Nasal epithelial and inflammatory response to ozone exposure: a review of laboratory-based studies published since 1985.
This article summarizes biological events in human and animal nasal epithelium after short- and long-term exposure to ozone, the principal agent in photochemical smog. Despite anatomical and histological interspecies differences, ozone exposures resulted in common nasal qualitative alterations with an anterior-posterior gradient of phenomena occurring immediately, and with a lag time postexposure: epithelial disruption and increased permeability, inflammatory cell influx, and proliferative and secretory responses. Described mechanisms of toxicity included a direct effect of ozone on epithelial lining fluid and cellular membranes and the subsequent release of cytokines and cyclooxygenase and lipoxygenase products. An indirect effect of ozone was indicated by a decreased mucociliary clearance, free radicals production interacting with a gene promoting factor, and increased DNA synthesis. Studies highlighted the pivotal role of activated neutrophils and mast cells leading to the release of deleterious enzymes (tryptase, eosinophil cationic protein) and numerous cytokines. Experiments performed with ozone exposure/allergen challenge reported that, besides the intrinsic deleterious properties of ozone, it also had a priming effect on the late-phase response to allergen challenge, providing new insights into the pathophysiology of respiratory allergic diseases.
Nikasinovic
L
L
Laboratoire d'Hygiène et de Santé Publique, Faculté des Sciences Pharmaceutiques et Biologiques, Université René Descartes, Paris, France.
Momas
I
I
Seta
N
N
D000818:Animals; D006801:Humans; D019570:Inhalation Exposure; D009297:Nasal Mucosa / Q000187:drug effects* / Q000378:metabolism; D010126:Ozone / Q000009:adverse effects*; D012220:Rhinitis / Q000139:chemically induced* / Q000473:pathology
D010126:Ozone