Association between Long-term Exposure to Air Pollution and Incident Chronic Kidney Disease among Adults in Beijing, China.
Abstract
Background
Chronic kidney disease (CKD) has become an increasing global health concern. The research objective was to explore the relationship between long-term exposure to atmospheric pollutants and the development of CKD.
Methods
A total of 15,580 participants were enrolled from the Beijing Air Pollution and Population Health Cohort. Incident CKD was identified by calculating estimated glomerular filtration rate (eGFR) based on biochemical measurements. Annual average concentrations of five ambient air pollutants (PM10, PM2.5, NO2, CO, and O3) in Beijing during the study period were collected. We applied time-varying Cox proportional hazards regression models to quantify the associations of individual air pollutants with incident CKD, reporting hazard ratios (HRs) and 95% confidence intervals (CIs). In addition, a composite air pollution score was constructed to evaluate the joint effect of multiple pollutants. Additionally, subgroup analyses were performed to examine potential modifying factors.
Results
Over the follow-up period from 2019 to 2025, 664 incident CKD cases occurred. Per 10μg/m3 increase, PM10(HR=1.18, 95%CI: 1.06-1.31) and CO (HR=1.02, 95%CI:1.01-1.03) were significantly associated with increased CKD risk. Both PM2.5 and NO2 showed positive risk associations, with HRs of 1.22 (95% CI: 0.99-1.50) and 1.17 (95% CI: 0.96-1.43), respectively. Conversely, O3 was inversely associated (HR=0.77, 95% CI: 0.68-0.87). Furthermore, each IQR increase in the composite air pollution score was associated with a 51% higher risk of CKD (HR, 1.51; 95% CI, 1.07-2.12). Subgroup analyses revealed stronger positive associations for PM2.5, PM10, CO, and combined exposure among females and older adults, and for PM2.5, NO2, and CO in urban residents.
Conclusion
Sustained PM10 and CO exposure was linked to elevated CKD risk, with O3 showing a potentially inverse pattern. The detrimental effects of air pollutants on renal function appeared to be amplified in several susceptible populations.