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OP0178 ASSOCIATION BETWEEN ENVIRONMENTAL AIR POLLUTION AND RHEUMATOID ARTHRITIS FLARES
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  1. G. Adami1,
  2. A. Fassio1,
  3. O. Viapiana1,
  4. G. Orsolini1,
  5. E. Bertoldo1,
  6. A. Giollo1,
  7. D. Gatti1,
  8. M. Rossini1
  1. 1University of Verona, Rheumatology Unit, Verona, Italy

Abstract

Background: Environmental air pollution has been linked to the pathogenesis of Rheumatoid Arthritis (RA). Nevertheless, evidence linking higher concentrations of air pollutants with the risk of RA reactivations is missing.

Objectives: The objective of the present study was to determine the association between RA flares and air pollution.

Methods: We collected longitudinal data of patients affected by RA and of the daily concentration of air pollutants in the Verona area. We designed a case-crossover study. In case-crossover studies, instead of obtaining information from two groups (cases and controls), the exposure information is obtained comparing two different periods of time in the same group of patients followed longitudinally. We compared the exposure to pollutants in the 30-day and 60-day periods preceding an arthritic flare referent to the 30-day and 60-day preceding a low-disease activity visit. Flare was defined as an increase in DAS28-CRP of >1.2 points with current DAS28-CRP ≥3.2 (OMERACT definition).

Results: 888 patients with RA with 3,396 follow-up visits were included in the study. 13,636 daily air pollution records were retrieved. We found an exposure-response relationship between the concentration of air pollutants and the risk of having abnormal CRP levels (Figure 1). Patients exposed to greater concentrations of air pollutants were at higher risk of having CRP levels ≥5 mg/L. Patients exposed to PM10 concentrations ≥50 μg/m3 had a 70% higher risk of having CRP levels ≥5 mg/L (OR 1.696 95% CI, 1.245-2.311). Among RA patients, 440 patients (49.5%) had at least 2 follow-up visits with a difference in DAS28-CRP of more than 1.2 points (with current DAS28-CRP ≥3.2), serving as our sample for the case-crossover study. Concentrations of CO, NO, NO2, NOx, PM10, PM2.5 and O3 were higher in the 60-day period preceding a flare (Table 1). Sensitivity analyses considering geometric mean and cumulative concentrations yielded similar results (data not shown). Remarkably, we found that the cumulative exposure to NO2 in the 60 days preceding a flare was approximately 500 µg/m3 higher than the low disease activity visit, an exposure that equates to approximately to 200 passively smoked cigarettes (3.5 cigarettes per day on a 60-day period).

Table 1.

Case-crossover study. Mean concentrations (mean and Area Under the Curve) of air pollutants in the 60 days before low-disease activity visit and flare visit (DAS28-CRP difference >1.2)

Figure 1.

Odds of having abnormal CRP serum levels (≥5 mg/L) at different exposures of PM10 and PM2.5 (mean concentration in the 60 days before assessment)

Conclusion: We found a striking association between air pollution and RA disease severity and reactivations in a cohort of patients followed over a 5-year period. The exposure to high levels of air pollutants was associated with increased CRP levels and a higher risk of experiencing a flare of arthritis. This excessive risk was evident at very low levels of exposure, even below the proposed threshold for the protection of human health. Our study has important and direct consequences. In order to reduce the burden of RA, public and environmental health policy makers should aim to diminish gaseous and PM emissions to a larger extent as currently recommended.

Disclosure of Interests: None declared

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