Further Information

A Review of the Epidemiology of ETS and Heart Disease | P.N. Lee
Article Published: 1997

Type: Meta-Analysis
Funding Source: see further information
Published By: P.N. Lee Statistics and Computing Ltd

Further Information

The false information that ETS “causes” heart disease is the product of most dishonest methodology, and a glaring example of intentional use of distorted information to scare and coerce an ignorant and gullible population through the mass-media. The executive summary of this thorough and massive meta-analysis is self-explanatory (emphasis added).

"It has been suggested that epidemiological studies of heart disease in nonsmokers support the hypothesis that environmental tobacco smoke (ETS) causes heart disease. This document examines this suggestion in detail, presenting an extensive review of the epidemiological evidence.

Data from 23 epidemiological studies of ETS and heart disease among lifelong nonsmokers have been considered. Nearly all the studies present results for females, with about half presenting results for males. A variety of indices of ETS exposure have been used in these studies. Most studies present results relating to smoking by the spouse, or other index of athome ETS exposure, with workplace ETS exposure the other commonly used index. Spousal results relate sometimes to current and sometimes to ever smoking by the husband/wife.

The epidemiological evidence relating ETS and heart disease is most unconvincing.

There is no significant association with ETS exposure in the workplace. While the overall data from the 23 studies do show a significant association with spousal smoking, whether ever smoking by the spouse (relative risk adjusted for covariates 1.07, 95% CI 1.03-1.10) or current smoking by the spouse (1.08, 95% CI 1.05-1.12) is used as the index, the association is quite
weak and could well be a result of various forms of bias. These include:
  1. misclassification of smoking habits - there is evidence suggesting that smokers with nonfatal myocardial infarction, who are at high risk of subsequent death from heart disease,often ignore advice by their doctors to give up smoking but deny smoking on interview;
  2. uncontrolled confounding - although adjustment for potential confounding factors was frequently found to modify spousal smoking relative risk estimates substantially, many studies had not controlled even for the major coronary risk factors;
  3. recall bias - independent validation of reported ETS exposure was hardly ever carried out, and one study that did so provided strongly suggestive evidence that presence of disease may affect responses to questions on ETS exposure; and
  4. publication bias - there was a clear tendency for spousal smoking relative risk estimates to be higher in smaller studies, consistent with publication bias.
There is also striking evidence of variation in spousal smoking relative risk estimates between three groups of studies:
  1. three recent studies without any apparent major weaknesses, each involving more than 1000 cases. In these there was no clear evidence of any increased risks (ever smoking by spouse 1.02, 95% CI 0.99-1.06; current smoking by spouse 1.04, 95% CI 1.00-1.08),
  2. five other studies also without major weaknesses but generally involving less than 1000 cases. In these the relative risk estimates were lower but still indicative of a positive association (ever or current smoking by spouse 1.22, 95% CI 1.11-1.34), and
  3. the remaining studies, which were reported only as abstracts or dissertations, involved less than 100 heart disease cases, and/or had identified major weaknesses. In such studies the spousal smoking relative risk estimates tended to be very high (ever smoking by spouse 1.50, 95% CI 1.30-1.72; current smoking by spouse 1.54, 95% CI 1.33-1.77).
It was also notable that, though there was some evidence of a dose-relationship in the last two groups of studies, there was no evidence of such a relationship in the first group, which included one study involving almost 15,000 heart disease deaths in nonsmokers. When all the evidence is considered, the epidemiological data do not demonstrate that exposure to ETS increases the risk of heart disease.

This document also contains a briefer commentary dismissing claims by Glantz and Parmley that clinical and laboratory evidence demonstrates that ETS causes heart disease."

But now, please believe nothing of what you read. Here is why:

"I thank Mrs B A Forey for considerable help in assembling the database and for programming, and Dr F J C Roe, Dr A Springall and Dr J S Fry for helpful comments. Dr Roe also assisted greatly in preparing Appendix D. I also thank Mrs P Wassell and Mrs F Lennard for typing the numerous drafts and Mrs K J Young for detailed checking of this report. I am grateful to various tobacco companies for providing financial support. I alone bear responsibility for the views expressed."

As "everyody knows," two plus two never equals four if just a penny in that equation comes from the tobacco industry. If it comes from the pharmaceutical industry, however, then anything goes — and it's all true.

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