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Background: Inhaled corticosteroid (ICS)-containing medications slow rate of decline of FEV 1 . Blood eosinophil (EOS) levels are associated with the degree of exacerbation reduction with ICS. Purpose: We investigated whether FEV 1 decline differs between patients with and without ICS, stratified by blood EOS level. Patients and methods: The UK Clinical Practice Research Datalink (primary care records) and Hospital Episode Statistics (hospital records) were used to identify COPD patients aged 35 years or older, who were current or ex-smokers with ≥2 FEV 1 measurements ≥6 months apart. Prevalent ICS use and the nearest EOS count to start of follow-up were identified. Patients were classified at baseline as higher stratum EOS (≥150 cell/µL) on ICS; higher stratum EOS not on ICS; lower stratum EOS (<150 cells/µL) on ICS; and lower stratum EOS not on ICS. In addition, an incident ICS cohort was used to investigate the rate of FEV 1 change by EOS and incident ICS use. Mixed-effects linear regression was used to compare rates of FEV 1 change in mL/year. Results: A total of 26,675 COPD patients met our inclusion criteria (median age 69, 46% female). The median duration of follow up was 4.2 years. The rate of FEV 1 change in prevalent ICS users was slower than non-ICS users (-12.6 mL/year vs -21.1 mL/year; P  =0.001). The rate of FEV 1 change was not significantly different when stratified by EOS level. The rate of FEV 1 change in incident ICS users increased (+4.2 mL/year) vs -21.2 mL/year loss in non-ICS users; P <0.001. In patients with high EOS, incident ICS patients showed an increase in FEV 1 (+12 mL/year) compared to non-ICS users whose FEV 1 decreased (-20.8 mL/year); P <0.001. No statistical difference was seen in low EOS patients. Incident ICS use is associated with an improvement in FEV 1 change, however, over time this association is lost. Conclusion: Regardless of blood EOS level, prevalent ICS use is associated with slower rates of FEV 1 decline in COPD., Competing Interests: Miss Whittaker reports grants from GlaxoSmithKline, during the conduct of the study; Dr Müllerova was employed by and reported personal fees from GlaxoSmithKline, during the conduct of the study; Dr Jarvis reports grants from European Union and Cystic Fibrosis Trust, outside the submitted work; she also reports grants from GlaxoSmithKline, during the conduct of the study. Dr Barnes is employed, holds shares and reports personal fees from GlaxoSmithKline, outside the submitted work; he also received grants from GlaxoSmithKline, during the conduct of the study. Dr Jones is employed by and reports personal fees from GlaxoSmithKline, during the conduct of the study; Dr Compton is employed, holds shares and reports personal fees from GlaxoSmithKline, during the conduct of the study; Dr Kiddle reports grants from MRC, during the conduct of the study; grants from Roche Diagnostics, Engineering and Physical Sciences Research Council, Biotechnology and Biological Sciences Research Council, National Institute for Health Research, Alzheimer’s Society, Eli Lily, and Jannsen, outside the submitted work; Dr Kiddle was supported by a MRC Career Development Award (MR/PO21573/1). Dr Quint reports grants from GlaxoSmithKline, during the conduct of the study; grants from The Health Foundation, MRC, Wellcome Trust, British Lung Foundation, Insmed, AstraZeneca, Bayer, Boehringer Ingelheim, Chiesi, Teva, and GlaxoSmithKline, outside the submitted work. The authors report no other conflicts of interest in this work.