Abstracts: ISEE 21st Annual Conference, Dublin, Ireland, August 25-29, 2009: Symposium Abstracts
*Department of Occupational and Environmental Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden; and †Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine, Umea University, Umea, Sweden.
Background and Objective:
Exposure to ambient air pollutants has been shown to induce airway inflammation. Measurement of fraction of nitric oxide in exhaled air (FENO) enables the calculation of the production of alveolar NO which has been suggested as a marker of distal airway inflammation. The aim of the study was to estimate whether short- term exposure to O3, NO2 and PM10 was associated with an increase of alveolar NO, a possible marker of inflammation in distal airways.
In this cross-sectional study we investigated 1606 adults in the age 25 to 75 years living in Göteborg, Sweden. Examination included FENO at flow-rates of 50, 100 and 270 mL/s and blood samples and a respiratory questionnaire. Alveolar NO was estimated by using Tsoukias two-compartment model. Atopy was defined as a positive Phadiatiopeâ -test. PM10 and O3 concentrations were measured at an urban background monitoring site and for cumulative mean exposure for 3, 24 and 120 hours were calculated. Ordinary least square regression was used to model the relation between FENO and alveolar NO and each of the studied pollutants, adjusted for potential confounding factors.
We found that an increase of one IQR in the 24 hour and 120 hour cumulative average of O3 (corresponding to 44.3 μg/m3 and 25.4 μg/m3) was associated with an increase in alveolar NO of 1.6% (95% CI 0.5–2.6) and 2.0% (95% CI 0.9–3.0). The effect was most pronounced in non-smoking non-atopic subjects. Alveolar NO remained significantly elevated for five days after exposure. Exposure to NO2 and PM10 did not affect alveolar NO or FENO.
Exposure to ozone appears to give rise to a small increase in alveolar nitric oxide, a possible marker for airway inflammation in the distal airways.