THE EFFECT OF 1 PPM NITROGEN-DIOXIDE ON BRONCHOALVEOLAR LAVAGE CELLS AND INFLAMMATORY MEDIATORS IN NORMAL AND ASTHMATIC SUBJECTS

Several studies have suggested that patients with bronchial asthma are more susceptible to the potential effects of nitrogen dioxide (NO2) t han healthy subjects, with respect to airway responsiveness and lung f unction. We investigated whether these differences are paralleled by d ifferences in the cellular and biochemical response within the airway lumen. Twelve subjects with mild extrinsic asthma and eight normal sub jects breathed either filtered air or 1 ppm NO2 in a single-blind mann er during intermittent exercise for 3 h. Bronchoscopy with bronchoalve olar lavage (BAL) was performed one hour after each exposure, and on a third day without exposure (baseline day), Prostanoids, leukotrienes and histamine were analysed in BAL fluid, and the cellular composition of BAL fluid was assessed. In the asthmatic subjects, NO2 induced a s mall mean drop in forced expiratory volume in one second (FEV(1)). Dif ferential cell counts in BAL fluid did not reveal significant effects of NO2. Levels of 6-keto-prostaglandin(1 alpha) (6-keto-PGF(1 alpha)) were decreased, and levels of thromboxane B-2 (TxB(2)) and prostagland in D-2 (PGD(2)) in BAL fluid were increased after NO2 compared to filt ered air exposure; whereas, prostaglandin E(2) (PGE(2)), prostaglandin F-2 alpha (PGF(2 alpha)), histamine and leukotriene levels did not ch ange significantly. The normal subjects showed no change in lung funct ion parameters and a small increase in TxB(2) after breathing NO2. We conclude that in subjects with mild asthma NO2 is capable of inducing an activation of cells, which is compatible with enhancement of airway inflammation, even if lung function parameters and cellular compositi on of BAL fluid are not markedly affected. The lower susceptibility to NO2 of normal subjects is also reflected in their lower response rega rding the soluble markers of inflammation in BAL.