Component-specific effects of PM2.5 on endoscopically identified erosive gastric mucosal lesions: a time-series study in Yixing, China.

BACKGROUND: PM2.5 has been increasingly linked to digestive morbidity, but evidence on its short-term association with gastric mucosal injury remains limited. Few epidemiological studies have examined component-specific associations of PM2.5 with endoscopically identified erosive gastric mucosal lesions (EGML), common indicators of impaired mucosal defense. METHODS: We consecutively enrolled individuals undergoing gastroscopy at Yixing People's Hospital from January 1, 2024 to December 31, 2025, and collected their basic characteristics and gastroscopic findings. Daily grid concentrations of PM2.5 and its five chemical components were also extracted. We applied generalized additive models to explore the lag-specific correlations between particulate pollutants and endoscopically identified EGML. Attributable burden analysis was further performed to estimate the preventable number of cases under hypothetical reduction scenarios, and the relative contribution of each component was quantified. RESULTS: A total of 60,789 individuals received gastroscopy, of whom 14,325 had EGML. A per interquartile range increase in PM2.5 concentration was associated with a 7.6% higher risk of EGML [incidence rate ratio (IRR): 1.076; 95% confidence interval (CI): 1.024, 1.132]. Among PM2.5 components, positive associations that remained significant after FDR correction were observed for sulfate (IRR: 1.070; 95% CI: 1.024, 1.118) and ammonium (IRR: 1.082; 95% CI: 1.026, 1.141). In contrast, no significant associations were found for nitrate (IRR: 1.012; 95% CI: 0.979, 1.046), organic matter (IRR: 1.012; 95% CI: 0.981, 1.043), and black carbon (IRR: 1.012; 95% CI: 0.982, 1.043). CONCLUSION: Short-term PM2.5 exposure is positively associated with EGML risk. Among the five components, sulfate and ammonium showed the strongest evidence of positive associations, although their independent contributions require further study. These findings extend existing epidemiological evidence on PM2.5 and gastric damage, and provide component-specific information that may inform targeted air quality management and population-level prevention of gastric mucosal diseases.