Smoking movies 2
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Glamourising: Audrey Hepburn in Breakfast at Tiffany's made cigarette holders stylish.
Introduction

I was looking YouTube and noticed in one of the comments that I was accused of advocating smoking as a "healthy food". It was nonsense, of course, but it set me wondering where the writer of the comment had got the idea from.

It turned out that it was from an article I have on this website about diesel smoke being worse than cigarette smoke, written by the late Dr Kitty Little in 1999.

Anyway, it got me looking at the evidence for and against smoking and heart disease again. And caused my to write the following article - because the issue is not as clear as it might appear.

The smoking debate


Smoking, particularly cigarette smoking, was first indicted as a cause of lung cancer in the 1950s. Subsequently, it was blamed for many other diseases including cardiovascular disease. But, while there are certainly many papers in the medical literature which attest to smoking as a causal factor in these diseases, there are also a worrying number which refute them.

In the history of heart disease, stopping smoking has been recommended consistently for over half a century, along with lowering cholesterol, dietary changes and exercise to prevent the disease; the four have gone together. Falling incidences of CHD in various countries during the middle of the last century are regarded as a result of national policies on reduction in smoking as well as dietare changes. However, graphs of the rise of heart disease in various age groups in the USA and its subsequent fall from 1900 to 1978, together with trends in smoking over the period, plotted by Stallones in 1980, showed a complete lack of evidence that they are linked.1

Other studies have come up with similar findings. After discussing the difficulties arising from changing international definitions, Marmot and colleagues looked at trends in deaths from heart disease in 18 countries throughout the world. They considered differences between men and women and between social classes in England and Wales, and changes in smoking and dietary habits, concluding that no one single factor has been responsible for all the changes.2

On smoking, they say:
"Not all of these factors fit the trends in IHD exactly. For example, the mortality from stroke was already falling in the 1950s and 1960s and the mortality from heart disease began to decline in the mid-1960s, whereas the big change in the proportion of hypertensives successfully treated probably did not occur until the 1970s. Nevertheless it seems likely that changes in diet, smoking and blood pressure control have all played a part in reducing ischaemic heart disease in American men."
They continue:
"The picture in women is less clear. American women have not reduced their level of smoking - in fact the proportion of those who smoke has risen in some groups - yet their death rates from heart disease began to fall before the men's."
It's no surprise, therefore, that the routine data which highlighted first the increased male proneness to heart attacks over and above their higher incidence of coronary heart disease, and that trends in mortality in both sexes from coronary heart disease do not follow the patterns anticipated by recent trends in cigarette smoking.3 Or that:
"Ischaemic heart disease is still a major public health problem in this country and current information suggests that preventive and curative medicine, regretfully, have made little impact."
In 1987, Dr J Shepherd and colleagues noted that the assumption that the falling rates of heart disease in USA, Finland, Israel, Australia was as a result of intervention in smoking and diet was wrong.

"Decreases in their prevalences have been attributed to the success of national policies aimed at the general population to stop cigarette smoking and to promote the consumption of a diet low in saturated fat." But they note that changes in mortality and morbidity started before interventions could be effective.4

Smoking might be beneficial

Published in 1989, the Framingham Heart Study examined the data on smoking in association with CHD in both men and women over a follow-up period of thirty years and found no evidence that smoking increases the risk of CHD - "Thus, in the Framingham Study's multivariable analyses, the former associations between cigarette smoking and CHD "disappear" when additional pertinent confounding factors are taken into account."5

Smoking might be beneficial - "...almost none of the risk ratios in women exceeds 1. In fact, most of the ratios are slightly below unity, suggesting that CHD may have a slightly higher incidence among nonsmokers than smokers."

"The effect of the duration of cigarette smoking is also shown indirectly by the decline, with increasing age, of CHD mortality and morbidity ratios for cigarette smokers, compared with nonsmokers. Older smokers in the Framingham data have a lower relative risk of CHD than younger smokers, despite the presumably greater duration of smoking in the older group."

"The results showed a striking surprise: the CHD rate was higher for never-smokers than for exsmokers. The respective age-adjusted incidence of CHD ... at 12-years of follow-up, after the 4th examination, was 8.3/1000 for ex-smokers and 12.0/1000 for never smokers."

On this last point, the investigators have publicly confirmed the finding by stating that "The Framingham data ... have always shown that men who never smoked had HIGHER mortality rates than men who quit..."

"...the odd implication that it is better to have smoked and stopped than never to have smoked at all."

Three other trials confirmed the Framingham data: The London Civil Servants single factor trial of smoking found no benefit in giving up (J Epidemiol Commun Med 1982; 36: 102-8); the Oslo two factor trial (diet and smoking) showed a CHD benefit but the results were confounded by changes in cholesterol (J Oslo City Hosp 1982; 32: 31-54); and the MRFIT showed no significant differences in total or CHD deaths although the magnitude of cigarette smoking was reduced beyond the anticipated goals (JAMA 1982; 249: 1465-77).

Passive smoking may also be beneficial

But smoking itself is not the only perceived problem. That may harm only the smoker, himself. What worries the legislators are the believed dangers from inhaling someone else's smoke, known as passive smoking. But this worry may also be unfounded.

Here is the biggest study we have been able to find into the effects of passive smoking. A study of 118,094 people over a period of almost forty years.

In late 1959 the American Cancer Society enrolled 118 094 adults in its cancer prevention study (CPSI). They were followed from 1960 until 1998. Particular focus was on the 35,561 who had never smoked but who had a spouse in the study who did smoke.

What the study aimed to measure was the relative risks for deaths from coronary heart disease, lung cancer, and chronic obstructive pulmonary disease related to smoking in spouses and active cigarette smoking.

What the study found was not what was expected. For the participants followed from 1960 until 1998 the age adjusted relative risk (95% confidence interval) for never smokers married to ever smokers compared with never smokers married to never smokers was:

Men (9619 )
  • 0.94 (0.85 to 1.05) for coronary heart disease,
  • 0.75 (0.42 to 1.35) for lung cancer, and
  • 1.27 (0.78 to 2.08) for chronic obstructive pulmonary disease
Women (25,942)
  • 1.01 (0.94 to 1.08) for coronary heart disease
  • 0.99 (0.72 to 1.37) for lung cancer,
  • 1.13 (0.80 to 1.58) for chronic obstructive pulmonary disease.
(Note that a risk figure less than 1.0 means benefit; over 1.0 indicates harm. Thus, in men, while passive smoking increased the risk of chronic obstructive pulmonary disease by a relative 27%, it reduced the risk of coronary heart disease by 6% and, perhaps surprisingly, reduced lung cancer risk by 25%. In women, passive smoking had little or no statistically significant effect other than a slight increased risk of chronic obstructive pulmonary disease.)

No significant associations were found for current or former exposure to environmental tobacco smoke before or after adjusting for seven confounders and before or after excluding participants with pre-existing disease.

The study concluded that "The results do not support a causal relation between environmental tobacco smoke and tobacco related mortality, although they do not rule out a small effect. The association between exposure to environmental tobacco smoke and coronary heart disease and lung cancer may be considerably weaker than generally believed."

Weaker? According to their figures, they should surely have concluded that passive smoking was beneficial in those two diseases, in men at least.

So how did the smoking get its bad name?

In 1976, Doll and Peto had issued a paper in which they reported that daily cigarette consumption by the British doctors who had been studied in connection with the 1964 Surgeon General's report had declined from 9.1 in 1951 to 3.6 in 1971. Doll and Peto claimed that, as a result there was a 38% reduction in lung cancer death rates amongst the doctors.

In a review of Doll and Peto's paper however, Philip R. J. Burch, a professor of Medical Physics at the University of Leeds, showed that Doll and Peto had made a critical error: they had compared the lung cancer death rates among the doctors with the lung cancer death rates for the entire British male population. Burch re-plotted the data to compare the doctors with themselves and showed that, on that basis, the risk for lung cancer amongst the doctors who had given up smoking had actually increased by 31%.7

In the same paper, Burch plotted cigarette consumption for women and men in England and Wales against lung cancer death rates, during the period 1890 to 1971. He showed that the largest increases in lung cancer death rates in both sexes came during the time periods 1916-1920 and 1931-35. Those periods were at a time when cigarette consumption among women in England and Wales was very small. From this Burch concluded that the rise in lung cancer was due to improved diagnosis, not smoking.

In England and Wales, there was, in fact, a 30 year gap between the time when males began smoking and females. So it is not surprising that the anti-smoking crowd in Britain made the argument that recent (in 1966) increases in lung cancer among women resulted from a "30 year incubation period".

Burch effectively refuted that argument by plotting lung cancer rates for males in 1906 through 1926, against female rates for 1936 to 1966, and showed that, if the incubation theory was correct, the two curves should have been similar; they were in fact completely different.

Nevertheless, Doll and Peto's hypothesis caught on with the anti-smoking lobby at the time and smoking came to be blamed for almost every disease known to Man.

Publication bias

There is also the problem of publication bias. Publication bias is where, if a study doesn't say what a journal editor wants it to say, or what advertisers want to see, or if it is not poltically correct, it won't get published

Publication bias is common throughout medical publications, but is considerably more obvious in the case of tobacco and smoking.

Below is the abstract of a paper looking at this very subject.

Abstract8

Two approaches are used to assess publication bias in the environmental tobacco smoke/coronary heart disease (ETS/CHD) literature:

(1) Statistical tests applied to all sex-specific relative risk (rr) estimates from 14 previously published studies indicate that publication bias is likely. A funnel graph of the studies' log relative risks plotted against their standard errors is asymmetrical, and weighted regression of the studies' log relative risks on their standard errors is significant (P < 0.01).

(2) Previously unpublished ETS/CHD relative risks from the American Cancer Society's Cancer Prevention Studies (CPS-I and CPS-II) and the National Mortality Followback Survey (NMFS) do not show an increased CHD risk associated with ETS exposure.
  • CPS-I: men, rr = 0.97 (0.90-1.05);
  • CPS-I: women, rr = 1.03 (0.98-1.08);
  • CPS-II: men, rr = 0.97 (0.87-1.08);
  • CPS-II: women, rr = 1.00 (0.88-1.14);
  • NMFS: men, rr = 0.97 (0.73-1.28);
  • NMFS: women, rr = 0.99 (0.84-1.16).
Comparison of pooled relative risk estimates from 14 previously published studies (rr = 1.29; 1.18-1.41) and unpublished results from three studies (rr = 1.00; 0.97-1.04) also indicates that published data overestimate the association of spousal smoking and CHD (chi 2 = 25.1; P < 0.0001).

The bottom Line

So, where does that leave smoking as a cause of heart disease? Well there are two sides to the debate - and a lot of money to be made out of staying with the status quo. I am not qualified to suggest that smoking does not cause many of the conditions that it is blamed for, including heart disease. But I do think that it is an argument that needs to be looked at with some caution.

References

1. Stallones RA. The Rise and Fall of Ischaemic Heart Disease. Scientific American 1980; 243: 43-9.

2. Marmot MG, Booth M, Beral V. Changes in heart disease mortality in England and Wales and other countries. Hlth Trends 1981; 13: 33-38.

3. Silman AJ. Routinely collected data and ischaemic heart disease in the United Kingdom. Hlth Trends 1981; 13: 39-42.

4. Shepherd J, Betteridge DJ, Durrington P, et al. Strategies for reducing coronary heart disease and desirable limits for blood lipid concentrations: guidelines of the British Hyperlipidaemia Association. BMJ 1987; 295: 1245-6

5. Seltzer CC. Framingham Study data and "established wisdom" about cigarette smoking and coronary heart disease. J Clin Epidemiol 1989; 42 (8): 743-50.

6. Enstrom JE, Kabat GC. Environmental tobacco smoke and tobacco related mortality in a prospective study of Californians, 1960-98. BMJ 2003;326:1057

7. Burch PRJ. Smoking and lung cancer: the problem of inferring cause. J Royal Statistical Society 1998; 141:437-477.

8. LeVois ME, Layard MW. Publication bias in the environmental tobacco smoke/coronary heart disease epidemiologic literature. Regul Toxicol Pharmacol. 1995;21:184-91.