OP0237 EXPOSURE TO ENVIRONMENTAL AIR POLLUTANTS AS A RISK FACTOR FOR PRIMARY SJÖGREN’S SYNDROME: A POPULATION-BASED COHORT STUDY

Abstract

Background: Recent studies suggest that air pollution may play a role in autoimmune diseases. However, few of them report the correlation between air pollution and primary Sjögren's syndrome (pSS). Objectives: We sought to determine whether people exposed to environmental fine particulate of air pollution have a higher risk of developing pSS. Methods: We performed a retrospective population-based cohort study from the National Health Insurance Research Database (NHIRD) of Taiwan's population, using the international Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM) to categorize each disease diagnosis. Air pollution data on Nitric oxide (NO), methane (CH4), and carbon monoxide (CO) were obtained from the Taiwan Air Quality-Monitoring Database (TAQMD), where daily air pollution data from community-based monitoring sites (78 sites since 1993) was available on a real-time basis. We followed up from January 1st, 1998 to the endpoint of SS diagnosis or to December 31, 2011.The daily average air pollutant concentrations were divided into 4 quartile-based groups (Q1-Q4). The incidence rate, hazard ratios (HRs), as well as 95% confidence intervals for pSS, were stratified by the quartiles of air pollutant concentration, and calculated with a Cox proportional regression model. Finally, Ingenuity Systems Pathway Analysis (IPA) was conducted to identify activated pathways among air way epithelial cells exposed to airborne coarse, fine, and ultrafine particles, and parotid gland tissues from pSS patients using Z-score visualization. Results: A total of 200 patients were diagnosed with SS. The mean age of patients with pSS was 53.1 years. The incidence of pSS was 0.11%. With the increase in exposure concentrations of nitrogen dioxide, methane, and carbon monoxide (from Q1 to Q4), the incidence rate for pSS of per 1000 person-years increased from 0.7 to 1.19, from 0.93 to 2.14, and from 0.57 to 1.06, respectively. Moreover, compared with Q1, the adjusted HR in Q4 after adjusting for age, gender, monthly income and urbanization levels increased to 1.86, 2.21 and 2.04, respectively. IPA analyses suggested that the underlying cellular mechanisms involved up-regulation of chronic inflammatory pathways including fibrosis signaling pathway. Conclusion: Exposure to air pollutants, specifically NO, CH4, and CO, was associated with SS development, mostly driven by fibrotic signaling cascades occurred during chronic inflammation.