Original Investigation Associations of Air Pollution and Serum Biomarker Abnormalities in Individuals with Hemodialysis- Dependent Kidney Failure

Background Ambient particles with a median aerodynamic diameter of ,2.5 mm (PM2.5) is a ubiquitous air pollutant with established adverse health consequences. While postulated to promote a systemic inflammatory response, limited studies have demonstrated changes in serum biomarkers related to PM2.5 exposure. We aim to examine associations between short-term PM2.5 exposure and commonly measured biomarkers known to be affected by inflammation among patients receiving maintenance in-center hemodialysis. Methods We conducted a retrospective open cohort study from January 1, 2008, to December 31, 2014. Adult hemodialysis patients were identified from the United States Renal Data System and linked at the patient level to laboratory data from a large dialysis organization. Daily ambient PM2.5 was estimated on a 1-km grid and assigned to cohort patients based on the ZIP codes of dialysis clinics. Serum albumin, serum ferritin, transferrin saturation (TSAT), and serum hemoglobin were ascertained from the dialysis provider organization database. Mixed-effect models were used to assess the changes in biomarker levels associated with PM2.5 exposure. Results The final cohort included 173,697 hemodialysis patients. Overall, the daily ZIP-level ambient PM2.5 averages were 8.4–8.5 mg/m3. A 10-mg/m3 increase in same-day ambient PM2.5 exposure was associated with higher relative risks of lower albumin (relative risk [RR], 1.01; 95% confidence interval [95% CI], 1.01 to 1.02) and lower hemoglobin (RR, 1.02; 95% CI, 1.01 to 1.03). Associations of same-day ambient PM2.5 exposure and higher ferritin and lower TSAT did not reach statistical significance. Conclusions Short-term PM2.5 exposure was associated with lower serum hemoglobin and albumin among patients receiving in-center hemodialysis. These findings lend support to the role of inflammation in PM2.5 exposure-outcome associations. KIDNEY360 4: 63–68, 2023. doi: https://doi.org/10.34067/KID.0003822022 Introduction Ambient exposure to particles with a median aerodynamic diameter of ,2.5 mm (PM2.5) is ubiquitous and an established contributor to respiratory and cardiovascular diseases and mortality.1 However, the pathologic mechanisms underlying PM2.5 exposure and clinical outcomes are incompletely understood. Various studies in cell culture and animal models have Department of Epidemiology, Gillings School of Global Public Health, University of North Carolina (UNC) at Chapel Hill, Chapel Hill, North Carolina Oak Ridge Institute for Science and Education at the United States Environmental Protection Agency, National Health and Environmental Effects Research Laboratory, Environmental Public Health Division, Research Triangle Park, North Carolina Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, Georgia UNC Kidney Center, Division of Nephrology and Hypertension, Department of Medicine, UNC School of Medicine, Chapel Hill, North Carolina Department of Medicine, School of Medicine, UNC at Chapel Hill, Chapel Hill, North Carolina United States Environmental Protection Agency, Center for Public Health and Environmental Assessment, Research Triangle Park, North