Abstract: OP0178
Authors: G. Adami et al.

zum Abstract

Key content:
In an elegant case-crossover study, these Italian investigators explored the association between RA flares and air pollution in the preceding weeks. A total of 888 patients with RA and 3’396 follow-up visits were analysed. The authors found a convincing dose (exposure)-response between the concentration of air pollutants and increased CRP levels: Patients exposed to PM10 concentrations ≥50 µg/m3 had a ~70% higher risk of having CRP levels ≥5 mg/L. Furthermore, concentrations of CO, NO, NO2, NOx, PM10, PM2.5 and O3 were significantly higher in the 60-day period preceding a flare and the cumulative exposure to NO2 in the 60 days preceding a flare was approximately 500 µg/m3 higher than for low disease activity visit, which represents an exposure that equates to approximately to 200 passively smoked cigarettes.

It has been known for a long time that active and passive smoking is a risk factor for developing RA. Once RA has developed, the impact of smoking on RA disease activity is less clear-cut and research has been conflicting. Similarly, epidemiologic studies have suggested that being exposed to traffic pollution or dusty environments may also increase the risk of RA, but studies of air pollution in established RA are scarce.

These authors nicely demonstrate a striking association between air pollution and CRP levels and RA-flares over a 5 year period. One criticism is that RA flare was defined by the DAS28-CRP, which is heavily dependent on acute phase reactants. It is not impossible that some of the flares were mainly driven by an increase of CRP levels, without much change in joint inflammation or joint pain. Perhaps in order to reduce the burden of RA, we should aim decrease our patient’s exposure to air pollution?

Prof. Dr. Axel Finckh