title: Acetaldehyde at a low concentration synergistically exacerbates allergic airway inflammation as an endocrine-disrupting chemical and as a volatile organic compound.
abstract: BACKGROUND
  Acetaldehyde is an endocrine-disrupting chemical (EDC) and a volatile organic compound (VOC). It is also a carcinogen and teratogen that causes bronchoconstriction in a subset of asthmatics. However, the mechanism through which acetaldehyde acts as an EDC/VOC causing allergic airway inflammation remains unknown.
  
  
  OBJECTIVE
  To determine the effects of a low concentration of acetaldehyde, which itself did not trigger airway inflammation, on extant allergic airway inflammation in a murine model of allergic asthma.
  
  
  METHODS
  We compared airway hyperresponsiveness (AHR), lung pathology, serum IgE and airway concentrations of cytokines among four groups of BALB/c mice [control, Dermatophagoides farinae(Df) allergen-sensitized (AS), intranasally acetaldehyde-injected (ALD) and AS-ALD mice].
  
  
  RESULTS
  Physiological and histological differences were not evident between ALD and control mice. AS mice developed AHR and allergic airway inflammation characterized by goblet cell hyperplasia and eosinophilic infiltration. Both AHR and airway eosinophilia were significantly enhanced in AS-ALD compared with AS mice. Serum total and Df-specific IgE were significantly increased in both AS and AS-ALD mice compared with control and ALD mice, but comparable between AS and AS-ALD mice. Mite allergen sensitization significantly increased interleukin-5 and granulocyte macrophage colony-stimulating factor, and decreased interferon-γ levels in the airways; injecting acetaldehyde into airways with allergic inflammation significantly increased the levels of these inflammatory cytokines.
  
  
  CONCLUSIONS
  Exposure to acetaldehyde can enhance allergic airway inflammation in asthma.
authors.affiliation: Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan.
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Kawano
authors.forename: Hiroto
authors.initials: H
authors.lastname: Matsuse
authors.forename: Susumu
authors.initials: S
authors.lastname: Fukahori
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tsuchida
authors.forename: Tomoya
authors.initials: T
authors.lastname: Nishino
authors.forename: Chizu
authors.initials: C
authors.lastname: Fukushima
authors.forename: Shigeru
authors.initials: S
authors.lastname: Kohno
mesh_terms: D000079:Acetaldehyde / Q000494:pharmacology*; D000281:Administration, Intranasal; D000818:Animals; D001249:Asthma / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D016084:Bronchoconstriction / Q000187:drug effects*; D004195:Disease Models, Animal; D052244:Endocrine Disruptors / Q000494:pharmacology*; D004802:Eosinophilia / Q000139:chemically induced / Q000378:metabolism; D005260:Female; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000378:metabolism; D006967:Hypersensitivity / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D007073:Immunoglobulin E / Q000097:blood; D007249:Inflammation / Q000209:etiology / Q000276:immunology / Q000503:physiopathology; D007371:Interferon-gamma / Q000378:metabolism; D015848:Interleukin-5 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D012137:Respiratory System / Q000187:drug effects* / Q000276:immunology / Q000473:pathology / Q000503:physiopathology; D055549:Volatile Organic Compounds / Q000494:pharmacology
chemical_list: D052244:Endocrine Disruptors; D015848:Interleukin-5; D055549:Volatile Organic Compounds; D007073:Immunoglobulin E; D007371:Interferon-gamma; D016178:Granulocyte-Macrophage Colony-Stimulating Factor; D000079:Acetaldehyde