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05; 95% CI 0.95�C1.15; p = 0.32). Variations in PM10 at lag day 3 correlated with neutrophils (p = 0.013), lymphocytes (p = 0.0031) and total cell count (p = 0.024) in BAL. Importantly, we only found an effect of PM10 on LB in patients not taking azithromycin. LB predisposed to chronic rejection (p http://www.selleck.cn/products/pf-06463922.html with BAL neutrophilia and lymphocytosis. Azithromycin was protective against this PM effect. Survival after lung transplantation (LTx), a last resort for selected patients with end-stage lung disease, has tremendously improved since 1963 (1). Survival, however, is still hampered by the development of chronic rejection or its clinical correlate bronchiolitis obliterans syndrome (BOS), as the lung experiences one of the highest rejection rates among solid organ transplantations (2). The higher susceptibility of lungs to be rejected could conceivably follow from its direct contact with the environment. Recently, we demonstrated that chronic exposure to (traffic-related) air pollution, indirectly http://www.selleckchem.com/products/erastin.html measured by proximity of the address of residence of each patient to a major road, increases the risk of chronic rejection and mortality in LTx patients (3). As a consequence, we hypothesized that daily variations in air pollution (""acute exposures"") may also http://www.selleckchem.com/products/3-deazaneplanocin-a-dznep.html affect the outcome of LTx. Various studies demonstrated that exposure to ambient particulate matter (PM) can contribute to pulmonary and systemic inflammation, causing the release of inflammatory mediators, and resulting in oxidative stress and accumulation of inflammatory cells like neutrophils (4), comparable to what happens during lymphocytic bronchiolitis (LB), the pathological correlate of acute airway rejection. In the early years, not much attention was given to LB until 2008 when Glanville reported a significant association between the occurrence of LB and the prevalence of chronic rejection (5). A-grade rejection, pathologically characterized by perivascular lymphocytic inflammation, is a common phenomenon, especially in the early phase after LTx: up to 40% of the patients experience at least one episode within the first year (1). Some established risk factors for A-grade rejection include human leukocyte antigen mismatching, low immunosuppressive trough levels, recipient age and genetics (6). External parameters, such as gastroesophageal reflux (7) may also impact on A-grade rejection, but the exact trigger remains unknown. In LTx patients, both A-grade rejection and LB are associated with higher total cell count and an increased broncho-alveolar lavage (BAL) neutrophilia compared to transplanted controls (8).