Association between long-term exposure to low level air pollutants and incident end-stage kidney disease in the UK Biobank: A prospective cohort
Jing Li, Liang Dai, Xiaowei Deng, Jingwen Zhang, Congying Song, Junjie Xu, Anxin Wang, Zuying Xiong, Ying Shan, Xiaoyan Huang
Abstract
Previous studies suggest that air pollution can increase the risk of incident chronic kidney disease. However, the association between end-stage kidney disease and relatively low-level air pollutants co-exposure remains unclear. A prospective cohort was designed based on UK Biobank. From 1 January 2010 to 12 November 2021, 453,347 participants were followed up over a median of 11.87 years. Principal component analysis was used to identify major patterns of five air pollutants, including PM2.5, PM2.5-10, PM10, NO2, and NOx. Sub-distribution hazards models were used to estimate the associations between air pollution individually or jointly, and incident end-stage kidney disease, chronic kidney disease, and all-cause death, respectively. Principal component analysis identified two principal components, namely RC1 (PM2.5, NO2, and NOx) and RC2 (PM2.5-10 and PM10). An elevated risk of incident end-stage kidney disease was associated with an interquartile range increase in PM2.5 (hazard ratio: 1.11, 95% confidence interval: 1.02–1.22), NO2 (1.16, 1.04–1.30), NOx (1.08, 1.00–1.17), and RC1 (1.12, 1.02–1.23). An elevated risk of incident chronic kidney disease was associated with an interquartile range increase in PM2.5 (1.05, 1.03–1.07), NO2 (1.04, 1.02–1.06), NOx (1.03, 1.02–1.05), and RC1 (1.04, 1.02–1.06). An increased risk of all-cause mortality was associated with an interquartile range increase in PM2.5 (1.02, 1.00–1.04). Restricted cubic spline analyses indicated a monotonic elevating association of PM2.5, NO2, NOx, and RC1 with ESKD incidence. Long-term exposure to PM2.5, NO2, NOx, and their complex were associated with elevated end-stage kidney disease incidence, even at relatively lower levels of air pollution.