Author + information
- Received December 15, 2009
- Revision received February 17, 2010
- Accepted March 18, 2010
- Published online June 29, 2010.
- Mark Hamer, PhD⁎,⁎ (, )
- Emmanuel Stamatakis, PhD⁎,
- Mika Kivimaki, PhD⁎,†,
- Gordon D. Lowe, DSc‡ and
- G. David Batty, PhD⁎,§
- ↵⁎Reprint requests and correspondence:
Dr. Mark Hamer, Department of Epidemiology and Public Health, University College London, 1-19 Torrington Place, London WC1E 6BT, United Kingdom
Objectives The aim of this study was to examine the association between objectively measured secondhand smoke (SHS) exposure and incident cardiovascular disease (CVD) death and assess the extent to which this association can be explained through novel circulating markers of inflammation and hemostasis.
Background Existing evidence suggests there is an association between SHS and CVD risk, although the mechanisms remain poorly understood.
Methods In a prospective study of 13,443 participants living in England and Scotland (age 53.5 ± 12.6 years, 52.3% women), we measured salivary cotinine (an objective marker of SHS exposure) and novel CVD biomarkers (C-reactive protein, fibrinogen) at baseline.
Results Of the sample, 20.8% had high SHS exposure on the basis of elevated levels of salivary cotinine (range 0.71 to 14.99 ng/ml). During a mean follow-up of 8 years, there were 1,221 all-cause deaths and 364 CVD deaths. High SHS was associated with all-cause (age-adjusted hazard ratio [HR]: 1.25, 95% confidence interval [CI]: 1.02 to 1.53) and CVD death (age-adjusted HR: 1.21, 95% CI: 0.85 to 1.73). High SHS was also associated with elevated CRP, which explained 48% of the association between SHS and CVD death. The excess risk of CVD associated with active smoking was exaggerated in relation to self report (age-adjusted HR: 3.27, 95% CI: 2.48 to 4.31) compared with objective assessment (age-adjusted HR: 2.44, 95% CI: 1.75 to 3.40).
Conclusions Among a large representative sample of British adults we observed elevated levels of low-grade inflammation in otherwise healthy participants exposed to high SHS, and this partly explained their elevated risk of CVD death.
The Scottish Health Survey is funded by the Scottish Executive. The views expressed in this article are those of the authors and not necessarily of the funding bodies. Dr. Hamer is supported by the British Heart Foundation(RG 05/006). Dr. Stamatakis is a National Institute for Health Research Fellow. Dr. Kivimaki is supported by the National Heart, Lung, and Blood Institute(R01HL036310) and the National Institute on Aging(R01AG034454), National Institutes of Health, U.S., and the Academy of Finland. Dr. Batty is a Wellcome Trust Career Development Fellow (WBS U.1300.00.006.00012.01). The Medical Research Council (MRC) Social and Public Health Sciences Unit receives funding from the UK MRCand the Chief Scientist Officeat the Scottish Government Health Directorates.
- Received December 15, 2009.
- Revision received February 17, 2010.
- Accepted March 18, 2010.
- American College of Cardiology Foundation