title: Occupational exposures, smoking and airway inflammation in refractory asthma.
abstract: BACKGROUND
  The influence of occupation and ex/passive smoking on inflammatory phenotype is not well understood. The aim of this study was to examine the relationship between occupation, past smoking and current passive smoking and airway inflammation in a population of adults with refractory asthma.
  
  
  METHODS
  Sixty-six participants with refractory asthma were characterised. Occupational exposure to asthma causing or worsening agents were identified with an asthma-specific job exposure matrix. Exposure to passive cigarette smoke was determined by questionnaire and exhaled carbon monoxide assessment. The carbon content of macrophages was assessed in a sub-group of participants.
  
  
  RESULTS
  Nineteen participants had smoked previously with low smoking pack years (median 1.7 years). Ex-smokers more commonly lived with a current smoker (26% vs. 9%, p = 0.11) and were more likely to allow smoking inside their home (26% vs. 4%, p = 0.02) compared to never smokers. Twenty participants had occupations with an identified exposure risk to an asthmagen; thirteen had exposures to irritants such as motor vehicle exhaust and environmental tobacco smoke. Sputum neutrophils were elevated in participants with asthma who had occupational exposures, particularly those who were diagnosed with asthma at a more than 30 years of age.
  
  
  CONCLUSIONS
  Sputum neutrophils are elevated in refractory asthma with exposure to occupational asthmagens. In addition to older age, exposure to both environmental and occupational particulate matter may contribute to the presence of neutrophilic asthma. This may help explain asthma heterogeneity and geographical variations in airway inflammatory phenotypes in asthma.
authors.affiliation: Centre for Asthma and Respiratory Disease, Faculty of Health and Medicine, The University of Newcastle, Callaghan, NSW, Australia. jodie.simpson@newcastle.edu.au.|Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. jodie.simpson@newcastle.edu.au.
authors.forename: Jodie L
authors.initials: JL
authors.lastname: Simpson
authors.affiliation: School of Health Sciences, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW, Australia. maya.guest@newcastle.edu.au.
authors.forename: Maya
authors.initials: M
authors.lastname: Guest
authors.affiliation: School of Health Sciences, Faculty of Health and Medicine, University of Newcastle, Callaghan, NSW, Australia. mboggess@asu.edu.|School of Mathematical and Statistical Sciences, Arizona State University, Tempe, AZ, USA. mboggess@asu.edu.
authors.forename: May M
authors.initials: MM
authors.lastname: Boggess
authors.affiliation: Centre for Asthma and Respiratory Disease, Faculty of Health and Medicine, The University of Newcastle, Callaghan, NSW, Australia. peter.gibson@hnehealth.nsw.gov.au.|Department of Respiratory and Sleep Medicine, Hunter Medical Research Institute, New Lambton Heights, NSW, Australia. peter.gibson@hnehealth.nsw.gov.au.
authors.forename: Peter G
authors.initials: PG
authors.lastname: Gibson
mesh_terms: D000368:Aged; D001249:Asthma / Q000453:epidemiology / Q000276:immunology; D059366:Asthma, Occupational / Q000453:epidemiology* / Q000276:immunology; D001315:Australia / Q000453:epidemiology; D001944:Breath Tests; D002248:Carbon Monoxide / Q000032:analysis; D002452:Cell Count; D005260:Female; D006801:Humans; D007249:Inflammation; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000166:cytology*; D016273:Occupational Exposure / Q000706:statistics & numerical data*; D012907:Smoking / Q000453:epidemiology* / Q000276:immunology; D013183:Sputum / Q000166:cytology; D014028:Tobacco Smoke Pollution / Q000706:statistics & numerical data*; D001335:Vehicle Emissions
chemical_list: D014028:Tobacco Smoke Pollution; D001335:Vehicle Emissions; D002248:Carbon Monoxide