In the present paper, we have reviewed experimental animal studies on the effects of the two most important oxidant airborne pollutants, nitrogen dioxide and ozone, on the respiratory system.
The toxic effects depend on concentration and length of exposure, and are generally similar for both oxidants, with ozone operative at lower concentrations.
High doses of both oxidants cause death due to lung oedema.
Exposure to sublethal levels causes functional alterations such as airflow limitation and airway hyperresponsiveness to bronchoconstrictor stimuli.
These effects, which are generally reversible, are associated with epithelial injury, oedema and airway and parenchymal infiltration by inflammatory cells.
Loss of cilia of airway epithelium and necrosis of type I alveolar epithelial cells are the most prominent consequences at the epithelial level.
Inflammation is characterized by early neutrophilic infiltration, followed by an increased number of mononuclear cells, predominantly alveolar macrophages.
After long-term exposure, whilst nitrogen dioxide causes predominantly emphysema, ozone produces mainly pulmonary fibrosis.
Biochemical effects include lipid peroxidation, increased antioxidant metabolism, and alteration of enzyme activity.
Nitrogen dioxide and ozone may also alter the immunological response and reduce the defence against infections, increasing the susceptibility of exposed animals to infections.
Mots-clés Pascal : Azote dioxyde, Ozone, Pollution air, Oxydant, Fonction respiratoire, Exploration, Toxicité, Animal
Mots-clés Pascal anglais : Nitrogen dioxide, Ozone, Air pollution, Oxidant, Lung function, Exploration, Toxicity, Animal
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 95-0508128
Code Inist : 002B03M02. Création : 01/03/1996.