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Diabetes mellitus (DM) has been suggested as a potential risk factor for tinnitus, but evidence remains inconclusive. This meta-analysis aimed to evaluate the association between DM and tinnitus by systematically reviewing and synthesizing data from observational studies. A comprehensive literature search was conducted in PubMed, Embase, and Web of Science up to August 16, 2024. Observational studies with a sample size of at least 100 participants that assessed the relationship between DM and tinnitus were included. Studies involving populations with specific diseases were excluded. Odds ratios (ORs) and 95% confidence intervals (CIs) were pooled using a random-effects model. Study quality was assessed using the Newcastle-Ottawa Scale (NOS), and sensitivity and subgroup analyses were performed. Publication bias was evaluated using funnel plots and Egger’s regression test. Twelve studies comprising 2,277,719 participants were included. The pooled analysis revealed a significant association between DM and tinnitus (OR: 1.18, 95% CI: 1.06–1.31, P = 0.002), with moderate heterogeneity (I² = 51%). Sensitivity analyses confirmed the robustness of these findings. Subgroup analyses showed no significant differences by geographical region, mean age, sex distribution, tinnitus diagnosis method, or model used for association estimation. Publication bias was not detected (Egger’s test P = 0.29). These findings suggest that DM is significantly associated with an increased risk of tinnitus. Further research is warranted to explore underlying mechanisms and causal relationships. Nonetheless, the results underscore the importance of monitoring tinnitus in patients with diabetes.

Background The pathogenesis of primary spontaneous pneumothorax (PSP) is unclear. Fine particles aggregated in the lung can be phagocytosed by alveolar macrophages (AMs) to induce an inflammatory reaction and damage local pulmonary tissue, which could be a mechanism of PSP. This project aimed to explore the pathological association between fine particulate matter and PSP. Methods Thirty pulmonary bullae tissues were obtained from surgery of PSP patients (B group). The adjacent normal tissues of the lungs were defined as the control S group. Another 30 normal lung tissues with nonpneumothorax disease (NPD) were applied as the control N group. Hematoxylin and eosin (H & E), Wright-Giemsa (W-G), Victoria blue, and immunohistochemical (IHC) staining experiments were performed to measure the levels of fine particulate matter, alveolar macrophages (AMs), pulmonary elastic fibers, monocyte chemoattractant protein-1 (MCP-1), and matrix metalloproteinase-9 (MMP-9) in the lung tissues. The serum levels of MCP-1 and MMP-9 were prospectively analyzed as well. Results Histopathological examinations revealed obvious deposition of fine particulate matter and inflammatory reactions (proliferation of AMs) in the B group, compared with those in the S group and the N group. These alterations were significantly associated with PSP. The numbers of AMs and pulmonary elastic fibers, the positive area of the H-score, as well as the concentrations of MCP-1 and MMP-9 in the lungs of the experimental group were obviously raised compared with the controls (P < 0.05). Conclusions Fine particulate matter aggregation, inflammation (macrophage hyperplasia), and overexpression of MCP-1 and MMP-9 may contribute to the pathogenesis of PSP. The overaccumulation of fine particulate matter may play a crucial part in the occurrence of adolescent and young adult PSP. Trial registration This project was enrolled on the Chinese Clinical Trial Registry: ChiCTR2100051460.