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5%, whereas COPD and pulmonary function were the strongest selleckchem affected by particulates with an aerodynamic diameter Enol air pollution exposure. COPD incidence was associated with the 35-year mean NO2 level (hazard ratio 1.08, 95% CI: 1.02�C1.14, per interquartile range of 5.8?mg/m3).18 Despite the fact that the authors have included a very long duration of air-pollutant concentration assessment, a 35-year accumulated exposure to traffic-related air pollution at home address, this study was limited by the lack of objective spirometric measurement for the diagnosis of COPD. Because there are few studies that have confirmed COPD by spirometry and the published data are conflicting, a causal relationship between outdoor air pollution and compound screening assay COPD cannot be drawn at this stage. Previous studies have shown that air pollutants have harmful effects on the airway. Particulate pollutants, ozone (O3) and NO2 can all produce deleterious effects on the airway, such as increases in bronchial reactivity,19 airway oxidative stress,20 pulmonary and systemic inflammation,21,22 amplification of viral infections,23 and reduction in airway ciliary activity.24 There is thus evidence of biological plausibility that air pollutants can cause damage in the lungs. Currently, there is insufficient evidence available to attribute outdoor air pollution as the causative factor for COPD due to the lack of long-term study with spirometric measurement. It would be ideal to follow up subjects from birth to over 60?years of age with serial assessment of their exposure to outdoor air pollutants in relation to their lung function. Analysis of the data from such studies would be expected to be very complex, as it would involve taking into account their indoor air-pollutant exposures, occupations and personal smoking history.