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Traffic-related particulate matter (PM) is a major source of outdoor air pollution worldwide. It has been recently hypothesized to cause cardiometabolic syndrome, including cardiovascular dysfunction, obesity, and diabetes. The environmental and toxicological factors involved in the processes, and the detailed mechanisms remain to be explored. The objective of this study is to assess the current scientific evidence of traffic-related PM-induced cardiometabolic syndrome. We conducted a literature review by searching the keywords of "traffic related air pollution", "particulate matter", "human health", and "metabolic syndrome" from 1980 to 2018. This resulted in 25 independent research studies for the final review. Both epidemiological and toxicological findings reveal consistent correlations between traffic-related PM exposure and the measured cardiometabolic health endpoints. Smaller sizes of PM, particularly ultrafine particles, are shown to be more harmful due to their greater concentrations, reactive compositions, longer lung retention, and bioavailability. The active components in traffic-related PM could be attributed to metals, black carbon, elemental carbon, polyaromatic hydrocarbons, and diesel exhaust particles. Existing evidence points out that the development of cardiometabolic symptoms can occur through chronic systemic inflammation and increased oxidative stress. The elderly (especially for women), children, genetically susceptible individuals, and people with pre-existing conditions are identified as vulnerable groups. To advance the characterization of the potential health risks of traffic-related PM, additional research is needed to investigate the detailed chemical compositions of PM constituents, atmospheric transformations, and the mode of action to induce adverse health effects. Furthermore, we recommend that future studies could explore the roles of genetic and epigenetic factors in influencing cardiometabolic health outcomes by integrating multi-omics approaches (e.g., genomics, epigenomics, and transcriptomics) to provide a comprehensive assessment of biological perturbations caused by traffic-related PM.

Objective: The noninvasive right ventricular pressure‐strain loop (PSL) represents a novel method for the quantitative assessment of right ventricular myocardial function. Given that atrial septal defect (ASD) is a prevalent congenital heart anomaly associated with right ventricular volume overload, this study aimed to quantitatively assess the myocardial function of the right ventricle in ASD patients pre‐ and post‐occlusion by noninvasive right ventricular PSL. Methods: This study included 36 patients diagnosed with secundum ASD group and 30 healthy adults (control group). We compared conventional right ventricular echocardiographic parameters, right ventricular strain, and myocardial work in the ASD group before occlusion, two days post‐occlusion, and three months post‐occlusion, with those in the control group. Results: Prior to and two days following occlusion, the ASD group exhibited higher right ventricular global work index (RVGWI), right ventricular global wasted work (RVGWW), and right ventricular global constructive work (RVGCW) compared to the control group (P <.05). Within the ASD group, post‐occlusion, RVGWI, RVGCW, and RVGWW values were significantly reduced compared to pre‐occlusion values (P <.001). Furthermore, RVGWI and RVGCW showed a significant decrease three months after occlusion compared to two days post‐occlusion (P <.05). Multivariate regression analysis identified ASD diameter and pulmonary artery systolic pressure (PASP) as independent predictors of RVGWI (β =.405, P <.001; β = 2.307, P =.037) and RVGCW(β =.350, P<.001; β = 1.967, P =.023). Conclusions: The noninvasive right ventricular PSL effectively demonstrates the alterations in right ventricular myocardial function in ASD patients, pre‐ and post‐occlusion. The metrics of right ventricular myocardial work (RVMW) offer a novel indicator for evaluating right ventricular myocardial function in these patients. Moreover, ASD diameter and PASP emerge as independent determinants of RVGWI and RVGCW. [ABSTRACT FROM AUTHOR]