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Objective To investigate the interplay between the genetic predisposition to successful ageing and air pollution on lung disease in healthy aged German women under the hypothesis that ageing and lung diseases share mechanisms of oxidative stress and inflammation that can be regulated by genetic predisposition and environmental factors.Design German Study on the influence of Air pollution on Lung function, Inflammation and Aging prospective cohort between baseline (1985–1994) and follow-up (2007–2010).Setting Urban Ruhr area and the adjacent rural Münsterland in Germany.Participants At baseline, 4874 women aged 55 years living between 1985 and 1994 in the setting and at follow-up examination, 834 of them participated.Main outcome measures Chronic lung disease was defined as any of asthma, chronic bronchitis, cough (with sputum) or chronic obstructive pulmonary disease. Chronic individual exposures to nitrogen dioxide (NO 2), nitrogen oxides, particulate matter with median aerodynamic diameters <2.5 (PM2.5), PM10, PMcoarse and PM2.5 absorbance based on European Study of Cohorts for Air Pollution Effects land-use regression models were used. Main and interaction effects between the genetic risk score (77 single-nucleotide polymorphisms (SNPs) related to successful ageing) and air pollutant exposures were investigated using adjusted logistic regression models.Results In 560 women (67–80 years), chronic lung disease was present in 156. Higher exposure to air pollution was associated with increased odds by up to 43% per IQR-increase in NO 2 (IQR=11.6 µg/m³, 95% CI 1.15 to 1.77). The genetic make-up reduced the negative impact of air pollution (gene–environment interaction with NO2: OR=0.66, 95% CI 0.45 to 0.96), while a healthy lifestyle further strengthens this association.Conclusions In elderly women, genetic predisposition based on successful ageing SNPs likely reduces the negative impact of air pollution on chronic lung disease, while a healthy lifestyle further strengthens this association.