Association between short-term air pollution exposure and perturbation in thyrotropin levels in 1.38 million Chinese women: A national longitudinal analysis, 2014-2019.

Prevalence of subclinical hypothyroidism substantially increased during the last decade in China, which has been commonly/clinically diagnosed as elevation in thyrotropin (thyroid-stimulating hormone [TSH]). Tobacco smoke containing toxic substances has been linked to thyroid dysfunction; however, data on perturbation of TSH following air pollution exposure in human has not been assessed at nationwide population level. We investigated the longitudinal impact of daily ambient air pollution estimated at residential level on serum TSH in 1.38 million women from China's 29 mainland provinces between 2014 and 2019. We observed that particulate matter with aerodynamic diameter ≤ 10 and ≤ 2.5 µm (PM10, PM2.5) and nitrogen dioxide (NO2) at cumulative lag 0-7 days of exposure were associated with percent elevations in TSH (0.88% [95% CI: 0.71, 1.05] per [interquartile range, IQR: 54.8 µg/m3] of PM10; 0.89% [95% CI, 0.71, 1.07] per IQR [40.3 µg/m3] of PM2.5; 2.01% [95% CI: 1.81, 2.22] per IQR [27.4 µg/m3] of NO2). Greater associations were observed in participants living in areas with ≥adequate iodine intake and those with low BMI levels and high inflammation status. Our results suggest that increased concentrations of recent ambient air pollutants at exposure ranges commonly encountered in Asia were associated with increases in TSH, supporting disturbing role of short-term air pollution exposure on the regulation of thyroid hormone homeostasis.

Occurrence, sources and risk of heavy metals in soil from a typical antimony mining area in Guizhou Province, China.

Antimony mining activities can result in serious contamination of soil by heavy metals, which represents a risk to human health. In this study, the contamination and sources of 14 heavy metals, and their risks to both ecosystem and public health from these metals at an antimony mining site in Guizhou Province in China were explored. The results showed that the mean concentrations of Hg, Cu, As, Se, Cd, Sn, Sb and Pb were 3.73, 2.49, 13.99, 38.32, 1.11, 1.61, 305.33, 1.59 times than their local background levels. Sb, Se, As and Hg presented the relatively heavy pollution, wherein Sb (EI = 2137.34 > 320), Hg (EI = 150.26 > 80) and As (EI = 139.92 > 80) also posed the strong ecological risk. The sources identification illustrated Hg, Pb, As, Bi, Cr, Sb, Cd and Zn were attributed to industrial activities, Ni, Co, Au and Cu (p < 0.01) were derived from a combination of a lithogeny origin and anthropogenic source, whereas Se was of natural origin. Health risk assessment demonstrated that Ni, Cr and As presented both the unacceptable noncarcinogenic and carcinogenic risk, and Sb (HI = 1.44E+03) and Cd (HI = 2.91E+00) posed unacceptable noncarcinogenic risk to the local resident. Furthermore, children in the 1-6 age group (HI = 7.83E+02) were more sensitive to noncarcinogenic risk, and the 6-18 age group (CRI = 2.39E-02) as more prone to carcinogenic risk. The dermal contact was the predominant exposure pathway of noncarcinogenic and carcinogenic risks with a contribution rate of over 97% for all age groups. Overall, this research provided the comprehensive information on heavy metals in an antimony mining sites, and the related heavy metals should be paid attention for ensuring soil safety and protecting local people's health.

Associations of climate variability driven by El Niño-southern oscillation with excess mortality and related medical costs in Chinese elderly.

Climate variability driven by El Niño-Southern Oscillation (ENSO) is a significant public health concern in parallel with global population aging; however, its role in healthy aging is less studied. We examined the longitudinal impacts of ENSO exposure on excess mortality and related medical costs in the elderly from 23 provinces of China. A total of 27,533 non-accidental all-cause deaths were recorded in 30,763 participants during 1998-2018. We found that both low and high levels of ENSO metrics over lags of 0-12 months were associated with increased mortality risks. Specifically, comparing the 10th percentile (-1.8) and 90th percentile (2.0) multivariate El Niño index (MEI) levels to the reference level with the minimum effect of MEI exposure, the risk of mortality was 1.87 (95 % confidence interval [CI], 1.75, 2.00) and 4.89 (95 % CI, 4.36, 5.49), respectively. ENSO exposure was also positively related to medical costs. Further, the associations were stronger among drinkers, lower-income participants, and those with higher blood pressure and heart rate measured at the most recent follow-ups. Our results suggested that ENSO exposure was capable of heightening mortality risks and medical burden among older elderly adults, highlighting that climate variability driven by ENSO could be a crucial determinant of healthy aging.

Combustion-Derived Particulate PAHs Associated with Small Airway Dysfunction in Elderly Patients with COPD.

Evidence of the respiratory effects of ambient organic aerosols (e.g., polycyclic aromatic hydrocarbons, PAHs) among patients with chronic diseases is limited. We aimed to assess whether exposure to ambient particle-bound PAHs could worsen small airway functions in patients with chronic obstructive pulmonary disease (COPD) and elucidate the underlying mechanisms involved. Forty-five COPD patients were recruited with four repeated visits in 2014-2015 in Beijing, China. Parameters of pulmonary function and pulmonary/systemic inflammation and oxidative stress were measured at each visit. Linear mixed-effect models were performed to evaluate the associations between PAHs and measurements. In this study, participants experienced an average PAH level of 61.7 ng/m3. Interquartile range increases in exposure to particulate PAHs at prior up to 7 days were associated with reduced small airway functions, namely, decreases of 17.7-35.5% in forced maximal mid-expiratory flow. Higher levels of particulate PAHs were also associated with heightened lung injury and inflammation and oxidative stress. Stronger overall effects were found for PAHs from traffic emissions and coal burning. Exposure to ambient particulate PAHs was capable of impairing small airway functions in elderly patients with COPD, potentially via inflammation and oxidative stress. These findings highlight the importance of control efforts on organic particulate matter from fossil fuel combustion emissions.

Maternal exposure to traffic-related ambient particles and risk of gestational diabetes mellitus with isolated fasting hyperglycaemia: A retrospective cohort study in Beijing, China.

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.

Association between air pollution and outpatient visits for allergic rhinitis: Effect modification by ambient temperature and relative humidity.

Mounting evidence indicated the associations between air pollution and outpatient visits for allergic rhinitis (AR), while few studies assessed the effect modification of these associations by ambient temperature and relative humidity (RH). In this study, dataset of AR outpatients was obtained from Chinese People's Liberation Army Strategic Support Force Characteristic Medical Center in Beijing during 2014 to 2019, and the average concentrations of air pollutants including particulate matter ≤2.5 µm in diameter (PM2.5) and ≤10 µm (PM10), nitrogen dioxide (NO2), sulfur dioxide (SO2), and meteorological factors (temperature and RH) at the same period were collected from one nearby air monitoring station. We performed a time-series study with Poisson regression model to examine the effects of air pollutants on AR outpatients after adjustment for potential confounders. And the effects modification analysis was further conducted by stratifying temperature and RH by tertiles into three groups of low, middle and high. In total of 33,599 outpatient visits for AR were recorded during the study period. Results found that a 10 µg/m3 increase in PM2.5, PM10, NO2 and SO2 was associated with significant increases in AR outpatients of 1.24% (95% confidence interval (CI): 0.69%, 1.78%), 0.79% (95% CI: 0.43%, 1.15%), 3.05% (95% CI: 1.72%, 4.40%) and 5.01% (95% CI: 1.18%, 8.96%), respectively. Stronger associations were observed in males than those in females, as well as in young adults (18-44 years) than those in other age groups. Air pollution effects on AR outpatients increased markedly at low temperature (<33.3th percentile) and high RH (>66.7th percentile). Findings in this study indicate that air pollution is associated with increased risk of AR outpatients, and the effects of air pollution on AR could be enhanced at low temperature and high RH.

The effect of using personal-level indoor air cleaners and respirators on biomarkers of cardiorespiratory health: a systematic review.

BACKGROUND: Emerging studies have investigated potential cardiovascular and respiratory health impacts from the use of personal-level intervention equipment against air pollution exposure. The objective of this systematic review is to assess the efficacy of personal-level air pollution intervention on mitigating adverse health effects from air pollution exposure by using portable air cleaner or wearing respirator. METHODS: In this systematic review, we searched PubMed and Web of Science for published literatures up to May 31, 2020, focusing on personal-level air pollution intervention studies. Among these studies, we investigated the impacts on cardio-respiratory responses to the use of these interventions. The intervention of review interest was the use of personal-level equipment against air pollution, including using portable air cleaner indoors or wearing respirator outdoors. The outcome of review interest was impacts on cardio-respiratory health endpoints following interventions, including level changes in blood pressure, heart rate variability (HRV), lung function, and biomarkers of inflammation and oxidative stress. Weighted mean differences or percent changes were pooled in meta-analyses for these health endpoints. The heterogeneity across studies was assessed using the Cochran's Q-statistic test, and the individual study quality was assessed using the Cochrane risk of bias tool version 2 (RoB 2). We further applied the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) method to evaluate the certainty of evidence. RESULTS: From systematic literature search and screening, we identified 29 related eligible intervention studies, including 21 studies on indoor portable air cleaner use and 8 studies on respirator use. For portable air cleaner intervention, we observed suggestive evidence of beneficial changes on cardio-respiratory health endpoints. Collectively in these studies, we found significantly beneficial changes of 2.01% decreases (95% CI: 0.50%, 3.52%) in systolic blood pressure, as well as non-significantly beneficial changes of 3.04% increases (95% CI: -2.65%, 8.74%) in reactive hyperemia index and 0.24% increases (95% CI: -0.82%, 1.31%) in forced expiratory volume in 1 s. We also observed non-significant reductions in levels of inflammation and oxidative stress biomarkers, including C-reactive protein, interleukin-6, fibrinogen, fractional exhaled nitric oxide and malondialdehyde. For respirator intervention, we observed some beneficial changes on cardiovascular health endpoints, such as significant increases in HRV parameters [SDNN (2.20%, 95% CI: 0.54%, 3.86%)], as well as non-significant decreases in blood pressure [SBP (0.63 mmHg, 95% CI: -0.39, 1.66)]; however, no sufficient data were available for meta-analyses on lung function and biomarkers. RoB 2 assessments suggested that most intervention studies were with a moderate to high overall risk of bias. The certainty of evidence for intervention outcome pairs was graded very low for either portable air cleaner or respirator intervention. The common reasons to downgrade study evidence included loss to follow-up, lack of blinding, lack of washout period, small sample size, and high heterogeneity across studies. CONCLUSIONS: The uses of indoor portable air cleaner and respirator could contribute to some beneficial changes on cardiovascular health, but with much limited evidence on respiratory health. Low certainty of the overall study evidence shed light on future research for larger sample size trials with more rigorous study design.

Traffic-related air pollution associated pulmonary pathophysiologic changes and cardiac injury in elderly patients with COPD.

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.

Maternal exposures to fine and ultrafine particles and the risk of preterm birth from a retrospective study in Beijing, China.

Maternal exposure to fine particulate matter (PM2.5) has been associated with increased risk of preterm birth (PTB), but evidence on particles in smaller sizes and PTB risk remains limited. In this retrospective analysis, we included birth records of 24,001 singleton live births from Haidian Maternal and Child Health Hospital in Beijing, China, 2014-2017. Concurrently, number concentrations of size-fractioned particles in size ranges of 5-560 nm (PNC5-560) and mass concentrations of PM2.5, black carbon (BC) and gaseous pollutants were measured from a fixed-location monitoring station in central Haidian District. Logistic regression models were used to estimate the odds ratio (OR) of air pollutants on PTB risk after controlling for temperature, relative humidity, and individual covariates (e.g., maternal age, ethnicity, gravidity, parity, gestational weight gain, fetal gender, the year and season of conception). Positive matrix factorization models were then used to apportion the sources of PNC5-560. Among the 1062 (4.4%) PTBs, increased PTB risk was observed during the third trimester of pregnancy per 10 µg/m3 increase in PM2.5 [OR = 1.92; 95% Confidence Interval (95% CI): 1.76, 2.09], per 1000 particles/cm3 increase in PNC25-100 (OR = 1.09; 95% CI: 1.03, 1.15) and PNC100-560 (OR = 1.22; 95% CI: 1.05, 1.42). Among the identified sources of PNC5-560, emissions from gasoline and diesel vehicles were significantly associated with increased PTB risk, with ORs of 1.14 (95% CI: 1.01, 1.29) and 1.11 (95% CI: 1.04, 1.18), respectively. Exposures to other traffic-related air pollutants, such as BC and nitrogen dioxide (NO2) were also significantly associated with increased PTB risk. Our findings highlight the importance of traffic emission reduction in urban areas.

Associations of ultrafine and fine particles with childhood emergency room visits for respiratory diseases in a megacity.

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.

The mediating role of vascular inflammation in traffic-related air pollution associated changes in insulin resistance in healthy adults.

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.

A review on reducing indoor particulate matter concentrations from personal-level air filtration intervention under real-world exposure situations.

Improving air quality in indoor environments where people live is of importance to protect human health. In this systematic review, we assessed the effectiveness of personal-level use of air filtration units in reducing indoor particulate matters (PM) concentrations under real-world situations following systematic review guidelines. A total of 54 articles were included in the review, in which 20 randomized controlled/crossover trials that reported the changes in indoor fine PM (PM2.5 ) concentrations were quantitatively assessed in meta-analysis. Standardized mean differences (SMDs) were calculated for changes in indoor PM concentrations following air filtration interventions. Moderate-to-large reductions of 11%-82% in indoor PM2.5  concentrations were observed with SMD of -1.19 (95% CI: -1.50, -0.88). The reductions in indoor PM concentrations varied by geographical locations, filtration technology employed, indoor environmental characteristics, and air pollution sources. Most studies were graded with low-to-moderate risk of bias; however, the overall certainty of evidence for indoor PM concentration reductions was graded at very low level. Considering the effectiveness of indoor air filtration under practical uses, socio-economic disparities across study populations, and costs of air filter replacement over time, our results highlight the importance of reducing air pollution exposure at the sources.

Combustion-derived particulate organic matter associated with hemodynamic abnormality and metabolic dysfunction in healthy adults.

Epidemiological evidence on cardiometabolic health of particulate organic matter (POM) and its sources is sparse. In a panel of 73 healthy adults in Beijing, China, daily concentrations of ambient fine particulate matter-bound polycyclic aromatic hydrocarbons (PAHs) and n-alkanes were measured throughout the study period, and Positive Matrix Factorization approach was used to identity PAHs sources. Linear mixed-effect models and mediation analyses were applied to examine the associations and potential interlink pathways between POM and biomarkers indicative of hemodynamics, insulin resistance, vascular calcification and immune inflammation. We found that significant alterations in cardiometabolic measures were associated with POM exposures. In specific, interquartile range increases in PAHs concentrations at prior up to 9 days were observed in association with significant elevations of 2.6-2.9% in diastolic blood pressure, 6.6-8.1% in soluble ST2, 10.5-14.5% in insulin, 40.9-45.7% in osteoprotegerin, and 36.3-48.7% in interleukin-17A. Greater associations were generally observed for PAHs originating from traffic emissions and coal burning. Mediation analyses revealed that POM exposures may prompt the genesis of hemodynamic abnormalities, possibly via worsening insulin resistance and calcification potential. These findings suggested that cardiometabolic health benefits would be achieved by reducing PM from combustion emissions.

Association between ambient temperature and childhood respiratory hospital visits in Beijing, China: a time-series study (2013-2017).

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.

Exercise training prevented endothelium dysfunction from particulate matter instillation in Wistar rats.

Exposure to fine particulate matter (PM2.5) can result in adverse cardiovascular responses including vascular endothelial dysfunction, whereas exercise training can promote cardiovascular health. However, whether exercise training can mitigate adverse vascular response to PM2.5 has been less studied. In the present study, we aimed to investigate the preventive effect of exercise training on vascular endothelial dysfunction induced by PM2.5 instillation. Six-week old male Wistar rats (n = 32) were divided into four groups (8 rats per group) by exercise status (sedentary vs. exercised) and PM2.5 exposure (instilled vs. non-instilled). Rats received treadmill training with moderate-intensity intervals in week 1 to 6, followed by three repeated PM2.5 instillation on every other day in week 7. Body weight and blood pressure were measured for each rat regularly during exercise training and before sacrifice. At sacrifice, thoracic aortas were isolated for functional response measurement to agonists. Nitric oxide bioavailability and high-density lipoprotein (HDL) function were also assessed. We observed that exercise training significantly reduced the body weight of rats, while PM2.5 instillation had little effect. Neither exercise training nor PM2.5 instillation had significant effects on blood pressure changes. However, exercise training effectively prevented endothelium-dependent vasorelaxation dysfunction and nitric oxide bioavailability reduction from subsequent PM2.5 instillation. In addition, exercise training promoted HDL function which were characterized as increased HDL cholesterol level, cholesterol efflux capacity, and reduced oxidization index; whereas PM2.5 instillation showed limited adverse impact on HDL function. Collectively, our results indicated that exercise training could promote HDL function and protect against endothelium dysfunction from PM2.5 instillation.

Health benefit of air quality improvement in Guangzhou, China: Results from a long time-series analysis (2006-2016).

Numerous epidemiologic studies on adverse health effects of air pollution have been well documented; however, assessment on health benefits of air quality improvement from air pollution control measures has been limited in developing countries. We assessed the mortality benefits associated with air pollution improvement over 11 years in Guangzhou, China (2006-2016). A time series analysis with Generalized additive Poisson models was used to estimate mortality effects of ozone (O3) and nitrogen dioxide (NO2), adjusting for time trend, day of week, public holiday, temperature and relative humidity. We further estimated the changes in mortality burden of O3 and NO2, including attributable fraction (AF, in %) and attributable mortality (AM, in number of death) during study period. We lastly estimated mortality effects during the 2010 Asian Games (November 12 to December 18, 2010) compared to a baseline period consisting of 4-week before and 4-week after the game. During the study period, average annual concentrations of NO2 decreased from 42.3 µg/m3 in 2006 to 33.8 µg/m3 in 2016; while O3 levels remained stable over time. We observed significant increases in mortality of O3 and NO2, with approximately linear exposure-response relationships. In specific, each increase of 10 µg/m3 in O3 and NO2 at 2 prior days was associated with increases of 0.60% (95% confidence interval (CI): 0.47, 0.74) and 1.89% (95%CI: 1.49, 2.29) in total mortality, respectively. We further estimated that AF on total mortality attributed to NO2 decreased from 1.38% (95%CI: 1.09, 1.68) in 2006-2010 to 0.43% (95%CI: 0.34, 0.52) in 2011-2016, corresponding to AM on total mortality of 2496 deaths (95%CI: 1964, 3033) to 1073 deaths (95%CI: 846, 1301). During the 2010 Asian Games, we observed decrease in total mortality of 9.3% (95%CI: -15.0, -3.2) in comparison with that observed in the baseline period. Similar mortality benefits in cardiovascular diseases were also observed. Our results showed reduced mortality burden from air pollution improvement in Guangzhou in recent years, which provide strong rationale for continuing to reduce air pollution through comprehensive and rigorous air quality management in the area.

Characterization of particulate-bound polycyclic aromatic compounds (PACs) and their oxidations in heavy polluted atmosphere: A case study in urban Beijing, China during haze events.

Characterizations on polycyclic aromatic compounds (PACs) during frequent haze periods have been conducted in an urban site of Beijing, China. Particulate polycyclic aromatic hydrocarbons (PAHs) and oxygenated-PAHs (OPAHs) and other carbonaceous matters were quantified. The average PM2.5 during haze events (256.3 ±â€¯103.7 µg/m3) were one magnitude over than that of clear periods (CRs, 24.7 ±â€¯27.7 µg/m3).The average total quantified PAHs (ΣPAHs) and OPAHs (ΣOPAHs) during haze events were 423.9 ±â€¯178.4 ng/m3 and 581.4 ±â€¯299.8 ng/m3, respectively, which were approximately 10 times higher than those of 40.3 ±â€¯68.2 ng/m3 and 54.4 ±â€¯82.4 ng/m3 in clear days. Four-rings PAHs had the highest compositions. 1,8-Naphthalic anhydride (1,8-NA) is the most abundant OPAHs, accounted for 49.8% of ∑OPAHs, followed by 9,10-anthraquinone (9,10-AQ) (13.8%) and benzo(a)anthracene-7,12-dione (BaAQ) (8.31%). In haze events, the contents of 5- to 7-rings PAHs decreased by 2.32% compared with those of clear days, while lower molecular weight fractions of 3- and 4-rings PAHs increased. The relationships between PAHs, OPAHs and relative humidity (RH) were found to be exponential. High oxygenation rate (R0) ratios of OPAH/PAH represents higher rates in secondary formation or degradation and gas- particle conversion for each PAH or OPAH during the wintertime. Significant positive correlation between BeP and OPAHs (r = 0.97), combined with the results of photochemical aging and negatively correlation with O3, suggest that secondary atmospheric reactions of PAHs played an important role in the burden of OPAHs.

Ambient Air Pollution Is Associated With HDL (High-Density Lipoprotein) Dysfunction in Healthy Adults.

Objective- We aimed to assess whether exposure to higher levels of ambient air pollution impairs HDL (high-density lipoprotein) function and to elucidate the underlying biological mechanisms potentially involved. Approach and Results- In the Beijing AIRCHD study (Air Pollution and Cardiovascular Dysfunction in Healthy Adults), 73 healthy adults (23.3±5.4 years) were followed-up with 4 repeated study visits in 2014 to 2016. During each visit, ambient air pollution concentrations, HDL function metrics, and parameters of inflammation and oxidative stress were measured. Average daily concentrations of ambient particulate matter in diameter <2.5 µm were 62.9 µg/m3 (8.1-331.0 µg/m3). We observed significant decreases in HDL cholesterol efflux capacity of 2.3% (95% CI, -4.3 to -0.3) to 5.0% (95% CI, -7.6 to -2.4) associated with interquartile range increases in moving average concentrations of particulate matter in diameter <2.5 µm and traffic-related air pollutants (black carbon, nitrogen dioxide, and carbon monoxide) during the 1 to 7 days before each participant's clinic visit. Higher ambient air pollutant levels were also associated with significant reductions in circulating HDL cholesterol and apoA-I (apolipoprotein A-I), as well as elevations in HDL oxidation index, oxidized LDL (low-density lipoprotein), malondialdehyde, and high-sensitivity C-reactive protein. Conclusions- Higher ambient air pollution concentrations were associated with impairments in HDL functionality, potentially because of systemic inflammation and oxidative stress. These novel findings further our understanding of the mechanisms whereby air pollutants promote cardiometabolic disorders.

Ambient air pollution is associated with cardiac repolarization abnormalities in healthy adults.

BACKGROUND: Ambient air pollution has been associated with acute cardiovascular events; however, the underlying mechanisms remain incompletely understood. We aimed to examine the impacts of ambient air pollutants on cardiac ventricular repolarization in a highly polluted urban region. METHODS: Seventy-three healthy non-smoking young adults (66% female, mean age of 23.3 ±â€¯5.4 years) were followed with four repeated 24-h electrocardiogram recordings in 2014-2016 in Beijing, China. Continuous concentrations of ambient particulates in size fractions of 5-560 nm diameter, black carbon (BC), nitrogen dioxide (NO2), carbon monoxide (CO), sulfur dioxide (SO2), and ozone (O3) were measured at a fixed-location air pollution monitoring station. Generalized linear mixed models, with adjustment for individual risk factors, time-varying factors and meteorological parameters, were used to evaluate the effects of air pollution on 5-min segments of heart rate-corrected QT interval (QTc), an index of cardiac ventricular repolarization. RESULTS: During the study period, the mean levels of number concentrations of particulates in size range of 5-560 nm (PNC5-560) were 20,711 particles/cm3. Significant increases in QTc of 0.56% (95% CI: 0.27, 0.84) to 1.76% (95% CI: 0.73, 2.79) were associated with interquartile range increases in PNC50-560 at prior 1-5 moving average days. Significant increases in QTc were also associated with increases in exposures to traffic-related air pollutants (BC, NO2 and CO), a combustion pollutant SO2, and the secondary pollutant O3. The associations were stronger in participants who were male, overweight, with abdominal obesity, and with higher levels of high-sensitivity C-reactive protein. CONCLUSIONS: Our findings suggest that exposures to higher levels of ambient particulates in small size fractions and traffic pollutants were associated with cardiac repolarization abnormalities in healthy adults, and the cardio-metabolic risks may modify the adverse cardiac effects attributable to air pollution.

High level of source-specific particulate matter air pollution associated with cardiac arrhythmias.

Epidemiological evidence linking source-specific ambient particulate matter with aerodynamic diameter <2.5 µm (PM2.5) and cardiac arrhythmias is limited. In this study, we investigated the impact of source-specific PM2.5 on cardiac arrhythmias in a panel of forty-five healthy adults living in Beijing, China, between 2015 and 2016. Repeated measures of 24-hour electrocardiograms were conducted during clinical visits, and daily counts of four arrhythmia events including supraventricular premature beat (SVPB), atrial tachycardia (AT), premature ventricular contraction (PVC) and ventricular tachycardia (VT) were recorded. One hundred forty-seven constituents in PM2.5 were analyzed for collected particulate samples, in which fifty-six of them above laboratory detection limits were selected for source apportionment analysis using positive matrix factorization. The average contributions of identified five major sources to PM2.5 were 45.9% from secondary nitrate/sulfate, 18.0% from coal combustion, 16.9% from crustal soil, 13.8% from biomass burning, and 5.4% from cooking. Generalized estimating equation models were used to estimate relative risks (RR) of arrhythmias in association with interquartile-range (IQR) increases in PM2.5 constituents and specific sources. Total PM2.5 mass as well as several combustion related constituents were found of significant impacts on increased risks of arrhythmia events. Among the identified sources of PM2.5, coal burning has been found the major source that associated with increased risks of SVPB, PVC and VT with RR of 1.19 [95% confidence intervals (CI): 1.04, 1.36] to 1.64 (95% CI: 1.35, 2.00). PM2.5 from combustion related secondary nitrate/sulfate was also found of significant impact on SVPB and AT, followed by PM2.5 from biomass burning and crustal soil. Our results indicated that PM2.5 from anthropogenic activity related sources were most responsible for increased risks of arrhythmia events. Our findings enhance the understanding of increased risks of arrhythmias from exposure to PM2.5, and provide evidence on source-specific PM control priorities.