Psoriasis burdens children and adults, but the impact of air pollution and aging is unclear. This study examines the association between air pollution exposure and psoriasis risk, considering the mediating role of biological aging. A prospective cohort study of 284,544 adults (51.3% female, mean age 56.26 ± 8.10 years) from the UK Biobank examined long-term exposure to air pollutants (PM2.5, PM10, PM2.5-10, NO2, and NOX). Biological aging was assessed using phenotypic age algorithms. Cox proportional hazards models were constructed to analyze the relationships with the risk of psoriasis, adjusting for demographic, socioeconomic, and health-related factors. Mediation analysis explored the role of biological aging. During a median follow-up of 15.58 years, 3,446 (1.21%) participants developed psoriasis. After adjusting for all confounders, each ten-unit increase (10 μg/m³) in PM2.5, PM10, NO2, and NOx, corresponded to the significantly increased risk of psoriasis by 95.7% (HR = 1.957, 95% CI 1.435-2.671), 19.7% (HR = 1.197, 95% CI 1.006-1.426), 9.0% (HR = 1.090, 95% CI 1.043-1.138) and 4.4% (HR = 1.044, 95% CI 1.024-1.066), respectively. Moreover, all air pollutants are significantly associated with biologically aging, while each one-year increase in PhenoAge was associated with a 5.0% higher risk of psoriasis (HR = 1.050, 95% CI 1.045-1.056). Finally, accelerated biological aging partially mediated 5.96%-13.86% of these air pollutants. Long-term exposure to air pollution significantly affects psoriasis risk, with biological aging as a partial mediator. Reducing pollution may lower the risk of psoriasis by slowing biological aging.

Keywords: air pollution; biological aging; cohort study; psoriasis.

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银屑病对儿童和成人造成了负担，但空气污染和衰老的影响尚不清楚。本研究探讨了长期接触空气污染物与银屑病风险之间的关联，并考虑生物衰老的中介作用。该研究使用英国生物银行（UK Biobank）的数据进行了一项前瞻性队列研究，共纳入284,544名成人参与者（女性占51.3%，平均年龄为56.26 ± 8.10岁），评估了长期接触空气污染物（PM2.5、PM10、PM2.5-10、NO2和NOX）的情况。生物衰老通过表型年龄算法进行评估。利用Cox比例风险模型分析银屑病风险的关系，并调整了人口统计学、社会经济及健康相关因素的影响。中介分析探索了生物衰老的作用。

在中位数为15.58年的随访期间，3,446名（1.21%）参与者新发银屑病。在校正所有混杂因素后，PM2.5、PM10、NO2和NOX每增加十单位（分别为10 μg/m³），银屑病风险分别显著增加了95.7%（HR = 1.957, 95% CI 1.435-2.671）、19.7%（HR = 1.197, 95% CI 1.006-1.426）、9.0%（HR = 1.090, 95% CI 1.043-1.138）和4.4%（HR = 1.044, 95% CI 1.024-1.066）。此外，所有空气污染物与生物衰老显著相关，PhenoAge每增加一岁，银屑病风险增加了5.0%（HR = 1.050, 95% CI 1.045-1.056）。最后，加速的生物衰老部分中介了这些空气污染物对银屑病的影响，占影响比例为5.96%-13.86%。长期接触空气污染显著影响银屑病风险，而生物衰老是其中的部分中介因素。减少污染可能通过减缓生物衰老来降低银屑病的风险。

关键词： 空气污染；生物老化；队列研究；银屑病。