Long-term air pollutants exposure on risk of psoriasis: the mediating role of accelerated biological aging among 284,544 participants.

Abstract

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.