J.G. Vos

The authors used a longitudinal observational design, with repeated measures, to study the association between traffic-related air pollutants (i.e., nitric oxide, nitrogen dioxide, carbon monoxide, and Black Smoke) and respiratory symptoms. Subjects (N = 82) attended an elementary school in either Utrecht (i.e., urban children) or Bilthoven (i.e., suburban children). These two geographic areas differed with respect to levels of Black Smoke (means = 53 microg/m3 and 18 microg/m3, respectively). Levels of nitric oxide, nitrogen dioxide, carbon monoxide, and Black Smoke were consistently higher in Utrecht than in Bilthoven (mean daily ratios were 8, 1.5, 1.8, and 2.7, respectively). The authors compared mean levels of short-term effects of the aforementioned air pollutants on suburban and urban children. Urban children had higher mean levels (p = .05) of interleukin-8 (32%), urea (39%), uric acid (26%), albumin (15%), and nitric oxide metabolites (21%) in nasal lavage than did suburban children. Peak expiratory flow, exhaled nitric oxide levels, and nasal markers were associated with levels of particulate matter with diameters less than or equal to 10 microm, Black Smoke, nitrogen dioxide, and nitric oxide. With respect to per-unit increases in air pollution, urban children had more increased peak expiratory flow, higher levels of exhaled nitric oxide, and more increased release of uric acid, urea, and nitric oxide metabolites than suburban children. In summary, urban children had increased levels of inflammatory nasal markers, and their responses were more pronounced than were the suburban children's responses to the same increments of air pollution.

The aim of this study was to assess the effect of outdoor air pollution on exhaled levels of endogenously released nitric oxide. To exclude bias from exogenous NO in the recovered exhaled air (residual NO or NO in dead volume) an experimental design was used that sampled NO of endogenous origin only. The validity of the presented experimental design was established in experiments where subjects were exposed to high levels of exogenous NO (cigarette smoke or 480 microg x m(-3) synthetic NO). Subsequent 1 min breathing and a final inhalation of NO-free air proved to be sufficient to attain pre-exposure values. Using the presented method detecting only endogenous NO in exhaled air, 18 subjects were sampled on 4 separate days with different levels of outdoor air pollution (read as an ambient NO level of 4, 30, 138 and 246 microg x m(-3)). On the 2 days with highest outdoor air pollution, exhaled NO was significantly (p<0.001) increased (67-78%) above the mean baseline value assessed on 4 days with virtually no outdoor air pollution. In conclusion, the level of endogenous nitric oxide in exhaled air is increased on days with high outdoor air pollution. The physiological implications of this findings need to be investigated further.