Independent and joint air pollutants exposure associated with kidney dysfunction mediating by hematocyte
- PMID: 40122905
- PMCID: PMC11930966
- DOI: 10.1038/s41598-025-95204-6
Independent and joint air pollutants exposure associated with kidney dysfunction mediating by hematocyte
Abstract
Air pollution is associated with hyperuricemia; however, its underlying mechanism remains poorly understood. In this retrospective analysis, 233 anonymous health data and urban air pollutants data were obtained. The mean daily exposure dose (DED) for combined air pollutants (CAPs) was 1.22 mg/day, which was defined as the threshold for dividing all individuals into two groups. The lower-exposure group (LEG) included those with a DED-CAPs less than or equal to 1.22 mg/day and the higher-exposure group (HEG) included those with a DED-CAPs that exceeded 1.22 mg/day. The peripheral blood cell counts of white blood cells, eosinophils, basophils, monocytes, and red blood cells were higher in the HEG than in the LEG, whereas peripheral platelet counts were lower in the HEG than in the LEG. In addition, serum uric acid (UA) levels were higher in the HEG than in the LEG. Multivariable-adjusted linear regression models suggested that with an increase in the daily exposure dose to air pollution, peripheral blood cells and serum UA levels increased. The results of mediation effect models further indicated that peripheral monocyte counts play a mediating role in the dose effect relationships between air pollutant exposures and serum UA levels. These results highlight that air pollution may increase serum UA levels by altering hematocytes inducing low-grade inflammation, which may ultimately increase the risk of kidney dysfunction.
Keywords: Air pollutant; Inflammation; Kidney dysfunction; Peripheral blood cells; Serum uric acid.
© 2025. The Author(s).
Conflict of interest statement
Declarations. Competing interests: The authors declare no competing interests.
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