Background:There is increasingly evidence that environmental air pollution is associated with both development of chronic inflammatory arthritides (CIA). The role of air pollutants on the treatment response of CIA (including psoriatic arthritis [PsA] and ankylosing spondylitis [AS]) is still unclear.Objectives:The objective of the present study is to determine the association between the concentration of air pollutants and biological drug retention rates in CIA.Methods:We retrieved longitudinal data of patients affected by CIA on biological therapies and of the daily concentration of air pollutants in the Verona area. We designed a case-crossover study to compare the exposure to pollutants in the 30-day and 60-day periods preceding a drug switch or swap due to disease progression referent to the 30-day and 60-day periods preceding a visit with stable treatment for at least 6 months.Results:1,286 patients with CIA (888 with RA, 260 with PsA and 138 with AS) with 5,454 follow-up visits were included in the study. 13,636 daily air pollution records were retrieved. We found an exposure-dependent relationship between exposure to air pollutants and CRP serum levels in CIA. At PM10 exposures of >50 μg/m3 and >40 μg/m3 we found a 150% and 65% higher risk of having CRP above 5 mg/L respectively (OR 2.564, 95% CI 2.114-3.110 and OR 1.659, 95% CI 1.440-1.910, respectively.). If the threshold was set at >30 μg/m3 of PM10 (below the European Union health protection limit) we still found a 38% higher risk of having altered CRP (OR 1.383, 95% CI 1.206-1.588). Among CIA patients, 280 patients (21.7%) had at least 2 follow-up visits with at least one drug switch or swap due to drug inefficacy and one visit with stable treatment for at least 6 months, serving as our sample for the case-crossover study. We found that air pollutants concentrations were higher before a switch or swap due to drug inefficacy (Figure 1A). Figure 1B shows the receiver operating characteristic (ROC) curve for the prediction of switch or swap due to drug inefficacy. Discriminatory capacity of disease activity alone was the highest (AUC 0.841) but when the prediction model included the concentrations of air pollutants in the 60 days before the visit the discriminatory capacity increased (AUC 0.879).Figure 1.A) Mean concentrations of air pollutants in the 60-day period before switch or swap visit compared to the stable treatment visit. p <0.001 between all groups. B) Receiving operating characteristics (ROC) curves for the prediction of switch or swap due to drug inefficacyConclusion:We found that environmental air pollution was a determinant of poor response to biological treatment in a cohort of patients with CIA followed over a 5-year period. Intervention aimed to decrease the fossil combustion emissions might have beneficial effects on biologics persistence rate of patients with CIA.Disclosure of Interests:None declared
Environmental Air Pollution Is a Predictor of Poor Response to Biological Drugs in Chronic Inflammatory Arthritides
