Currently, our understanding of the impact of particulate matter on nephrotoxicity is limited. Oxidative stress has been identified as a mechanism involved in the adverse health effects due to exposure to this air pollutant, to their inorganic, organic, and aerobiological constituents (e.g. endotoxin). The goal of the present study was to correlate the endotoxin content of particulate matter with urinary oxidative stress biomarkers to explain early decline in renal dysfunction. Adult male Sprague-Dawley rats exposed to subchronic inhalation to particles less 2.5 micrometers in aerodynamic diameter, also known as fine particles or PM2.5 (8 weeks, 4 days/week, 5 hours/day). The control group was exposed to filtered air. Biomarkers of oxidative stress were assessed in urine samples per week harvested by metabolic cage. The assessed oxidative stress biomarkers were methylglyoxal, non-esterified fatty acids, malondialdehyde, advanced oxidative protein products, arginase, myeloperoxidase, glutathione-S-transferase, and gamma-glutamyl transferase. Subchronic exposure to PM2.5 increased five evaluated biomarkers in urine. Endotoxin content in PM2.5 positively correlated with urinary oxidative stress biomarkers evaluated. Positively correlation of urinary oxidative stress biomarkers was found with urinary early kidney damage biomarkers (e.g., β-2-microglobulin and cystatin-C). The subchronic inhalation exposure to PM2.5 induce the presence of oxidative stress reflected in urine, based on statistical correlations, suggests early kidney damage related to endotoxin content.