The potential effects of short-term exposure to major ambient gaseous pollutants (ozone: O₃, carbon monoxide: CO, and sulfur dioxide: SO₂) on platelet mitochondrial DNA (mtDNA) methylation have been uncertain and no studies have examined whether platelet mtDNA methylation levels could modify the associations between ambient gaseous pollutants and the risks of ST-segment depression (STDE) and T-wave inversion events (TIE), two indicators of myocardial ischemia. This study used data from a randomized, double-blind, placebo-controlled intervention study with a standardized 24-hour exposure protocol among 110 participants in Beijing. Absolute changes in platelet mtDNA methylation (ACmtDNAm) levels were determined by two repeated measurements on platelet mtDNA methylation levels in blood samples collected before and after the 24-hour exposure period. A multivariable linear regression model and a generalized linear model with a Poisson link function were used to investigate the associations of ambient gaseous pollutants with platelet mtDNA methylation levels, STDE, and TIE, respectively. Short-term O₃ exposure was significantly associated with decreased ACmtDNAm at ATP6_P1 but increased ACmtDNAm at mt12sRNA, MT-COX1, and MT-COX1_P2; short-term CO and SO₂ exposures were significantly associated with decreased ACmtDNAm at D-loop, MT-COX3- and ATP-related genes. Moreover, short-term O₃ exposure was significantly associated with increased risks of STDE and TIE, and ACmtDNAm at MT-COX1 and MT-COX1_P2 modified the association between short-term O₃ exposure and STDE events. L-Arg supplementation attenuated the effects of ambient gaseous pollutants, particularly O₃, on ACmtDNAm and STDE. Platelet mtDNA methylation levels are promising biomarkers of short-term exposure to ambient gaseous air pollution, and are likely implicated in the mechanism behind the association of ambient O₃ pollution with adverse cardiovascular effects. L-Arg supplementation showed the potential to mitigate the adverse effects of ambient O₃ pollution.

This study characterizes the impacts of transported peat-forest (PF) burning smoke on an urban environment and evaluates associated source burning conditions based on carbon properties of PM2.5 at the receptor site. We developed and validated a three-step classification that enables systematic and more rapid identification of PF smoke impacts on a tropical urban environment with diverse emissions and complex atmospheric processes. This approach was used to characterize over 300 daily PM2.5 data collected during 2011-2013, 2015 and 2019 in Singapore. A levoglucosan concentration of ≥0.1 μg/m3 criterion indicates dominant impacts of transported PF smoke on urban fine aerosols. This approach can be used in other ambient environments for practical and location-dependent applications. Organic carbon (OC) concentrations (as OC indicator) can be an alternate to levoglucosan for assessing smoke impacts on urban environments. Applying the OC concentration indicator identifies smoke impacts on ∼80% of daily samples in 2019 and shows an accuracy of 51-86% for hourly evaluation. Following the systematic identification of urban PM2.5 predominantly affected by PF smoke in 2011-2013, 2015 and 2019, we assessed the concentration ratio of char-EC/soot-EC as an indicator of smoldering- or flaming-dominated burning emissions. When under the influence of transported PF smoke, the mean concentration ratio of char-EC to soot-EC in urban PM2.5 decreased by >70% from 8.2 in 2011 to 2.3 in 2015 but increased to 3.8 in 2019 (p < 0.05). The reversed trend with a 65% increase from 2015 to 2019 shows stronger smoldering relative to flaming, indicating a higher level of soil moisture at smoke origins, possibly associated with rewetting and revegetating peatlands since 2016.

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.

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.

Black carbon (BC), a key toxic constituent of ambient PM_2.5, and psychosocial stress, heightened by socioeconomic instability, both impair cardiovascular health. While epidemiological studies suggest that psychosocial stress could amplify the cardiovascular risks associated with air pollution, experimental evidence on the acute effects and mechanisms of joint exposure to BC and psychosocial stress is still lacking. In this study, a psychosocial stress model of male Sprague Dawley rats was exposed to different doses of BC by intratracheal instillation, followed by measurement of the hippocampal glucocorticoid receptor (GR) methylation, DNA methyltransferase (DNMT) and GR expressions, hypothalamic-pituitary-adrenal (HPA) axis-associated glucocorticoid secretion and cardiovascular indicators. Rats were additionally treated with a DNMT inhibitor (SGI-1027) to further validate the upstream regulatory role of hippocampal GR methylation. The results demonstrated that joint exposure to BC and psychosocial stress induces hypermethylation of the hippocampal GR-encoding gene NR3C1 via upregulation of DNMT3b, leading to decreased GR expression. This, in turn, weakens the negative feedback on the HPA axis, thereby contributing to the sustained elevation of stress hormones including corticosterone. Consequently, joint exposure induces more apparent acute cardiovascular dysfunction, including reduced ejection fraction, elevated blood pressure, increased myocardial enzymes (e.g., CK, CK-MB) and oxidative stress (e.g., MDA) compared to separate exposures. This study demonstrated that acute joint exposure to air pollution and psychosocial stress impairs cardiovascular function via hippocampal GR epigenetic reprogramming and HPA-axis dysregulation, and established a novel paradigm for investigating "environmental-psychological-biological" interactions.