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Background: Ambient fine particulate matter with aerodynamic diameter less than 2.5 µm (PM2.5) has been associated with deteriorated respiratory health, but evidence on particles in smaller sizes and childhood respiratory health has been limited.Methods: We collected time-series data on daily respiratory emergency room visits (ERVs) among children under 14 years old in Beijing, China, during 2015-2017. Concurrently, size-fractioned number concentrations of particles in size ranges of 5-560 nm (PNC5-560) and mass concentrations of PM2.5, black carbon (BC) and nitrogen dioxide (NO2) were measured from a fixed-location monitoring station in the urban area of Beijing. Confounder-adjusted Poisson regression models were used to estimate excessive risks (ERs) of particle size fractions on childhood respiratory ERVs, and positive matrix factorisation models were applied to apportion the sources of PNC5-560.Results: Among the 136 925 cases of all-respiratory ERVs, increased risks were associated with IQR increases in PNC25-100 (ER=5.4%, 95% CI 2.4% to 8.6%), PNC100-560 (4.9%, 95% CI 2.5% to 7.3%) and PM2.5 (1.3%, 95% CI 0.1% to 2.5%) at current and 1 prior days (lag0-1). Major sources of PNC5-560 were identified, including nucleation (36.5%), gasoline vehicle emissions (27.9%), diesel vehicle emissions (18.9%) and secondary aerosols (10.6%). Emissions from gasoline and diesel vehicles were found of significant associations with all-respiratory ERVs, with increased ERs of 6.0% (95% CI 2.5% to 9.7%) and 4.4% (95% CI 1.7% to 7.1%) at lag0-1 days, respectively. Exposures to other traffic-related pollutants (BC and NO2) were also associated with increased respiratory ERVs.Conclusion: Our findings suggest that exposures to higher levels of PNC5-560 from traffic emissions could be attributed to increased childhood respiratory morbidity, which supports traffic emission control priority in urban areas. [ABSTRACT FROM AUTHOR]

Little is known on the potential impact of temperature on respiratory morbidity, especially for children whose respiratory system can be more vulnerable to climate changes. In this time-series study, Poisson generalized additive models combined with distributed lag nonlinear models were used to assess the associations between ambient temperature and childhood respiratory morbidity. The impacts of extreme cold and hot temperatures were calculated as cumulative relative risks (cum.RRs) at the 1st and 99th temperature percentiles relative to the minimum morbidity temperature percentile. Attributable fractions of respiratory morbidity due to cold or heat were calculated for temperatures below or above the minimum morbidity temperature. Effect modifications by air pollution, age, and sex were assessed in stratified analyses. A total of 877,793 respiratory hospital visits of children under 14 years old between 2013 and 2017 were collected from Beijing Children's Hospital. Overall, we observed J-shaped associations with greater respiratory morbidity risks for exposure to lower temperatures, and higher fraction of all-cause respiratory hospital visits was caused by cold (33.1%) than by heat (0.9%). Relative to the minimum morbidity temperature (25 °C, except for rhinitis, which is 31 °C), the cum.RRs for extreme cold temperature (-6 °C) were 2.64 (95%CI: 1.51–4.61) for all-cause respiratory hospital visits, 2.73 (95%CI: 1.44–5.18) for upper respiratory infection, 2.76 (95%CI: 1.56–4.89) for bronchitis, 2.12 (95%CI: 1.30–3.47) for pneumonia, 2.06 (95%CI: 1.27–3.34) for rhinitis, and 4.02 (95%CI: 2.14–7.55) for asthma, whereas the associations between extreme hot temperature (29 °C) and respiratory hospital visits were not significant. The impacts of extreme cold temperature on asthma hospital visits were greater at higher levels of ozone (O3) exposure (> 50th percentile). Our findings suggest significantly increased childhood respiratory morbidity risks at extreme cold temperature, and the impact of extreme cold temperature on asthma hospital visits can be enhanced under higher level exposure to O3. [ABSTRACT FROM AUTHOR]

Air pollution has been associated with the development of atherosclerosis; however, the pathophysiological mechanisms underlying pro-atherosclerotic effects of air pollution exposure remain unclear. We conducted a prospective panel study in Beijing and recruited 152 participants with four monthly visits from September 2019 to January 2020. Linear mixed-effect models were applied to estimate the associations linking short-term air pollution exposure to biomarkers relevant to ceramide metabolism, pro-inflammation (neutrophil extracellular traps formation and systemic inflammation) and pro-atherosclerotic responses (endothelial stimulation, plaque instability, coagulation activation, and elevated blood pressure). We further explored whether ceramides and inflammatory indicators could mediate the alterations in the profiles of pro-atherosclerotic responses. We found that significant increases in levels of circulating ceramides of 9.7% (95% CIs: 0.7, 19.5) to 96.9% (95% CIs: 23.1, 214.9) were associated with interquartile range increases in moving averages of ambient air pollutant metrics, including fine particulate matter (PM 2.5), black carbon, particles in size fractions of 100–560 nm, nitrogen dioxide, carbon monoxide and sulfur dioxide at prior up to 7 days. Higher air pollution levels were also associated with activated neutrophils (increases in citrullinated histone H3, neutrophil elastase, double-stranded DNA, and myeloperoxidase) and exacerbation of pro-atherosclerotic responses (e.g., increases in vascular endothelial growth factor, lipoprotein-associated phospholipase A2, matrix metalloproteinase-8, P-selectin, and blood pressure). Mediation analyses further showed that dysregulated ceramide metabolism and potentiated inflammation could mediate PM 2.5 -associated pro-atherosclerotic responses. Our findings extend the understanding on potential mechanisms of air pollution-associated atherosclerosis, and suggest the significance of reducing air pollution as priority in urban environments. [Display omitted] • Ambient air pollution exposure showed pro-atherosclerotic effects. • Air pollution was associated with dysregulated ceramide metabolism. • Air pollutants promoted neutrophil extracellular traps (NETs) formation. • Ceramides and NETs mediated pro-atherosclerotic effects of air pollution exposure. [ABSTRACT FROM AUTHOR]

Evidence of impact of ambient oxidant pollution on cardiometabolic responses remains limited. We aimed to examine associations of oxidant pollutants with cardiometabolic responses, and effect modification by ceramides. During 2019–2020, 152 healthy adults were visited 4 times in Beijing, China, and indicators of ceramides, glucose homeostasis, and vascular function were measured. We found significant increases in ceramides of 13.9% (p = 0.020) to 110.1% (p = 0.005) associated with an interquartile increase in oxidant pollutants at prior 1–7 days. Exposure to oxidant pollutants was also related to elevations in insulin and reductions in adiponectin, and elevations in systolic and diastolic blood pressure. Further, stratified analyses revealed larger changes in oxidant pollutant related cardiometabolic responses among participants with higher ceramide levels compared to those with lower levels. Our findings suggested cardiometabolic effects associated with exposure to oxidant pollutants, which may be modified by ceramide levels. • Elevated ceramides were associated with ambient O 3 , NO X and O X exposures. • Exposure to oxidant pollutants could induce changes of glucose homeostasis. • Exposure to oxidant pollutants prompted elevated blood pressure. • Ceramides may modify oxidant pollutant-related cardiometabolic effects. [ABSTRACT FROM AUTHOR]

Background: Ambient particles have been associated with gestational diabetes mellitus (GDM), however, no study has evaluated the effects of traffic-related ambient particles on the risks of GDM subgroups classified by oral glucose tolerance test (OGTT) values.Methods: A retrospective analysis was conducted among 24,001 pregnant women who underwent regular prenatal care and received OGTT at Haidian Maternal and Child Health Hospital in Beijing, China, 2014-2017. A total of 3,168 (13.2%) pregnant women were diagnosed with GDM, including 1,206 with isolated fasting hyperglycaemia (GDM-IFH). At a fixed-location monitoring station, routinely monitored ambient particles included fine particulate matter (PM2.5), black carbon (BC) and particles in size ranges of 5-560 nm (PNC5-560). Contributions of PNC5-560 sources were apportioned by positive matrix factorization model. Logistic regression model was applied to estimate odds ratio (OR) of ambient particles on GDM risk.Results: Among the 24,001 pregnancy women recruited in this study, 3,168 (13.2%) were diagnosed with GDM, including 1,206 with isolated fasting hyperglycaemia (GDM-IFH) and 1,295 with isolated post-load hyperglycaemia (GDM-IPH). We observed increased GDM-IFH risk with per interquartile range increase in first-trimester exposures to PM2.5 (OR = 1.94; 95% Confidence Intervals: 1.23-3.07), BC (OR = 2.14; 1.73-2.66) and PNC5-560 (OR = 2.46; 1.90-3.19). PNC5-560 originated from diesel and gasoline vehicle emissions were found in associations with increases in GDM-IFH risk, but not in GDM-IPH risk.Conclusion: Our findings suggest that exposure to traffic-related ambient particles may increase GDM risk by exerting adverse effects on fasting glucose levels during pregnancy, and support continuing efforts to reduce traffic emissions for protecting vulnerable population who are at greater risk of glucose metabolism disorder. [ABSTRACT FROM AUTHOR]

Traffic-related air pollution (TRAP) has shown enormous environmental toxicity, but its cardiorespiratory health impact on chronic obstructive pulmonary disease (COPD) has been less studied. We followed a panel of 45 COPD patients with 4 repeated clinical visits across 14 months in a traffic-predominated urban area of Beijing, China, with concurrent measurements of TRAP metrics (fine particulate matter, black carbon, oxides of nitrogen and carbon monoxide). Linear mixed-effect models were performed to evaluate the associations and potential pathways linking traffic pollution to indicators of spirometry, cardiac injury, inflammation and oxidative stress. We observed that interquartile range increases in moving averages of TRAP exposures at prior up to 7 days were associated with significant reductions in large and small airway functions, namely decreases in forced vital capacity of 3.1–9.3% and forced expiratory flow 25–75% of 5.9–16.4%. Higher TRAP levels were also associated with worsening of biomarkers relevant to lung injury (hepatocyte growth factor and surfactant protein D) and cardiac injury (high-sensitivity cardiac troponin I, B-type natriuretic peptide and soluble ST2), as well as enhanced airway/systemic inflammation and oxidative stress. Mediation analyses showed that TRAP exposures may prompt cardiac injury, possibly via worsening pulmonary pathophysiology. These findings highlight the importance of traffic pollution control priority in urban areas. [Display omitted] • Exposure to TRAP could prompt dysfunction on small airway in COPD patients. • TRAP was associated with heightened cardiac injury potential. • Higher TRAP levels prompted airway/systemic inflammation and oxidative stress. • Pulmonary pathophysiologic change due to TRAP may possibly heighten cardiac injury. [ABSTRACT FROM AUTHOR]

Aim: The precise pathophysiologic pathway linking traffic-related air pollution (TRAP) to diabetes mellitus is not well elucidated. We aimed to investigate whether activation of vascular inflammation can be a mechanistic linkage between ambient TRAP and insulin resistance.Methods: Study outcomes were determined by assessing a series of circulating biomarkers indicative of insulin resistance and vascular inflammation among 73 healthy adults who underwent repeated clinical visits in Beijing, China, 2014-2016. Concomitantly, concentrations of ambient TRAP indices, including particulate matter in diameter <2.5 μm (PM2.5), particles in size fractions of 5-560 nm, black carbon, carbon monoxide, nitrogen dioxide, and oxides of nitrogen, were continuously monitored.Results: Participants experienced extremely high levels of TRAP exposures, with mean (standard deviation) PM2.5 concentrations of 91.8 (48.3) μg/m3, throughout the study. We found that interquartile range increases in exposure to moving average concentrations of various TRAP indices at prior up to 7 days were associated with significant elevations of 8.9-49.6% in insulin levels. Higher pollutant levels were also related to worsening metrics of insulin resistance (soluble insulin receptor ectodomain, adipokines, and homeostasis model assessment of insulin resistance) and heightened vascular inflammatory responses, particularly disruptions of the receptor activator of nuclear factor κB ligand/osteoprotegerin system balance and elevations of monocyte/macrophage and T cell activation markers. Mediation analyses showed that activation of vascular inflammation could explain up to 66% of the alterations in metrics of insulin resistance attributable to air pollution.Conclusion: Our results suggest that ambient traffic pollution exposure was capable of promoting insulin resistance possibly via generating vascular inflammation. [ABSTRACT FROM AUTHOR]