title: The interactions between cigarette smoking and reduced lung function on systemic inflammation.
abstract: BACKGROUND
  Low-grade systemic inflammation is commonly observed in conditions associated with reduced FEV(1). Active cigarette smoking, which is a leading risk factor for decreased FEV(1), can also independently induce systemic inflammation.
  
  
  OBJECTIVE
  To determine the independent contributions of active cigarette smoking and reduced FEV(1) (as well as their potential interactions) on systemic inflammation.
  
  
  METHODS
  Cross-sectional survey.
  
  
  METHODS
  The US general population.
  
  
  METHODS
  A total of 7,685 adult participants, >/= 40 years of age, in the Third National Health and Nutrition Examination Survey, who had acceptable data on spirometry and laboratory measurements such as serum C-reactive protein (CRP).
  
  
  METHODS
  The participants were stratified into four equal groups (quartiles) based on the percent predicted FEV(1) values. Each group was further categorized as active smokers or nonsmokers according to serum cotinine level (ie, >/= 10 or < 10 ng/mL). Serum levels of CRP, plasma fibrinogen, blood leukocytes, and platelets were compared across the predicted FEV(1) quartile groups and across smoking status using multiple logistic regression models.
  
  
  RESULTS
  We found that active smoking by itself increased the odds of having elevated CRP levels by 63% (adjusted odds ratio [OR], 1.63; 95% confidence interval, 1.28 to 2.09). The adjusted OR for reduced FEV(1) was 2.27 (95% confidence interval, 1.92 to 2.70). Having both risk factors increased the OR to 3.31 (95% confidence interval, 2.73 to 4.02). Similar findings were observed for blood leukocytes and plasma fibrinogen.
  
  
  CONCLUSIONS
  These findings suggest an additive effect of active smoking and reduced FEV(1) on markers of systemic inflammation and suggest their potential interactions in the pathogenesis of systemic complications observed in patients with poor lung function.
authors.affiliation: James Hogg iCAPTURE Center for Cardiovascular and Pulmonary Research, St. Paul's Hospital, Room No. 368A, 1081 Burrard St, Vancouver, BC, V6Z 1Y6 Canada.
authors.forename: Wen Qi
authors.initials: WQ
authors.lastname: Gan
authors.forename: S F Paul
authors.initials: SF
authors.lastname: Man
authors.forename: Don D
authors.initials: DD
authors.lastname: Sin
mesh_terms: D000328:Adult; D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D015984:Causality; D003367:Cotinine / Q000097:blood; D003430:Cross-Sectional Studies; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005541:Forced Expiratory Volume / Q000502:physiology; D006306:Health Surveys; D006801:Humans; D007958:Leukocyte Count; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D010976:Platelet Count; D029424:Pulmonary Disease, Chronic Obstructive / Q000453:epidemiology / Q000503:physiopathology*; D012307:Risk Factors; D012907:Smoking / Q000009:adverse effects* / Q000453:epidemiology / Q000503:physiopathology; D013223:Statistics as Topic; D018746:Systemic Inflammatory Response Syndrome / Q000453:epidemiology / Q000503:physiopathology*; D014481:United States
chemical_list: D005340:Fibrinogen; D002097:C-Reactive Protein; D003367:Cotinine