OZONE EXPOSURE IN HUMANS - INFLAMMATORY, SMALL AND PERIPHERAL AIRWAY RESPONSES

We exposed eight normal adults to filtered air (FA) and 0.35 ppm ozone (O-3) and compared responses in spirometry, including isovolume (isoV ) flows at intermediate-to-low lung volumes, against levels of inflamm atory markers in bronchoalveolar ravage fluid (BALF) and peripheral lu ng resistance (Rp) measured through a wedged bronchoscope. Spriometry was performed at the end, 25 min and 24 h after exposure, bronchoscopy at 24 h after exposure. The percentages of neutrophils, fibrinogen, a lbumin, PGE(2), PGF(2 alpha), and kinins were elevated in BALF after O -3 compared with FA. The percentage reduction in (isoV) FEF(25-75) at 25 min and 24 h after administration of O-3 correlated closely with th e rise in fibrinogen concentrations in BALF, a marker of altered vascu lar permeability. Rp, a measurement dominated by very small or periphe ral airways, was unaffected in 7 of 8 subjects. The absence of change in Rp might have reflected insufficient penetration of O-3 into these airways to produce or sustain an effect far 24 h; alternatively, the b ronchoscopic procedure which included atropine and lidocaine pretreatm ent may have reversed an O-3 effect. An unexpected finding was the sig nificant association between baseline Rp (after FA) and the magnitude of the spirometric response to O-3. Our results suggest that small air way dysfunction in the immediate post-O-3 period is a marker of lung i nflammation.