title: Asthma/allergic airways disease: does postnatal exposure to environmental toxicants promote airway pathobiology?
abstract: The recent, dramatic increase in the incidence of childhood asthma suggests a role for environmental contaminants in the promotion of interactions between allergens and the respiratory system of young children. To establish whether exposure to an environmental stressor, ozone (O3), and an allergen, house dust mite (HDMA), during early childhood promotes remodeling of the epithelial-mesenchymal trophic unit (EMTU) of the tracheobronchial airway wall by altering postnatal development, infant rhesus monkeys were exposed to cyclic episodes of filtered air (FA), HDMA, O3, or HDMA plus O3. The following alterations in the EMTU were found after exposure to HDMA, O3, or HDMA plus O3: (1) reduced airway number; (2) hyperplasia of bronchial epithelium; (3) increased mucous cells; (4) shifts in distal airway smooth muscle bundle orientation and abundance to favor hyperreactivity; (5) interrupted postnatal basement membrane zone differentiation; (6) modified epithelial nerve fiber distribution; and (7) reorganization of the airway vascular and immune system.
  
  
  CONCLUSIONS
  cyclic challenge of infants to toxic stress during postnatal lung development modifies the EMTU. This exacerbates the allergen response to favor development of intermittent airway obstruction associated with wheeze. And, exposure of infants during early postnatal lung development initiates compromises in airway growth and development that persist or worsen as growth continues, even with cessation of exposure.
authors.affiliation: Department of Anatomy, Physiology, and Cell Biology, University of California, Davis, CA 95616, USA. cgplopper@ucdavis.edu
authors.forename: Charles G
authors.initials: CG
authors.lastname: Plopper
authors.forename: Suzette M
authors.initials: SM
authors.lastname: Smiley-Jewell
authors.forename: Lisa A
authors.initials: LA
authors.lastname: Miller
authors.forename: Michelle V
authors.initials: MV
authors.lastname: Fanucchi
authors.forename: Michael J
authors.initials: MJ
authors.lastname: Evans
authors.forename: Alan R
authors.initials: AR
authors.lastname: Buckpitt
authors.forename: Mark
authors.initials: M
authors.lastname: Avdalovic
authors.forename: Laurel J
authors.initials: LJ
authors.lastname: Gershwin
authors.forename: Jesse P
authors.initials: JP
authors.lastname: Joad
authors.forename: Radhika
authors.initials: R
authors.lastname: Kajekar
authors.forename: Shawnessy
authors.initials: S
authors.lastname: Larson
authors.forename: Kent E
authors.initials: KE
authors.lastname: Pinkerton
authors.forename: Laura S
authors.initials: LS
authors.lastname: Van Winkle
authors.forename: Edward S
authors.initials: ES
authors.lastname: Schelegle
authors.forename: Emily M
authors.initials: EM
authors.lastname: Pieczarka
authors.forename: Reen
authors.initials: R
authors.lastname: Wu
authors.forename: Dalla M
authors.initials: DM
authors.lastname: Hyde
mesh_terms: D000393:Air Pollutants / Q000009:adverse effects* / Q000276:immunology; D000485:Allergens / Q000009:adverse effects* / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000276:immunology / Q000517:prevention & control; D001980:Bronchi / Q000187:drug effects* / Q000254:growth & development / Q000503:physiopathology; D002648:Child; D002657:Child Development / Q000187:drug effects* / Q000502:physiology; D040001:Dermatophagoides farinae / Q000276:immunology; D004195:Disease Models, Animal; D048788:Growth and Development / Q000187:drug effects*; D006801:Humans; D019570:Inhalation Exposure; D008253:Macaca mulatta; D010083:Oxidants, Photochemical / Q000009:adverse effects; D010126:Ozone / Q000009:adverse effects
chemical_list: D000393:Air Pollutants; D000485:Allergens; D010083:Oxidants, Photochemical; D010126:Ozone