Letters

Passive smoking and heart disease

Authors need to analyse the same data

Evidence on passive smoking and heart disease needs re-evaluation

BMJ should encourage open debate of available evidence

There must be better uses for money spent on vilifying passive smoking

Authors' reply

Authors need to analyse the same data

EDITORIn their meta-analysis Law et al¹ reject results we published ^{2 3} on environmental tobacco smoke and coronary heart disease, using data from the two large cancer prevention studies by the American Cancer Society and the national mortality followback survey. They reject our results because they disagree with our interpretation of data from other studies and because our analysis was funded by the tobacco industry (table 1).

By excluding our results Law et al discard 16 280 relevant deaths from coronary heart disease with spousal smoking data and retain 6600 cases. They give no hint that their meta-analysis includes under a third of the available published data. The reasons for rejecting so many data should be considered. If Law et al believe we have misrepresented the data, they should analyse the same data from the American Cancer Society and the national mortality followback survey, and report their results.

Law et al's argument that our data from the second cancer prevention study disagree appreciably with data reported by Steenland et al⁴ is wrong.⁵ They incorrectly compare our results for ever-smoking spouse exposure with Steenland et al's results for current-smoking spouse exposure. Both studies present comparable results for subjects in the second cancer prevention study who are married to a current smoker. We calculate the relative risk for men to be 1.30 (95% confidence interval 1.11 to 1.51), for women 1.08 (0.89 to 1.32), and for both sexes combined 1.21 (1.07 to 1.37). These results are similar to those reported by Steenland et al (men 1.22 (1.07 to 1.40), women 1.10 (0.96 to 1.27)),⁴ which we have combined to give a relative risk of 1.16 (1.05 to 1.27) for both sexes.

Both sets of analyses report a barely significant association between environmental tobacco smoke and coronary heart disease in men, with a negative dose response. There is no significant association between spousal smoking and death from coronary heart disease in women, nor any sign of a dose response. Nearly twice as many women as men died of coronary heart disease in the second cancer prevention study, which makes the data for women particularly relevant to any meta-analysis.

Law et al's selective rejection of two thirds of the relevant data on environmental tobacco smoke and coronary heart disease raises additional questions about their interpretation of other data. We have noted significant publication bias in the pooled results on environmental tobacco smoke and coronary heart disease, for example.² In reaching the opposite conclusion, Law et al ignore the significant association between study size and relative risk in the previously published spousal smoking studies as well as the significant difference between published and unpublished results on environmental tobacco smoke and coronary heart disease.

^* M E LeVois and M W Layard hold outside consultancies with the Tobacco Institute, 1901 K Street, Washington, DC 20001, USA.

1. Law MR, Morris JK, Wald NJ. Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence. BMJ 1997; 313: 973-980. (18 October.)
2. LeVois ME, Layard MW. Publication bias in the environmental tobacco smoke/coronary heart disease epidemiologic literature. Regul Toxicol Pharmacol 1995; 21: 184-191[Medline].
3. Layard MW. Ischemic heart disease and spousal smoking in the national mortality followback survey. Regul Toxicol Pharmacol 1995; 21: 180-183[Medline].
4. Steenland K, Thun M, Lally C, Heath Jr C. Environmental tobacco smoke and coronary heart disease in the American Cancer Society CPS-II cohort. Circulation 1996; 94: 622-628[Abstract/Free Full Text].
5. LeVois ME, Layard MW. Letter to the editor re: Steenland et al. Circulation 1997; 96: 2086-2087.

Evidence on passive smoking and heart disease needs re-evaluation

EDITORLaw et al estimate that there is a 30% excess risk associated with spousal smoking on the basis of 6600 deaths from heart disease in 19 epidemiological studies.¹ They distort the estimate by omitting results that are based on 15 000 deaths from heart disease from the first cancer prevention study by the American Cancer Society. That study reported on spousal smoking and lung cancer in 1981.² Ten years ago the society told me that the study showed no effect on heart disease, but it never published its findings. Law et al reject published analyses of this study by LeVois and Layard³ because they are tobacco consultants and their analyses of the second cancer prevention study cited different relative risks from those reported by the American Cancer Society.⁴ Both analyses actually reported similar findingsa small decrease in risk for spouses who were former smokers and a small, non-dose related, increase for spouses who were current smokers. The "difference" arose because LeVois and Layard followed precedent in concentrating on the index "spouse ever smoked" whereas the society emphasised results for "spouse current smoker." For the first cancer prevention study the risk was not increased for either index. If Law et al wish to reject analyses by tobacco consultants, they should have analysed the study themselves in order to avoid publication bias.

Law et al dismiss smoking misclassification bias as unimportant, ignoring recent evidence that smokers who deny smoking have a risk of heart disease that is 4.0 times higher (95% confidence interval 1.8 to 9.1) than that of smokers who admit to smoking.⁵ Their consideration of confounding relates only to a few of the many risk factors for heart disease.

Law et al say that the risks from passive smoking and smoking one cigarette a day are similaran acute response to effects on platelets. This is based on a questionable backward linear extrapolation from data on risk by amount smoked (ignoring the known relative risk of 1.0 in non-smokers) and unjustified reliance on results from one single study of platelet aggregation in 10 subjects exposed to passive smoking in a hospital corridor.

This argument implies virtually no dose-response relation between risk in non-smokers and the extent of their exposure to environmental smoke, but Law et al never consider the dose-response data for passive smoking. The table shows that the results from the studies tend to fall into two groupssmall studies reporting a moderate association and marked dose response and large studies reporting essentially no overall association or dose response. Neither group of results is consistent with the authors' theories.

The conclusion that passive smoking is an important cause of heart disease is premature. The data require further evaluation.

^* Peter Lee acts as a consultant to the tobacco industry.

1. Law MR, Morris JK, Wald NJ. Environmental tobacco smoke exposure and ischaemic heart disease: an evaluation of the evidence. BMJ 1997; 315: 973-980[Abstract/Free Full Text]. (18 October.)
2. Garfinkel L. Time trends in lung cancer mortality among nonsmokers and a note on passive smoking. J Natl Cancer Inst 1981; 66: 1061-1066.
3. LeVois ME, Layard MW. Publication bias in the environmental tobacco smoke/coronary heart disease epidemiologic literature. Regul Toxicol Pharmacol 1995; 21: 184-191.
4. Steenland K, Thun M, Lally C, Heath C. Environmental tobacco smoke and coronary heart disease in the American Cancer Society CPS-II cohort. Circulation 1996; 94: 622-628.
5. Suadicani P, Hein HO, Gyntelberg F. Mortality and morbidity of potentially misclassified smokers. Int J Epidemiol 1997; 26: 321-327[Abstract/Free Full Text].

BMJ should encourage open debate of available evidence

EDITORAs a principal scientist for Philip Morris I am aware that many readers will take the views expressed in this letter somewhat cynically. I appeal to readers' scientific objectivity and urge them to give due consideration to the issues raised below.

Law et al claim a potential relation between environmental tobacco smoke and ischaemic heart disease.¹ They exclude the largest datasets available on the subject because they have "been published by Layard and LeVois, consultants to the tobacco industry."¹ These data represent about twice as many ischaemic heart disease events as the other 19 studies added together. Law et al also mislead readers into believing that LeVois and Layard's analyses are inconsistent with the rest of the evidence. This is not the case: several of the 19 studies they selected for analysis report similar findings to those of LeVois and Layard. The results of one of the three studies published by LeVois and Layard² are not inconsistent with the findings of an independent analysis of the same data by the American Cancer Society.³ A straightforward comparison shows mostly similaritiesthe only apparent differences are caused by the emphasis the different authors give to different reference groups.

This type of exclusion is symptomatic of the one-sided nature of the debate surrounding tobacco. There are other scientific flaws in Law et al's study. Unfortunately, even though many other scientists with no particular affection for the tobacco industry may share my views, few will speak out on this issue for fear of being branded as sympathisers of the industry. This is a disservice to science and erodes one of the fundamental tools of scientific investigationthe opportunity to debate.

Would the BMJ be willing to try to rectify some of the damage done to the scientific process and encourage correspondence from independent scientists whose views may be contrary to those of Law et al? Perhaps a direct invitation from the BMJ's editor would diminish the reluctance of such scientists to participate in the debate.

The issues raised by such papers have important implications for public health. It is therefore vital that they have a sound scientific basis. I believe that there are scientifically valid grounds for doubting the interpretation of the evidence given by Law et al. A fear of repercussions affecting anyone who voices an opinion that could be favourable to the tobacco industry seems to be preventing this process from taking place. We should all be striving to open up the debate, allowing sound scientific principles to decide on the best interpretation of the available evidence. I hope that the BMJ will play its part in facilitating this.