Ozone increases both in humans and in experimental animals air tract responsivity to aspecific bronchoconstrictor stimuli (histamine and/or cholinergic agents). In groups of 6 sheep, mean weight 34.5 Kg, exposed to inhaled gaseous pollutants, the following experiments were performed. Sheep were exposed in an exposure chamber to variable concentrations of O 3 and SO 2, and pathophysiological effects were evaluated after administration of aereosols containing 3H histamine. Exposure to 0,5 ppm ozone increased both lung resistance to flow (% Δ Re) and appearance velocity of 3H in the blood. In addition, O 3 inhalation increased mucus secretion and decreased mucociliary clearance. In fact, in sheep exposed to 0,5 ppm ozone per 4h/day per 2 days, basal secretion of 35SO 4/ 3H glycoprotein ratio suggests qualitative mucus alterations with relative increase of sulfonated glycoproteins, which are more viscous. In addition, a significant reduction of tracheal mucus velocity, was also observed. Exposure to gaseous (O 3 and SO 2) environmental pollutants modifies air tract responsivity and decreases mucociliary clearance. These functional alterations may be explained, at least in part, by the production of inflammatory mediators by damaged bronchial cells or by inflammatory cells recruited within the air tract, with mucociliary clearance impairment, because of both mucus alteration and impairment of the physiologic transport mechanism. In particular, sheep is a suitable experimental animal for mimicking pathophysiologic alterations of the air tract induced in humans by gaseous pollutants.
|Translated title of the contribution||Mucociliary disfunction by exposure to gaseous pollutants|
|Number of pages||9|
|Journal||GIMT - Giornale Italiano delle Malattie del Torace|
|Publication status||Published - 2008|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine