title: Objectively measured secondhand smoke exposure and risk of cardiovascular disease: what is the mediating role of inflammatory and hemostatic factors?
abstract: OBJECTIVE
  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.
authors.affiliation: Department of Epidemiology and Public Health, University College London, London, United Kingdom. m.hamer@ucl.ac.uk
authors.forename: Mark
authors.initials: M
authors.lastname: Hamer
authors.forename: Emmanuel
authors.initials: E
authors.lastname: Stamatakis
authors.forename: Mika
authors.initials: M
authors.lastname: Kivimaki
authors.forename: Gordon D
authors.initials: GD
authors.lastname: Lowe
authors.forename: G David
authors.initials: GD
authors.lastname: Batty
mesh_terms: D015415:Biomarkers / Q000097:blood*; D002097:C-Reactive Protein / Q000032:analysis*; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000401:mortality; D003367:Cotinine / Q000032:analysis; D005260:Female; D005340:Fibrinogen / Q000032:analysis*; D005500:Follow-Up Studies; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000097:blood; D008297:Male; D008875:Middle Aged; D012463:Saliva / Q000737:chemistry; D014028:Tobacco Smoke Pollution / Q000032:analysis*
chemical_list: D015415:Biomarkers; D014028:Tobacco Smoke Pollution; D005340:Fibrinogen; D002097:C-Reactive Protein; D003367:Cotinine