title: Different airway inflammatory responses in asthmatic and healthy humans exposed to diesel.
abstract: Particulate matter (PM) pollution adversely affects the airways, with asthmatic subjects thought to be especially sensitive. The authors hypothesised that exposure to diesel exhaust (DE), a major source of PM, would induce airway neutrophilia in healthy subjects, and that either these responses would be exaggerated in subjects with mild allergic asthma, or DE would exacerbate pre-existent allergic airways. Healthy and mild asthmatic subjects were exposed for 2 h to ambient levels of DE (particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10) 108 microg x m(-3)) and lung function and airway inflammation were assessed. Both groups showed an increase in airway resistance of similar magnitude after DE exposure. Healthy subjects developed airway inflammation 6 h after DE exposure, with airways neutrophilia and lymphocytosis together with an increase in interleukin-8 (IL-8) protein in lavage fluid, increased IL-8 messenger ribonucleic acid expression in the bronchial mucosa and upregulation of the endothelial adhesion molecules. In asthmatic subjects, DE exposure did not induce a neutrophilic response or exacerbate their pre-existing eosinophilic airway inflammation. Epithelial staining for the cytokine IL-10 was increased after DE in the asthmatic group. Differential effects on the airways of healthy subjects and asthmatics of particles with a 50% cut-off aerodynamic diameter of 10 microm at concentrations below current World Health Organisation air quality standards have been observed in this study. Further work is required to elucidate the significance of these differential responses.
authors.affiliation: Dept of Respiratory Medicine and Allergy, University Hospital, Umeå, Sweden.
authors.forename: N
authors.initials: N
authors.lastname: Stenfors
authors.forename: C
authors.initials: C
authors.lastname: Nordenhäll
authors.forename: S S
authors.initials: SS
authors.lastname: Salvi
authors.forename: I
authors.initials: I
authors.lastname: Mudway
authors.forename: M
authors.initials: M
authors.lastname: Söderberg
authors.forename: A
authors.initials: A
authors.lastname: Blomberg
authors.forename: R
authors.initials: R
authors.lastname: Helleday
authors.forename: J O
authors.initials: JO
authors.lastname: Levin
authors.forename: S T
authors.initials: ST
authors.lastname: Holgate
authors.forename: F J
authors.initials: FJ
authors.lastname: Kelly
authors.forename: A J
authors.initials: AJ
authors.lastname: Frew
authors.forename: T
authors.initials: T
authors.lastname: Sandström
mesh_terms: D000328:Adult; D000403:Airway Resistance / Q000187:drug effects; D001249:Asthma / Q000503:physiopathology*; D001980:Bronchi / Q000737:chemistry; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D015815:Cell Adhesion Molecules / Q000032:analysis; D004781:Environmental Exposure; D005260:Female; D006801:Humans; D007249:Inflammation / Q000139:chemically induced; D016753:Interleukin-10 / Q000032:analysis; D016209:Interleukin-8 / Q000032:analysis / Q000235:genetics; D008218:Lymphocytosis / Q000139:chemically induced; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000473:pathology; D012333:RNA, Messenger / Q000032:analysis; D020545:Respiratory Mucosa / Q000737:chemistry; D012137:Respiratory System / Q000187:drug effects* / Q000473:pathology; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D015815:Cell Adhesion Molecules; D016209:Interleukin-8; D012333:RNA, Messenger; D001335:Vehicle Emissions; D016753:Interleukin-10