title: Inhalation of concentrated ambient particulate matter near a heavily trafficked road stimulates antigen-induced airway responses in mice.
abstract: The goal of this study was to test the following hypotheses: (1) exposure to mobile emissions from mobile sources close to a heavily trafficked roadway will exacerbate airway inflammation and allergic airway responses in a sensitized mouse model, and (2) the magnitude of allergic airway disease responses will decrease with increasing distance from the roadway. A particle concentrator and a mobile exposure facility were used to expose ovalbumin (OVA)-sensitized BALB/c mice to purified air and concentrated fine and concentrated ultrafine ambient particles at 50 m and 150 m downwind from a roadway that was heavily impacted by emissions from heavy duty diesel-powered vehicles. After exposure, we assessed interleukin (IL)-5, IL-13, OVA-specific immunoglobulin E, OVA-specific immunoglobulin G1, and eosinophil influx as biomarkers of allergic responses and numbers of polymorphonuclear leukocytes as a marker of inflammation. The study was performed over a two-year period, and there were differences in the concentrations and compositions of ambient particulate matter across those years that could have influenced our results. However, averaged over the two-year period, exposure to concentrated ambient particles (CAPs) increased the biomarkers associated with airway allergies (IL-5, immunoglobulin E, immunoglobulin G1 and eosinophils). In addition, mice exposed to CAPs 50 m downwind of the roadway had, on the average, greater allergic responses and showed greater indications of inflammation than did mice exposed to CAPs 150 m downwind. This study is consistent with the hypothesis that exposure to CAPs close to a heavily trafficked roadway influenced allergic airway responses.
authors.affiliation: Southern California Particle Center and Supersite, USA. mtkleinm@uci.edu
authors.forename: Michael T
authors.initials: MT
authors.lastname: Kleinman
authors.forename: Ali
authors.initials: A
authors.lastname: Hamade
authors.forename: Dianne
authors.initials: D
authors.lastname: Meacher
authors.forename: Michael
authors.initials: M
authors.lastname: Oldham
authors.forename: Constantinos
authors.initials: C
authors.lastname: Sioutas
authors.forename: Bhabesh
authors.initials: B
authors.lastname: Chakrabarti
authors.forename: Dan
authors.initials: D
authors.lastname: Stram
authors.forename: John R
authors.initials: JR
authors.lastname: Froines
authors.forename: Arthur K
authors.initials: AK
authors.lastname: Cho
mesh_terms: D000393:Air Pollutants / Q000633:toxicity*; D000818:Animals; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry / Q000166:cytology; D002140:California; D004804:Eosinophils / Q000166:cytology; D007073:Immunoglobulin E / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D019570:Inhalation Exposure; D018793:Interleukin-13 / Q000096:biosynthesis; D015848:Interleukin-5 / Q000096:biosynthesis; D015141:Los Angeles; D008168:Lung / Q000187:drug effects* / Q000276:immunology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009504:Neutrophils / Q000166:cytology; D010047:Ovalbumin / Q000276:immunology; D012130:Respiratory Hypersensitivity / Q000139:chemically induced* / Q000276:immunology; D001335:Vehicle Emissions / Q000633:toxicity*
chemical_list: D000393:Air Pollutants; D007074:Immunoglobulin G; D018793:Interleukin-13; D015848:Interleukin-5; D001335:Vehicle Emissions; D007073:Immunoglobulin E; D010047:Ovalbumin