EFFECTS OF NITRIC-ACID GAS ALONE OR IN COMBINATION WITH OZONE ON HEALTHY-VOLUNTEERS

Nitric acid (HNO3) is the most prevalent acid air pollutant in the wes tern United States and has the potential to cause adverse respiratory effects through both acidification and oxidation reactions. To study t his potential, we measured physiologic (specific airway resistance, SR aw, FEV1, and FVC) and bronchoalveolar lavage (total and differential cell counts, LDH, fibronectin, and total protein) end points in a grou p of 10 healthy, athletic subjects who were exposed to 500 mug/m3 of H NO3 gas or filtered air for 4 h during moderate exercise (ventilatory rate, 40 L/min) and underwent bronchoscopy 18 h later. Under an identi cal protocol, 10 healthy subjects were exposed to 500 mug/m3 of HNO3 g as plus 0.20 ppm ozone (O3) or 0.20 PPM O3 alone to determine if HNO3 might enhance the toxicity of O3. In addition to bronchoalveolar lavag e (BAL), we employed the techniques of isolated left mainstem bronchia l lavage and bronchial biopsy to determine if proximal airway injury w as caused by pollutant exposure and whether there was any correlation with the degree of distal lung injury as assessed by BAL. We found no significant differences in pulmonary function tests or in the cellular or biochemical constituents in either the BAL or the left mainstem la vage fluids between the HNO3 and the air exposures. Similarly, there w ere no differences in these end points between the HNO3/O3 and the O3 exposures. Furthermore, there were no significant differences in the b ronchial biopsy specimens between the HNO3 and air exposures or betwee n the HNO3/O3 and O3 exposures. In conclusion, the data gathered to da te do not suggest that HNO3 gas causes either proximal airway or dista l lung injury or that HNO3 potentiates the inflammatory response produ ced by O3 in healthy individuals.