School of Nursing, Peking University, Beijing, China.
Ministry of Education Key Laboratory of Environment and Health, and State Key Laboratory of Environmental Health (Incubating), School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
JAMA Netw Open. 2024 Jul 1;7(7):e2421665. doi: 10.1001/jamanetworkopen.2024.21665.
Psoriasis is a common autoinflammatory disease influenced by complex interactions between environmental and genetic factors. The influence of long-term air pollution exposure on psoriasis remains underexplored.
To examine the association between long-term exposure to air pollution and psoriasis and the interaction between air pollution and genetic susceptibility for incident psoriasis.
DESIGN, SETTING, AND PARTICIPANTS: This prospective cohort study used data from the UK Biobank. The analysis sample included individuals who were psoriasis free at baseline and had available data on air pollution exposure. Genetic analyses were restricted to White participants. Data were analyzed between November 1 and December 10, 2023.
Exposure to nitrogen dioxide (NO2), nitrogen oxides (NOx), fine particulate matter with a diameter less than 2.5 µm (PM2.5), and particulate matter with a diameter less than 10 µm (PM10) and genetic susceptibility for psoriasis.
To ascertain the association of long-term exposure to NO2, NOx, PM2.5, and PM10 with the risk of psoriasis, a Cox proportional hazards model with time-varying air pollution exposure was used. Cox models were also used to explore the potential interplay between air pollutant exposure and genetic susceptibility for the risk of psoriasis incidence.
A total of 474 055 individuals were included, with a mean (SD) age of 56.54 (8.09) years and 257 686 (54.36%) female participants. There were 9186 participants (1.94%) identified as Asian or Asian British, 7542 (1.59%) as Black or Black British, and 446 637 (94.22%) as White European. During a median (IQR) follow-up of 11.91 (11.21-12.59) years, 4031 incident psoriasis events were recorded. There was a positive association between the risk of psoriasis and air pollutant exposure. For every IQR increase in PM2.5, PM10, NO2, and NOx, the hazard ratios (HRs) were 1.41 (95% CI, 1.35-1.46), 1.47 (95% CI, 1.41-1.52), 1.28 (95% CI, 1.23-1.33), and 1.19 (95% CI, 1.14-1.24), respectively. When comparing individuals in the lowest exposure quartile (Q1) with those in the highest exposure quartile (Q4), the multivariate-adjusted HRs were 2.01 (95% CI, 1.83-2.20) for PM2.5, 2.21 (95% CI, 2.02-2.43) for PM10, 1.64 (95% CI, 1.49-1.80) for NO2, and 1.34 (95% CI, 1.22-1.47) for NOx. Moreover, significant interactions between air pollution and genetic predisposition for incident psoriasis were observed. In the subset of 446 637 White individuals, the findings indicated a substantial risk of psoriasis development in participants exposed to the highest quartile of air pollution levels concomitant with high genetic risk compared with those in the lowest quartile of air pollution levels with low genetic risk (PM2.5: HR, 4.11; 95% CI, 3.46-4.90; PM10: HR, 4.29; 95% CI, 3.61-5.08; NO2: HR, 2.95; 95% CI, 2.49-3.50; NOx: HR, 2.44; 95% CI, 2.08-2.87).
In this prospective cohort study of the association between air pollution and psoriasis, long-term exposure to air pollution was associated with increased psoriasis risk. There was an interaction between air pollution and genetic susceptibility on psoriasis risk.
银屑病是一种常见的自身炎症性疾病,受环境和遗传因素之间复杂相互作用的影响。长期暴露于空气污染对银屑病的影响仍未得到充分探索。
研究长期暴露于空气污染与银屑病之间的关联,以及空气污染与银屑病遗传易感性之间的相互作用。
设计、地点和参与者:本前瞻性队列研究使用了英国生物库的数据。分析样本包括基线时无银屑病且可获得空气污染暴露数据的个体。遗传分析仅限于白种人参与者。数据分析于 2023 年 11 月 1 日至 12 月 10 日进行。
二氧化氮(NO2)、氮氧化物(NOx)、直径小于 2.5 µm 的细颗粒物(PM2.5)和直径小于 10 µm 的颗粒物(PM10)的长期暴露以及银屑病的遗传易感性。
为了确定长期暴露于 NO2、NOx、PM2.5 和 PM10 与银屑病风险之间的关联,使用了时间变化的空气污染暴露 Cox 比例风险模型。还使用 Cox 模型探索了空气污染暴露与银屑病发病遗传易感性之间的潜在相互作用。
共纳入 474055 名参与者,平均(标准差)年龄为 56.54(8.09)岁,257686 名(54.36%)为女性参与者。有 9186 名参与者(1.94%)为亚洲或亚裔英国人,7542 名(1.59%)为黑人或黑人英国人,446637 名(94.22%)为白种欧洲人。在中位数(IQR)随访 11.91(11.21-12.59)年期间,记录了 4031 例银屑病发病事件。银屑病发病风险与空气污染物暴露呈正相关。与 PM2.5、PM10、NO2 和 NOx 的 IQR 每增加一个单位,风险比(HR)分别为 1.41(95%CI,1.35-1.46)、1.47(95%CI,1.41-1.52)、1.28(95%CI,1.23-1.33)和 1.19(95%CI,1.14-1.24)。与处于最低暴露四分位数(Q1)的个体相比,处于最高暴露四分位数(Q4)的个体,多变量调整后的 HR 分别为 PM2.5 2.01(95%CI,1.83-2.20)、PM10 2.21(95%CI,2.02-2.43)、NO2 1.64(95%CI,1.49-1.80)和 NOx 1.34(95%CI,1.22-1.47)。此外,还观察到空气污染与银屑病遗传易感性之间存在显著的相互作用。在 446637 名白种人个体的亚组中,与空气污染水平最低四分位数且遗传风险低的个体相比,暴露于空气污染水平最高四分位数且遗传风险高的个体发生银屑病的风险显著增加(PM2.5:HR,4.11;95%CI,3.46-4.90;PM10:HR,4.29;95%CI,3.61-5.08;NO2:HR,2.95;95%CI,2.49-3.50;NOx:HR,2.44;95%CI,2.08-2.87)。
在这项关于空气污染与银屑病关联的前瞻性队列研究中,长期暴露于空气污染与银屑病风险增加相关。空气污染与银屑病遗传易感性之间存在相互作用。