Lihong Ye, Ding Ye, Yu Qian, Jiayu Li, Bin Liu, Jiacheng Ying, Manli Wang, Hao Lin, Jing Guo, Xiaohui Sun, Zhixing He, Chengping Wen, Yingying Mao
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引用次数: 0
Abstract
The relationship between air pollution and the risk of systemic lupus erythematosus (SLE) remains inconclusive. Here, we investigated the associations between long-term exposure to ambient air pollutants and incident SLE, based on a cohort of 502,004 participants free of SLE at baseline from UK Biobank. During a median of 13.65 follow-up years, 638 patients with SLE were identified. For each increase of interquartile range in air pollutant concentrations, the hazard ratios (HRs) and 95% confidence intervals (CIs) of SLE were 1.15 (1.04-1.27) for nitrogen dioxide (NO2), 1.08 (1.00-1.17) for nitrogen oxides (NOx), 1.13 (1.03-1.24) for particulate matter with the diameters ≤2.5 μm (PM2.5), 1.06 (0.99-1.14) for particulate matter with diameter between 2.5 μm and 10 μm (PMcoarse), and 1.10 (1.02-1.18) for particulate matter with diameter ≤10 μm (PM10), respectively. A non-linear relationship of PMcoarse with SLE risk was detected by using restricted cubic spline models (Pnon-linearity = 0.009), but not for the remaining air pollutants. Furthermore, smoking and long-term exposure to PM pollutants had significant additive interaction on SLE risk, with a relative excess risk of additive interaction (RERI) of 0.07 (95% CI: 0.02-0.09) for PM2.5, and 0.05 (95% CI: 0.01-0.08) for PM10. Additive interactions were also observed for genetic risk and PMcoarse (RERI: 0.04, 95% CI: 0.00-0.07) and PM10 (RERI: 0.04, 95% CI: 0.02-0.06) on SLE risk. In conclusion, our findings emphasize the significance of evaluating the impacts of long-term exposure to ambient air pollutants in preventing SLE, and highlight the necessity to identify individuals who smoke and have a high genetic risk to minimize the harmful effects of air pollution on the development of SLE.