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J Am Coll Cardiol, 2010; 56:18-23, doi:10.1016/j.jacc.2010.03.032
© 2010 by the American College of Cardiology Foundation
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QUARTERLY FOCUS ISSUE: PREVENTION/OUTCOMES: CLINICAL RESEARCH: CARDIOVASCULAR RISK

Objectively Measured Secondhand Smoke Exposure and Risk of Cardiovascular Disease

What Is the Mediating Role of Inflammatory and Hemostatic Factors?

Mark Hamer, PhD*,*, Emmanuel Stamatakis, PhD*, Mika Kivimaki, PhD*,{dagger}, Gordon D. Lowe, DSc{ddagger} and G. David Batty, PhD*,§

* Department of Epidemiology and Public Health, University College London, London, United Kingdom
{dagger} Finnish Institute of Occupational Health and University of Helsinki, Helsinki, Finland
{ddagger} Division of Cardiovascular and Medical Sciences, University of Glasgow, and Haemophilia and Thrombosis Centre, Royal Infirmary, Glasgow, United Kingdom
§ Medical Research Council Social and Public Health Sciences Unit, Glasgow, United Kingdom

Manuscript received December 15, 2009; revised manuscript received February 17, 2010, accepted March 18, 2010.

* 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 (Email: m.hamer{at}ucl.ac.uk).

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.

Key Words: cotinine • epidemiology • inflammation • mortality • nicotine • passive smoke

Abbreviations and Acronyms
  CI = confidence interval
  CRP = C-reactive protein
  CV = coefficient of variation
  CVD = cardiovascular disease
  HDL = high-density lipoprotein
  SHS = secondhand smoke


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