title: The course of persistent airflow limitation in subjects with and without asthma.
abstract: BACKGROUND
  Most patients who develop persistent airflow limitation do so either as a manifestation of chronic obstructive pulmonary disease that is largely related to smoking or as a consequence of persistent asthma. We sought to compare the natural course of lung function associated with persistent airflow limitation in subjects with and without asthma from early to late adult life.
  
  
  METHODS
  We studied 2552 participants aged 25 or more who had multiple questionnaire and lung function data from the long-term prospective population-based Tucson Epidemiological Study of Airway Obstructive Disease. Persistent airflow limitation was defined as FEV(1)/FVC ratio consistently < 70% in all completed surveys subsequent to the first survey with airflow limitation. Participants were divided into nine groups based on the combination of their physician-confirmed asthma status (never, onset < or = 25 years, or onset > 25 years) and the presence of airflow limitation during the study follow-up (never, inconsistent, or persistent).
  
  
  RESULTS
  Among subjects with an asthma onset < or = 25 years, blood eosinophilia increased significantly the odds of developing persistent airflow limitation (adjusted ORs: 3.7, 1.4-9.5), whereas cigarette smoking was the strongest risk factor for persistent airflow limitation among non-asthmatics and among subjects with asthma onset after age 25 years. Among subjects with persistent airflow limitation, the natural course of lung function differed between subjects with asthma onset < or = 25 years and non-asthmatics, with the former having lower FEV(1) levels at age 25 (predicted value for a 175-cm tall male of 3400 versus 4090 ml, respectively; p<0.001) and the latter having greater FEV(1) loss between age 25 and 75 (1590 versus 2140 ml; p=0.003).
  
  
  CONCLUSIONS
  In subjects who have asthma onset before 25 years of age and persistent airflow limitation in adult life, the bulk of the FEV(1) deficit is already established before age 25 years.
authors.affiliation: Arizona Respiratory Center, University of Arizona, Tucson, AZ, USA. sguerra@arc.arizona.edu
authors.forename: Stefano
authors.initials: S
authors.lastname: Guerra
authors.forename: Duane L
authors.initials: DL
authors.lastname: Sherrill
authors.forename: Margaret
authors.initials: M
authors.lastname: Kurzius-Spencer
authors.forename: Claire
authors.initials: C
authors.lastname: Venker
authors.forename: Marilyn
authors.initials: M
authors.lastname: Halonen
authors.forename: Stuart F
authors.initials: SF
authors.lastname: Quan
authors.forename: Fernando D
authors.initials: FD
authors.lastname: Martinez
mesh_terms: D000328:Adult; D000367:Age Factors; D017668:Age of Onset; D000368:Aged; D001249:Asthma / Q000276:immunology / Q000503:physiopathology*; D016022:Case-Control Studies; D004802:Eosinophilia / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D005541:Forced Expiratory Volume; D006801:Humans; D016015:Logistic Models; D008168:Lung / Q000276:immunology / Q000503:physiopathology*; D008173:Lung Diseases, Obstructive / Q000276:immunology / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D012907:Smoking / Q000009:adverse effects; D013997:Time Factors; D055815:Young Adult