Objective. Recent studies in animal models and on human cells have shown an effect of sodium chloride (NaCl) on Th17 cells promoting inflammation. The aim of this study was to evaluate the impact of NaCl intake on the risk of development of RA.

Methods. A nested case–control study was performed using population-based prospective data from the Västerbotten Intervention Programme. The study included 386 individuals who had stated their dietary habits as part of a community intervention programme a median of 7.7 years before the onset of symptoms of RA. For comparison, 1886 matched controls were identified from the same database and co-analysed.

Results. No significant association was found between sodium intake and the development of RA when all of the individuals were included. In analyses stratified for smoking status at the time of the examination, sodium intake more than doubled the risk for RA among smokers [odds ratio (OR) 2.26 (95% CI 1.06, 4.81)]. This was not observed among non-smokers. Additive interaction analysis of smoking and cases with the highest tertile of sodium intake revealed that 54% of the increased risk of developing RA from these exposures was due to interaction between them [attributable proportion 0.54 (95% CI 0.26, 0.82)]. The risk was further increased for the development of anti-CCP-positive and/or HLA shared epitope–positive RA.

Conclusion. Although we were unable to confirm our stated hypothesis, our results that high sodium consumption among smokers was associated with the risk of RA may provide new insights into the impact of smoking in RA development.