Jiaqi Zhu

Increasing studies are indicating a potential association between ambient air pollution exposure and fasting blood glucose (FBG), an indicator of prediabetes and diabetes. However, there is inconsistency within the existing literature. The aim of this study was to summarize the associations of exposures to particulate matters (PMs) (with aerodynamic diameters of ≤1 μm (PM₁), ≤2.5 μm (PM_2.5), and ≤10 μm (PM₁₀), respectively) and gaseous pollutants (sulfur dioxide (SO₂), nitrogen dioxide (NO₂) and ozone (O₃)) with FBG based on the existing epidemiological research for a better understanding of the relationship between air pollution and diabetes. Up to 2 July 2024, we performed a comprehensive literature retrieval from various electronic databases (PubMed, Web of Science, Scopus, and Embase). Random-effect and fixed-effect models were utilized to estimate the pooled percent changes (%) and 95% confidence intervals (CIs). Then, subgroup meta-analyses and meta-regression analyses were applied to recognize the sources of heterogeneity. There were 33 studies eligible for the meta-analysis. The results showed that for each 10 μg/m³ increase in long-term exposures to PM₁, PM_2.5, PM₁₀, and SO₂, the pooled percent changes in FBG were 2.24% (95% CI: 0.54%, 3.96%), 1.72% (95% CI: 0.93%, 2.25%), 1.19% (95% CI: 0.41%, 1.97%), and 0.52% (95% CI:0.40%, 0.63%), respectively. Long-term exposures to ambient NO₂ and O₃ were not related to alterations in FBG. In conclusion, our findings support that long-term exposures to PMs of various aerodynamic diameters and SO₂ are associated with significantly elevated FBG levels.

Background: The burden of cardiovascular diseases caused by ambient particulate air pollution is universal. An increasing number of studies have investigated the potential effects of exposure to particulate air pollution on endothelial function, which is one of the important mechanisms for the onset and development of cardiovascular disease. However, no previous study has conducted a summary analysis of the potential effects of particulate air pollution on endothelial function. Objectives: To summarize the evidence for the potential effects of short-term exposure to ambient particulate air pollution on endothelial function based on existing studies. Methods: A systematic literature search on the relationship between ambient particulate air pollution and biomarkers of endothelial function including endothelin-1 (ET-1), E-selectin, intercellular cell adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) was conducted in PubMed, Scopus, EMBASE, and Web of Science up to 20 May 2023. Subsequently, a meta-analysis was conducted using a random effects model. Results: A total of 18 studies were included in this meta-analysis. A 10 μg/m³ increase in short-term exposure to ambient PM_2.5 was associated with a 1.55% (95% CI: 0.89%, 2.22%) increase in ICAM-1 and a 1.97% (95% CI: 0.86%, 3.08%) increase in VCAM-1. The associations of ET-1 (0.22%, 95% CI: −4.94%, 5.65%) and E-selectin (3.21%, 95% CI: −0.90% 7.49%) with short-term exposure to ambient PM_2.5 were statistically insignificant. Conclusion: Short-term exposure to ambient PM_2.5 pollution may significantly increase the levels of typical markers of endothelial function, including ICAM-1 and VCAM-1, suggesting potential endothelial dysfunction following ambient air pollution exposure.