclusion come to was that “No significant associations were seen...” where lung cancer was concerned. “The data do not indicate any association at all between risk of lung cancer and exposure to ETS...in childhood”.
Asthmatic patients used to be advised to smoke: there were even special asthma cigarettes. [65 & 66] Then in 1975, as already mentioned, C.F Tate came up with the lady and the 34 million like her who suffered from ETS. [13] Among them, he said, were 9 million asthmatics. In 1984 Muramatsu et al. reported that “a nonsmoker exposed to environmental tobacco smoke under these conditions [that is, in offices, laboratories, conference rooms, hotel lobbies, tea rooms, restaurants, cafeterias, bus and railway waiting rooms, automobiles, trains, domestic airplanes, hospital lobbies, and dwellings – which seems to include most places where people might smoke] might inhale nicotine equivalent to smoking 0.001 to 0.044 ordinary cigarettes per hour.” [67] Hinds & First reported on similar lines. [68] At another posh WHO conference held in Stockholm (another nice place) in 1979, Stahle & Tibbling brought up the theory again: that tobacco smoke is an allergen and likely to provoke acute bronchial asthma. [69]
They based this on a report that Swedish asthmatic patients had a positive reaction to skin testing with tobacco leaf extract. This is not really the same as breathing tobacco smoke. (No doubt there are many other plants that mixed up and applied to the skin would be irritating). The difference was stressed by a Swedish colleague, G. Bylin, in an article significantly entitled Tobacco Allergy – Does It Exist? [70]
In the USA, Dahms et al. reported on discomfort felt by asthmatics exposed to very high levels of smoke. Indeed, the level was recognised as unrealistic by the researchers themselves, and there were no controls in the form of non-asthmatics, which was also recognised as a mistake. Several other studies showed no reaction. [71-74] White & Froeb reported that nonsmokers exposed to ETS in their workplace for 20 years had “lower values of small-airways function”. [75]
Lenfant & Liu, in an editorial, stated:
“There is no proof as yet that the reported reduction in airways function has any physiological or clinical consequences.” [76]
D.M. Aviado also wondered where White & Froeb had managed to find a really typical group of people who had worked for 20 years without exposure to tobacco smoke, for comparison. [77] Freedman said that the study was “flawed” [78], and Lebowitz criticized it as improperly designed. [79] In general, there are four studies that describe no relationship between ETS and respiratory disease. [77, 80-83]
Certainly respiratory complaints apparently caused by ETS have been growing in number and severity. However, Aviado says that it is his conclusion that “a causal relationship has not been established”, and this is confirmed by the four other studies mentioned above. [84]
We all know people who collect diseases. They are like the people who were all bitten by “Alsatians” a few years ago – never by any other kind of dog. In fact, one suspects that they are the same people. Are they now allergic to tobacco smoke? Professor Glantz was being unusually honest, in his celebrated outburst: at least he spoke of people who “don’t like cigarette smoke”. [5]
Anyone, of course, has a right not to like cigarette smoke. We all have a right not to like something: cigarette smoke, dogs, or, in my case, garlic on the breath and dirty jeans. What I don’t think we have a right to do is to elevate our dislikes to a disease.
Of course, it is more impressive if we can. My aversion to dirty jeans is “passiver Schmutzigebaumwollehosenbestinkendesyndrom”, (this is very bad German: I meant it to be), and as such produces severe symptoms, if you give me time to think about it.
The weight of evidence on ETS shows that air quality standard levels in public places do not amount to anything that might be considered dangerous in any sense. [85] The idea that patients with angina can suffer from ETS was put forward by a researcher (Aronow) whose work has been questioned by two US government health agencies. [14 & 48]
It has not been shown that human beings are allergic to tobacco smoke. Studies on children and ETS are not conclusive. There is equally no adequate evidence to show that ETS causes respiratory disease, including bronchial asthma, in adults. Lung cancer in non-smoking women cannot be shown to be caused by their husbands’ (or presumably anyone else’s) smoking. [86]
But there is no doubt that people have symptoms. “It has been suggested” says Aviado cautiously, “that many of the symptoms reported by non-smokers may be due to psychological factors”. [87] Rummel et al. conducted a survey in which students were asked about their feelings about tobacco smoke. Those who disliked it had higher pulse rates when exposed to it than those who expressed indifference. [88] An article in the New York Times suggested that symptoms might be caused by anger rather than by the smoke itself. [89] Feinhandler, as reported by Aviado, has the very interesting suggestion that “upheavals in society and overcrowding have made people supersensitive to other people’s behaviour. Since cigarette smoke is highly visible, some individuals have reacted against the smoker as ’a ready target for general frustrations, anxiety and discontent.’” [90]
Which brings us back to the victim who is wanted. Indeed, he is necessary. We can’t persecute people for their religion, race, or sexual preferences, at least in the West. So if our “frustrations, anxiety and discontent” lead us to seek relief in making other people as unhappy as we are, there is only the smoker to seek out and hurt.
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