Evidence on the effects of fine particulate matter (PM) constituents and sources on kidney injury is limited. We designed a panel study with 4 repeated measurements to investigate the association of acute exposure to chemical constituents and source-specific PM with kidney function and renal tubular injury. We further evaluated the modifying effect of Nrf2 promoter polymorphism. In this study, a total of 64 participants were recruited and ambient PM constituents were monitored at a fixed-site station. We used a positive matrix factorization (PMF) model to identify emission sources and linear mixed-effect models to explore the associations. An interquartile range (IQR) increase in PM concentration was associated with a 1.40 % and 3.15 % decrease in eGFR-Cr (eGFR assessed by creatinine) and eGFR-Cys (eGFR assessed by cystatin-C), respectively, and 10.2 % higher kidney injury molecule 1 (KIM-1) levels. Carbonaceous components (EC and OC), metallic elements (Cr, K, Pb, Zn) and Cl were robustly responsible for kidney injury. Per IQR increase in these constituents accounted for 0.57 % to 1.62 % declines in eGFR-Cr; 1.36 % to 3.66 % declines in eGFR-Cys; and 7.50 % to 19.83 % increments in KIM-1. Specific source analysis revealed that PM emitted by combustion was associated with the largest reduction in eGFR, while the secondary source played a more prominent role in renal tubular injury. The dominant models showed that the magnitudes of the effect estimates of PM and its constituents were generally larger in the participants with minor alleles of the Nrf2 promoter. These findings suggest that acute exposure to EC, OC, Cl and several metallic constituents may be responsible for kidney injury induced by PM, especially in individuals with unfavorable Nrf2 genotypes. PM from combustion and secondary sources impairs kidney health, highlighting the importance of source-oriented PM control strategies.
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