You are here:
Chronic Kidney Disease (CKD) and Exposure to Fine Particulate Matter and Ozone: A Cross-Sectional Study Utilizing North Carolina Electronic Healthcare Records
Citation:
Dillon, D., C. Ward-Caviness, A. Kshirsagar, J. Moyer, J. Schwartz, Q. Di, AND A. Weaver. Chronic Kidney Disease (CKD) and Exposure to Fine Particulate Matter and Ozone: A Cross-Sectional Study Utilizing North Carolina Electronic Healthcare Records. International Society of Environmental Epidemiology, Athens, GREECE, September 18 - 21, 2022.
Impact/Purpose:
Chronic kidney disease is a common chronic condition, affecting more than 38 million people in the United States. Environmental exposures, including air pollution, may contribute to chronic kidney disease. We examined associations between PM2.5 and ozone air pollution with kidney function, measured as estimated glomerular filtration rate (eGFR). We used data from a random sample of electronic health records from the University of North Carolina healthcare system to estimate eGFR. We observed associations between poorer kidney funciton and PM2.5 and, to a lesser extent, ozone.
Description:
Background and aims: Chronic kidney disease (CKD) affects more than 38 million people in the United States, predominantly those over 65 years of age. While CKD etiology is complex, recent research suggests associations with certain environmental exposures. Additional studies are needed to understand the strength of associations. We examine estimated glomerular filtration rate (eGFR) using a random sample of North Carolina electronic healthcare records (EHRs) and potential relationships with PM2.5 and O3. Methods: Patient data came from a random sample of 7,065 EHRs within the EPA CARES resource, with recorded serum creatinine concentrations. Patients were seen at a University of North Carolina Healthcare System affiliated hospital or clinic from 2004-2017. We estimated eGFR using CKD-EPI equations. PM2.5 data comes from a hybrid model using 1x1 km grids and O3 data from CMAQ 12x12 km grids. Exposures were annual average PM2.5 and O3 based on the creatinine lab test date. We used multiple linear regression to estimate eGFR per IQR increase of PM2.5 & O3. We adjusted for patient sex, race, age, comorbidities, and 2010 census block group measures of sociodemographic and economic factors. Results: Patients averaged 55.3 (SD: 16.2) years of age, with 58.3% female. There were 1,001 patients (14.2%) diagnosed with CKD, identified by ICD-9 & 10 codes. Mean concentrations for the study period of PM2.5 and O3 were 9.92 (IQR: 1.61) µg/m3 and 40.20 (IQR: 2.53) ppb respectively. eGFR decreased 8.45 mL/min/1.73m2 (95% CI: 7.92, 8.98) per IQR increase of PM2.5 and a more modest decrease of 0.66 mL/min/1.73m2 (95% CI: -.08, 1.40) per IQR of O3. Conclusions: Annual average PM2.5, and to a lesser extent O3, were associated with lower (poorer) eGFR. Future work will examine the relationship between air pollution and onset of CKD and impaired renal function. This abstract does not reflect EPA policy.