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We studied the role of chronic exposure to ambiant air pollution on lung function level and evolution in lung transplant patients. The lung function of 525 lung transplant (LT) patients from the COLT cohort was followed-up. The 12-month average levels of air pollutants (Nitrogen dioxide (NO 2 ), fine particulate matters (PM 2.5 , PM 10 ) and ozone (O 3 )) were estimated at the home addresses of each patient. The effect of air pollutant exposure on FEV 1 level and change in FEV 1 both during the recovery and decline periodes were estimated using mixed linear regression models adjusted on recipient age, sex, smoking (donor and patient), body mass index, donor age, type of LT, underlying disease, sex and HLA mismatch, ischemia time, anti-HLA antibodies, Pseudomonas colonization, CMV infections, immunosuppression induction and acute rejection. The population included 54% of men and 81% of double LT (mean age 43yrs). The main underlying diseases were cystic fibrosis (40%), emphysema/COPD (34%) and pulmonary arterial hypertension (14%). Mean (sd) individual exposure levels were 15.2 (2.1), 22.1 (3.1), 18.1 (7.3) and 51.7 (8.2) µg/m 3 for PM 2.5 , PM 10 , NO 2 and O 3 , respectively. NO 2 exposure was significantly associated with lower FEV 1 levels measured during the recovery period and a non-significant trend was observed in the decline period (estimate (se) = -3.39(1.48) p=0.02 and -1.96(1.47) p=0.18). None of the air pollutants exposure was associated with change in FEV 1 . Our results suggest a potential deleterious effect of chronic exposure to NO 2 on FEV 1 level following LT and did not evidence an effect of air pollution on change in FEV 1 . Fundings: EU-FP7 SYSCLAD, Vaincre la Mucoviscidose, Association Gregory Lemarchal.