Long-term exposure of adults to outdoor air pollution is associated with increased airway obstruction and higher prevalence of bronchial hyperresponsiveness.

The authors studied the association between long-term exposure (i.e., > 10 y) to outdoor air pollution and the severity of obstructive pulmonary disease and prevalence of bronchial hyperreactivity to beta2 agonists in two groups of adult patients who were of similar ages and who had similar smoking habits. The subjects lived in downtown districts or in the outer suburbs of Marseilles, the neighborhood that contained air samplers. The regions were similar with respect to sulfur dioxide levels, but levels of nitric oxides and particulate matter (10 millimeters or less) were higher in the downtown area than the suburbs. The authors assessed airway obstruction, as determined by a decrease in forced expiratory volume in 1 s, mean forced expiratory flow measured between 25% and 75% of vital capacity, and an elevated value of central airway resistance. The authors tested the changes in these variables induced by inhalation of a beta2 agonist. Baseline lung function was altered more significantly in both male and female patients who lived in downtown Marseilles than in those who resided in the suburbs, and the differences persisted regardless of the season during which the study occurred. Prevalence of bronchial hyperreactivity and symptoms of asthma (but not of rhinitis) were higher in the downtown than suburban male subjects. The results of this study suggest that an association exists between actual environmental exposure to outdoor air pollution (i.e., nitrogen oxides and/or particulate matter of 10 millimeters or less) and respiratory effects in sensitive adults represented by patients with chronic obstructive pulmonary disease or asthma.

The changes in leg blood flow during and after mild or severe acute hypoxaemia in healthy humans.

The present study examines the leg blood flow changes in resting healthy humans during and after a 10-min period of mild (PaO2=5.60 kPa) or severe hypoxaemia (PaO2=4.53 kPa) induced by breathing hypoxic gas mixtures. A Colour Duplex Scan system allowed to measure the cross-sectional area (CSA) and mean blood flow (Q) in a femoral artery (FA) and a femoral vein (FV) and also in an artery supplying leg muscles (medial gastrocnemius artery, MGA). During the mild as well as the severe hypoxaemia and their recovery periods, no significant variations of Q and CSA occurred in FA and FV. During the mild hypoxaemia and the first 10 min of the recovery period, Q and CSA of MGA increased (maximal changes: +84 and +20%, respectively). By contrast, a marked Q decrease and a reduced CSA were measured in MGA during the severe hypoxaemia (-67 and -60%, respectively). This reduced muscle blood flow was followed by a vasodilatation (CSA increase = +30%), which began 10 min after the hypoxaemia ended and persisted for a further 10-min period. This study shows that the time course of muscle blood flow changes in response to acute hypoxaemia depends on the PaO2 level. Reverse effects were measured during the mild or the severe hypoxaemia, whereas a post-hypoxaemic vasodilatation occurred in all circumstances.