The ESPOIR cohort is a prospective cohort study monitoring clinical, biologic, and radiographic data for patients with inflammatory arthritis lasting 6 weeks to 6 months. We examined the influence of smoking status on disease presentation (baseline characteristics) and therapeutic response at 1 year. Risk of structural progression at 12 months, defined as change in the modified Sharp/van der Heijde score ≥1, was analyzed by multivariate regression adjusted for potential confounders (age, sex, joint erosion at inclusion, educational level, positivity for rheumatoid factor or anti-cyclic citrullinated peptide 2 antibodies, and shared HLA-DRB1 epitope).

A total of 813 patients were included; 641 (79%) fulfilled the 2010 American College of Rheumatology/European League Against Rheumatism (EULAR) criteria for rheumatoid arthritis (RA). At inclusion, 138 (21.5%) were S patients, 168 (26.2%) were EX patients, and 335 (52.3%) were NS patients. Baseline acute-phase indicator values were significantly lower for S patients than EX and NS patients (mean ± SD erythrocyte sedimentation rate was 24.2 ± 18.2 mm/hour versus 33.4 ± 28.0 and 31.4 ± 25.0 [P = 0.02], respectively, and mean ± SD C-reactive protein level was 17.7 ± 28.0 mg/dl versus 28.5 ± 42.5 and 21.4 ± 29.0 [P = 0.01], respectively). Smoking status had no influence on Disease Activity Score in 28 joints, Health Assessment Questionnaire score, EULAR response, or use of disease-modifying antirheumatic drugs and biologic therapy in the first 12 months of followup (P > 0.05). The adjusted risk for structural disease progression was associated with active smokers (odds ratio 0.50 [95% confidence interval 0.27-0.93], P = 0.028). Sixteen patients had stopped smoking at 12 months, with no significant difference in observed outcomes from other patients.

In this large prospective cohort of patients with early arthritis, smoking status had no significant effect on disease activity and disability but did reduce 1-year radiographic disease progression. The antiinflammatory role of nicotine may explain the lower systemic inflammation and structural disease progression in current smokers with early RA.