title: Systemic inflammation and lung function: A longitudinal analysis.
abstract: BACKGROUND
  Systemic inflammation is associated with impaired lung function in healthy adults as well as in patients with lung disease. The mechanism for this association is unknown and it is unclear if systemic inflammation leads to impaired lung function or if poor lung function leads to inflammation. We explored the temporal associations between blood C-reactive protein (CRP), fibrinogen, and white blood cells, and lung function in young adults.
  
  
  METHODS
  Spirometry, plethysmography, and diffusion capacity were measured in a population-based cohort at ages 32 and 38 years. High-sensitivity CRP, fibrinogen, and white blood cells were measured at the same ages.
  
  
  RESULTS
  Higher levels of CRP and, to a lesser extent, fibrinogen were associated with lower lung volumes in cross-sectional analyses at both ages 32 and 38 years. Higher CRP and fibrinogen at age 32 were associated with higher FEV1 and FEV1/FVC at age 38, but not other measures of lung function. Lower lung volumes (total lung capacity, functional residual capacity, and residual volume) but not airflow obstruction (FEV1/FVC) at age 32 were associated with higher CRP at age 38. Associations between age 32 lung function and fibrinogen at follow-up were weaker, but consistent. There were no longitudinal associations between white blood cells and lung function.
  
  
  CONCLUSIONS
  We found no evidence that systemic inflammation causes a decline in lung function. However, lower lung volumes were associated with higher CRP and fibrinogen at follow-up indicating that pulmonary restriction may be a risk factor for systemic inflammation. The mechanism for this association remains unclear.
authors.affiliation: Department of Preventive & Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand. Electronic address: bob.hancox@otago.ac.nz.
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Hancox
authors.affiliation: Department of Preventive & Social Medicine, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
authors.forename: Andrew R
authors.initials: AR
authors.lastname: Gray
authors.affiliation: Department of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada.
authors.forename: Malcolm R
authors.initials: MR
authors.lastname: Sears
authors.affiliation: Department of Psychology, University of Otago, Dunedin, New Zealand.
authors.forename: Richie
authors.initials: R
authors.lastname: Poulton
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D015331:Cohort Studies; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000503:physiopathology*; D008137:Longitudinal Studies; D008168:Lung / Q000378:metabolism / Q000503:physiopathology*; D008297:Male; D010991:Plethysmography / Q000379:methods; D011653:Pulmonary Diffusing Capacity / Q000379:methods; D012129:Respiratory Function Tests / Q000379:methods; D013147:Spirometry / Q000379:methods
chemical_list: D002097:C-Reactive Protein
keywords: C-reactive protein; Cohort studies; Inflammation; Pulmonary function