LUNG-FUNCTION RESPONSE OF HEALTHY WOMEN AFTER SEQUENTIAL EXPOSURES TONO2 AND O-3

Since NOx emissions bear a precursor-product relation with ambient ozo ne (O-3) levels, the sequence of peak ambient concentrations is first nitrogen dioxide (NO2) followed later in the day by ozone (O-3). We as certained whether preliminary exposure to 0.6 parts per million (ppm) NO2 would affect the lung function response to subsequent exposure to 0.3 ppm O-3. Twenty-one healthy young nonsmoking women (18 to 35 yr of age) underwent two sets of exposures on two different days separated by a minimum of 2 wk. On one day, subjects were exposed to air for 2 h followed 3 h later by a 2-h exposure to O-3. On the other day, the fi rst exposure was to NO2; order of the days was randomized. During each exposure subjects intermittently exercised, alternating 15 min of res t with 15 min of exercise (VE similar to 40 L/min). Spirometry was per formed before the first exposure and at 1-h intervals until the end of the 2-h (O-3) exposure. Plethysmography measurements were made before and after NO2 and O-3 exposures. Nonspecific airway reactivity (AR) w as determined at least 1 wk prior to the first exposure and following each O-3 exposure. AR to methacholine (MCh) was expressed as dose requ ired to decrease FEV(1) by 10% (PD(10)FEV(1)). Nitrogen dioxide exposu re alone did not reduce FEV(1) but did significantly enhance O-3-induc ed spirometric changes. No significant effects were observed in plethy smography. On both exposure days, the median PD(10)FEV(1) was signific antly reduced (p < 0.05) from control PD(10)FEV(1) (14.3 mg/ml). Follo wing the NO2-O-3 sequence, the median PD(10)FEV(1) was significantly r educed from 5.6 mg/ml to 1.7 mg/ml compared with the air-O-3 sequence (n = 16, p < 0.05), suggesting a delayed latent effect of NO2 on the a irways.