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Air pollution is associated with a substantial burden on human health; however, the most important pollutants may vary with location. Proper monitoring is necessary to determine the effect of these pollutants on respiratory health.This study was designed to evaluate the role of outdoor, indoor and personal exposure to combustion-related pollutants NO(2) and O(3) on respiratory health of children in a non-affluent urban area of São Paulo, Brazil.Levels of NO(2) and O(3) were continuously measured in outdoor and indoor air, as well as personal exposure, for 30 days using passive measurement monitors. Respiratory health was assessed with a Brazilian version of the ISAAC questionnaire.Complete data were available from 64 children, aged 6-10 years. Respiratory morbidity was high, with 43 (67.2%) reporting having had wheezing at any time, 27 (42.2%) wheezing in the last month, 17 (26.6%) asthma at any time and 21 (32.8%) pneumonia at any time. Correlations between levels of NO(2) and O(3) measured in the three locations evaluated were poor. Levels of NO(2) in indoor air and personal exposure to O(3) were independently associated with asthma (both cases P=.02), pneumonia (O(3), P=.02) and wheezing at any time (both cases P.01). No associations were seen between outdoor NO(2) and O(3) and respiratory health.Exposure to higher levels of NO(2) and O(3) was associated with increased risk for asthma and pneumonia in children. Nonetheless, the place where the pollutants are measured influences the results. The measurements taken in indoor and personal exposure were the most accurate.

Clinical evidence has identified the pulmonary circulation as an important target of air pollution. It was previously demonstrated that in vitro exposure to fine particulate matter (aerodynamic diameter ≤2.5μm, PM2.5) induces endothelial dysfunction in isolated pulmonary arteries. We aimed to investigate the effects of in vivo exposure to urban concentrated PM2.5 on rat pulmonary artery reactivity and the mechanisms involved. For this, adult Wistar rats were exposed to 2 weeks of concentrated São Paulo city air PM2.5 at an accumulated daily dose of approximately 600μg/m3. Pulmonary arteries isolated from PM2.5-exposed animals exhibited impaired endothelium-dependent relaxation to acetylcholine without significant changes in nitric oxide donor response compared to control rats. PM2.5 caused vascular oxidative stress and enhanced protein expression of Cu/Zn- and Mn-superoxide dismutase in the pulmonary artery. Protein expression of endothelial nitric oxide synthase (eNOS) was reduced, while tumor necrosis factor (TNF)-α was enhanced by PM2.5 inhalation in pulmonary artery. There was a significant positive correlation between eNOS expression and maximal relaxation response (Emax) to acetylcholine. A negative correlation was found between vascular TNF-α expression and Emax to acetylcholine. Plasma cytokine levels, blood cells count and coagulation parameters were similar between control and PM2.5-exposed rats. The present findings showed that in vivo daily exposure to concentrated urban PM2.5 could decrease endothelium-dependent relaxation and eNOS expression on pulmonary arteries associated with local high TNF-α level but not systemic pro-inflammatory factors. Taken together, the present results elucidate the mechanisms underlying the trigger of cardiopulmonary diseases induced by urban ambient levels of PM2.5.