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(Circulation. 2007;116:1845-1854.)
© 2007 American Heart Association, Inc.

Special Report

Tobacco Industry Efforts Undermining Evidence Linking Secondhand Smoke With Cardiovascular Disease

Elisa K. Tong, MD, MA; Stanton A. Glantz, PhD

From the Division of General Internal Medicine, Department of Medicine, University of California, Davis (E.K.T.), and Division of Cardiology, Department of Medicine, Cardiovascular Research Institute, and Center of Tobacco Control Research and Education, University of California, San Francisco (S.A.G.).

Correspondence to Stanton Glantz, 530 Parnassus, Ste 366, University of California, San Francisco, San Francisco, CA 94143–1390. E-mail glantz{at}medicine.ucsf.edu

Background— The scientific consensus that secondhand smoke (SHS) increases cardiovascular disease (CVD) risk by 30% is based on epidemiological and biological evidence. The tobacco industry has contested this evidence that SHS causes CVD, but how and why they have done it has not been described.

Methods and Results— About 50 million pages of tobacco industry documents were searched using general keywords and names of industry consultants and scientists. Tobacco industry–funded epidemiological analyses of large data sets were used to argue against an epidemiological association between SHS and CVD and smoke-free regulations, but these analyses all suffered from exposure misclassification problems that biased the results toward the null. More recent industry-funded publications report an increased risk of CVD associated with SHS but claim a low magnitude of risk. When early tobacco industry–funded work demonstrated that SHS increased atherosclerosis, the industry criticized the findings and withdrew funding. RJ Reynolds focused on attacking the biological plausibility of the association between SHS and CVD by conducting indirect platelet aggregation studies, exposure chamber experiments, and literature reviews. Although these studies also suffered from exposure misclassification problems, several produced results that were consistent with a direct effect of SHS on blood and vascular function. Instead, RJ Reynolds attributed these results to an unproven epinephrine-related stress response from odor or large smoke exposure, which supported their regulatory and "reduced-harm" product development efforts. Philip Morris’ recent "reduced-harm" efforts seem supportive of a similar corporate agenda.

Conclusions— The tobacco industry attempted to undermine the evidence that SHS causes CVD to fight smoke-free regulations while developing approaches to support new products that claim to reduce harm. The industry interest in preserving corporate viability has affected the design and interpretation of their cardiovascular studies, indicating the need for great caution in current debates about future tobacco industry regulation and development of reduced-harm tobacco products.

Key Words: epidemiology • lipids • platelets • public policy • tobacco smoke pollution