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Introduction: Long-term exposure to fine particulate matter (≤2.5 µm (PM 2.5 )) has been associated with pulmonary tuberculosis (TB) notifications or incidence in recent publications. Studies quantifying the relative contribution of long-term PM 2.5 on TB notifications have not been documented. We sought to perform a health impact assessment to estimate the PM 2.5 - attributable TB notifications during 2007-2017 in Ningxia Hui Autonomous Region (NHAR), China., Methods: PM 2.5 attributable TB notifications were estimated at township level (n=358), stratified by age group and summed across NHAR. PM 2.5 -associated TB-notifications were estimated for total and anthropogenic PM 2.5 mass and expressed as population attributable fractions (PAFs). The main analysis used effect and uncertainty estimates from our previous study in NHAR, defining a counterfactual of the lowest annual PM 2.5 (30 µg/m 3 ) level, above which we assumed excess TB notifications. Sensitivity analyses included counterfactuals based on the 5th (31 µg/m 3 ) and 25th percentiles (38 µg/m 3 ), and substituting effect estimates from a recent meta-analysis. We estimated the influence of PM 2.5 concentrations, population growth and baseline TB-notification rates on PM 2.5 attributable TB notifications., Results: Over 2007-2017, annual PM 2.5 had an estimated average PAF of 31.2% (95% CI 22.4% to 38.7%) of TB notifications while the anthropogenic PAF was 12.2% (95% CI 9.2% to 14.5%). With 31 and 38 µg/m 3 as counterfactuals, the PAFs were 29.2% (95% CI 20.9% to 36.3%) and 15.4% (95% CI 10.9% to 19.6%), respectively. PAF estimates under other assumptions ranged between 6.5% (95% CI 2.9% to 9.6%) and 13.7% (95% CI 6.2% to 19.9%) for total PM 2.5 , and 2.6% (95% CI 1.2% to 3.8%) to 5.8% (95% CI 2.7% to 8.2%) for anthropogenic PM 2.5 . Relative to 2007, overall changes in PM 2.5 attributable TB notifications were due to reduced TB-notification rates (-23.8%), followed by decreasing PM2.5 (-6.2%), and population growth (+4.9%)., Conclusion: We have demonstrated how the potential impact of historical or hypothetical air pollution reduction scenarios on TB notifications can be estimated, using public domain, PM 2.5 and population data. The method may be transferrable to other settings where comparable TB-notification data are available., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

This prospective birth cohort study evaluated the association of exposure to PM 2.5 (diameter ≤2.5 μm), PM 1-2.5 (1-2.5 μm), and PM 1 (≤1 μm) with maternal thyroid autoimmunity and function during early pregnancy. A total of 15,664 pregnant women were included at 6 to 13 +6 gestation weeks in China from 2018 to 2020. Single-pollutant models using generalized linear models (GLMs) showed that each 10 μg/m 3 increase in PM 2.5 and PM 1-2.5 was related with 6% (odds ratio [OR] = 1.06, 95% confidence interval [CI]: 1.01, 1.12) and 15% (OR = 1.15, 95% CI: 1.08, 1.22) increases in the risk of thyroid autoimmunity, respectively. The odds of thyroid autoimmunity significantly increased with each interquartile range increase in PM 2.5 and PM 1-2.5 exposure ( P for trend <0.001). PM 1 exposure was not significantly associated with thyroid autoimmunity. GLM with natural cubic splines demonstrated that increases in PM 2.5 and PM 1-2.5 exposure were associated with lower maternal FT4 levels, while a negative association between PM 1 and FT4 levels was found when exposure exceeded 32.13 μg/m 3 . Only PM 2.5 exposure was positively associated with thyrotropin (TSH) levels. Our findings suggest that high PM exposure is associated with maternal thyroid disruption during the early pregnancy.

The sources, sizes, components, and toxicological responses of particulate matter (PM) have demonstrated remarkable spatiotemporal variability. However, associations between components, sources, and toxicological effects in different-sized PM remain unclear. The purposes of this study were to 1) determine the sources of PM chemical components, 2) investigate the associations between components and toxicology of PM from Guangzhou high air pollution season. We collected size-segregated PM samples (PM 10-2.5 , PM 2.5-1 , PM 1-0.2 , PM 0.2 ) from December 2017 to March 2018 in Guangzhou. PM sources and components were analyzed. RAW264.7 mouse macrophages were treated with PM samples for 24 h followed by measurements of toxicological responses. The concentrations of PM 10 - 2.5 and PM 1 - 0.2 were relatively high in all samples. Water-soluble ions and PAHs were more abundant in smaller-diameter PM, while metallic elements were more enriched in larger-diameter PM. Traffic exhaust, soil dust, and biomass burning/petrochemical were the most important sources of PAHs, metals and ions, respectively. The main contributions to PM were soil dust, coal combustion, and biomass burning/petrochemical. Exposure to PM 10 - 2.5 induced the most significant reduction of cell mitochondrial activity, oxidative stress and inflammatory response, whereas DNA damage, an increase of Sub G1/G0 population, and impaired cell membrane integrity were most evident with PM 1 - 0.2 exposure. There were moderate or strong correlations between most single chemicals and almost all toxicological endpoints as well as between various toxicological outcomes. Our findings highlight those various size-segregated PM-induced toxicological effects in cells, and identify chemical components and sources of PM that play the key role in adverse intracellular responses. Although fine and ultrafine PM have attracted much attention, the inflammatory damage caused by coarse PM cannot be ignored., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Little evidence is available regarding the impact of different sizes of inhaled particulate matter (PM) on inflammatory responses in healthy young adults in connection with toxicological responses. We conducted a five-time repeated measurement panel study on 88 healthy young college students in Guangzhou, China from December 2017 to January 2018. Blood samples were collected from each participant and tested for tumor necrosis factor alpha (TNF-α) levels every week for 5 consecutive weeks. Mass concentrations of ambient PM 2.5 , PM 1 , PM 0.5 and number concentrations of ambient PM 0.1 were measured. RAW 264.7 macrophages were exposed to PM (PM 10 - 2.5 , PM 2.5 - 1 , PM 1 - 0.2 , PM 0.2 ) collected at the same time as the panel study. Cytotoxicity, oxidation and inflammatory parameters, cell cycle and genotoxicity were tested. Particles were characterized for their chemical composition. The trends of associations between PM 2.5 , PM 1 , PM 0.5 and TNF-α level were consistent in lag 0 and 3 days, and the relative risk decreased as the particle size decreased. All the ambient air pollutants had the similar change trends in lag 1, 4 and 5 days. Similar results in RAW 264.7 macrophages were found; PM 10 - 2.5 induced the greatest TNF-α and macrophage inflammatory protein 2 (MIP-2) productions and oxidative damage. PM 1 - 0.2 and PM 0.2 induced more significant dose-dependent increases of cell cycle and genotoxic response. In the component concentrations of PM samples, metal elements were PM 10 - 2.5 > PM 2.5 - 1 > PM 0.2 ≥ PM 1 - 0.2 ; ions and polycyclic aromatic hydrocarbons (PAHs) were PM 0.2 > PM 1 - 0.2 > PM 2.5 - 1 > PM 10 - 2.5 . Our results suggested that exposure to all particle sizes was significantly associated with inflammation among healthy young adults and toxicological responses in RAW 264.7 macrophages. Different human and toxicological reactions caused by PM samples indicated the importance of investigating various particle sizes., Competing Interests: Declaration of competing interest The authors declare they have no actual or potential competing interests., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background Although several studies have focused on the associations between particle size and constituents and blood pressure, results have been inconsistent. Methods and Results We conducted a panel study, between December 2017 and January 2018, in 88 healthy university students in Guangzhou, China. Weekly systolic blood pressure and diastolic blood pressure were measured for each participant for 5 consecutive weeks, resulting in a total of 440 visits. Mass concentrations of particles with an aerodynamic diameter of ≤2.5 µm (PM 2.5 ), ≤1.0 µm (PM 1.0 ), ≤0.5 µm (PM 0.5 ), ≤0.2 µm (PM 0.2 ), and number concentrations of airborne particulates of diameter ≤0.1 μm were measured. Linear mixed-effect models were used to estimate the associations between blood pressure and particles and PM 2.5 constituents 0 to 48 hours before blood pressure measurement. PM of all the fractions in the 0.2- to 2.5-μm range were positively associated with systolic blood pressure in the first 24 hours, with the percent changes of effect estimates ranging from 3.5% to 8.8% for an interquartile range increment of PM. PM 0.2 was also positively associated with diastolic blood pressure, with an increase of 5.9% (95% CI, 1.0%-11.0%) for an interquartile range increment (5.8 μg/m 3 ) at lag 0 to 24 hours. For PM 2.5 constituents, we found positive associations between chloride and diastolic blood pressure (1.7% [95% CI, 0.1%-3.3%]), and negative associations between vanadium and diastolic blood pressure (-1.6% [95% CI, -3.0% to -0.1%]). Conclusions Both particle size and constituent exposure are significantly associated with blood pressure in the first 24 hours following exposure in healthy Chinese adults.

Experimental data suggests that PM 1 is more toxic than PM 2.5 although the epidemiologic evidence suggests that the health associations are similar. However, few objective exposure data are available to compare the associations of PM 1 and PM 2.5 with children lung function. Our objectives are a) to evaluate associations between long-term exposure to PM 1 , PM 2.5 and children's lung function, and b) to compare the associations between PM 1 and PM 2.5 . From 2012 to 2013, we enrolled 6,740 children (7-14 years), randomly recruited from primary and middle schools located in seven cities in northeast China. We measured lung function including forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), peak expiratory flow (PEF), and maximal mid-expiratory flow (MMEF) utilizing two portable electronic spirometers. We dichotomized continuous lung function measures according the expected values for gender and age. The spatial resolution at which PM 1 and PM 2.5 estimated were estimated using a machine learning method and the temporal average concentrations were averaged from 2009 to 2012. A multilevel regression model was used to estimate the associations of PM 1 , PM 2.5 exposure and lung function measures, adjusted for confounding factors. Associations with lower lung function were consistently larger for PM 1 than for PM 2.5 . Adjusted odds ratios (OR) per interquartile range greater PM 1 ranged from 1.53 for MMEF (95% confidence interval [CI]: 1.20-1.96) to 2.14 for FEV1 (95% CI: 1.66-2.76) and ORs for PM 2.5 ranged from 1.36 for MMEF (95%CI: 1.12-1.66) to 1.82 for FEV1 (95%CI: 1.49-2.22), respectively. PM 1 and PM 2.5 had significant associations with FVC and FEV1 in primary school children, and on PEF and MMEF in middle school children. Long-term PM 1 and PM 2.5 exposure can lead to decreased lung function in children, and the associations of PM 1 are stronger than PM 2.5 . Therefore, PM 1 may be more hazardous to children's respiratory health than PM 2.5 exposure., (Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Evidence on the associations between airborne particulates of diameter ≤1 μm (PM 1 ) and airborne particulates of diameter ≤2.5 μm (PM 2.5 ) and childhood blood pressure (BP) is scarce. To help to address this literature gap, we conducted a study to explore the associations in Chinese children. Between 2012 and 2013, we recruited 9354 children, aged 5 to 17 years, from 62 schools in 7 northeastern Chinese cities. We measured their BP with a mercury sphygmomanometer. We used a spatiotemporal model to estimate daily ambient PM 1 and PM 2.5 exposures, which we assigned to participants' home addresses. Associations between particulate matter exposure and BP were evaluated with generalized linear mixed regression models. The findings indicated that exposure to each 10 mg/m 3 greater PM 1 was significantly associated with 2.56 mm Hg (95% CI, 1.47-3.65) higher systolic BP and 61% greater odds for hypertension (odds ratio=1.61 [95% CI, 1.18-2.18]). PM 1 appears to play an important role in associations reported between PM 2.5 exposure and BP, and we found that the ambient PM 1 /PM 2.5 ratio (range, 0.80-0.96) was associated with BP and with hypertension. Age and body weight modified associations between air pollutants and BP ( P <0.01), with stronger associations among younger (aged ≤11 years) and overweight/obese children. This study provides the first evidence that long-term exposure to PM 1 is associated with hypertension in children, and that PM 1 might be a leading contributor to the hypertensive effect of PM 2.5 . Researchers and policy makers should pay closer attention to the potential health impacts of PM 1 .

No evidence exists concerning the association between blood pressure and ambient particles with aerodynamic diameter ≤ 1.0 µm (PM 1 ), a major component of PM 2.5 (≤ 2.5 µm) particles, and potentially causing more hazardous health effects than PM 2.5 . We aimed to examine the associations of blood pressure in adults with both PM 1 and PM 2.5 in China. In 2009, we randomly selected 24,845 participants aged 18-74 years from 33 communities in China. Using a standardized mercuric-column sphygmomanometer, we measured blood pressure. Long-term exposure (2006-08) to PM 1 and PM 2.5 were estimated using a spatial statistical model. Generalized linear mixed models were used to evaluate the associations between air pollutants and blood pressure and hypertension prevalence, controlling for multiple covariates. A 10-μg/m 3 increase in PM 1 was significantly associated with an increase of 0.57 (95% CI 0.31-0.83) mmHg in systolic blood pressure (SBP), 0.19 (95% CI 0.03-0.35) mmHg increase in diastolic blood pressure (DBP), and a 5% (OR=1.05; 95% CI 1.01-1.10) increase in odds for hypertension. Similar associations were detected for PM 2.5 . Furthermore, PM 1-2.5 showed no association with blood pressure or hypertension. In summary, both PM 1 and PM 2.5 exposures were associated with elevated blood pressure levels and hypertension prevalence in Chinese adults. In addition, most of the pro-hypertensive effects of PM 2.5 may come from PM 1 . Further longitudinal designed studies are warranted to validate our findings., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Importance: Which cardiometabolic risk factors (eg, hypertension, type 2 diabetes, overweight or obesity, and dyslipidemia) are more sensitive to long-term exposure to ambient air pollution and whether participants with these conditions are more susceptible to the cardiovascular effects of air pollution remain unclear., Objectives: To evaluate the associations among long-term exposure to air pollutants, cardiometabolic risk factors, and cardiovascular disease (CVD) prevalence., Design, Setting, and Participants: This population-based cross-sectional study was conducted from April 1 through December 31, 2009, in 3 cities in Northeastern China. Participants were adults aged 18 to 74 years who had lived in study area for 5 years or longer. Data analysis was performed from May 1 through December 31, 2018., Exposures: Long-term (2006-2008) exposure to air pollutants was measured using a spatiotemporal statistical model (particulate matter with an aerodynamic diameter of ≤2.5 μm [PM2.5] and ≤1.0 μm [PM1.0]) and data from air monitoring stations (particulate matter with an aerodynamic diameter of ≤10.0 μm [PM10.0], sulfur dioxide [SO2], nitrogen dioxide [NO2], and ozone [O3])., Main Outcomes and Measures: Cardiovascular disease was determined by self-report of physician-diagnosed CVD. Blood pressure, body mass index, and levels of triglycerides and low-density lipoprotein cholesterol were measured using standard methods., Results: Participants included 15 477 adults (47.3% women) with a mean (SD) age of 45.0 (13.5) years. The prevalence of CVD was 4.8%, and the prevalence of cardiometabolic risk factors ranged from 8.6% (hyperbetalipoproteinemia) to 40.5% (overweight or obesity). Mean (SD) air pollutant concentrations ranged from 35.3 (5.5) μg/m3 (for NO2) to 123.1 (14.6) μg/m3 (for PM10.0). Associations with air pollutants were identified for individuals with hyperbetalipoproteinemia (eg, odds ratio [OR], 1.36 [95% CI, 1.03-1.78] for a 10-μg/m3 increase in PM1.0) and the weakest association for those with for overweight or obesity (eg, OR, 1.06 [95% CI, 1.02-1.09] for a 10-μg/m3 increase in PM1.0). Cardiometabolic risk factors only partially mediated associations between air pollution and CVD. However, they modified the associations such that greater associations were found in participants with these cardiometabolic conditions (eg, ORs for CVD and per 10-μg/m3 increase in PM1.0, 1.22 [95% CI, 1.12-1.33] in participants with hyperbetalipoproteinemia and 1.07 [95% CI, 0.98-1.16] in participants without hyperbetalipoproteinemia)., Conclusions and Relevance: In this population-based study of Chinese adults with CVD, long-term exposure to air pollution was associated with a higher prevalence of cardiometabolic risk factors, and the strongest associations were observed for hyperbetalipoproteinemia. In addition, participants with cardiometabolic risk factors may have been more vulnerable to the effects of air pollution on CVD.

Backgrounds: Evidence on the association between long-term exposure to particulate matter with aerodynamic diameter ≤2.5 μm (PM 2.5 ) and cardiovascular disease (CVD) is scarce in developing countries. Moreover, few studies assessed the role of the PM 1 (≤1.0 μm) size fraction and CVD. We investigated the associations between PM 1 and PM 2.5 and CVD prevalence in Chinese adults., Methods: In 2009, we randomly recruited 24,845 adults at the age of 18-74 years from 33 communities in Northeastern China. CVD status was determined by self-report of doctor-diagnosed CVD. Three-year (2006-08) average concentrations of PM 1 and PM 2.5 were assigned using a satellite-based exposure. We used spatial Generalized Linear Mixed Models to evaluate the associations between air pollutants and CVD prevalence, adjusting for multiple covariates. Stratified and interaction analyses and sensitivity analyses were also performed., Results: A 10 μg/m 3 increase in long-term exposure to ambient PM 1 levels was associated a 12% higher odds for having CVD (OR = 1.12; 95% CI = 1.05-1.20). Compared to PM 1 , association between PM 2.5 and CVD was lower (OR = 1.06; 95% CI = 1.01-1.11). No significant association was observed for PM 1-2.5 (1-2.5 μm) size fraction (OR = 0.98; 95% CI = 0.85-1.13). Stratified analyses showed greater effect estimates in men and the elder., Conclusions: Long-term PM 1 exposure was positively related to CVD, especially in men and the elder. In addition, PM 1 may play a greater role than PM 2.5 in associations with CVD. Further longitudinal studies are warranted to confirm our findings., (Copyright © 2018 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background and Objectives: Little is known about PM 1 effects on respiratory health, relative to larger size fractions (PM 2.5 ). To address this literature gap, we assessed associations between PM 1 exposure and asthmatic symptoms in Chinese children and adolescents, compared with PM 2.5 ., Methods: A total of 59,754 children, aged 2-17 years, were recruited from 94 kindergartens, elementary and middle schools in the Seven Northeast Cities (SNEC) study, during 2012-2013. We obtained information on asthma and asthma-related symptoms including wheeze, persistent phlegm, and persistent cough using a standardized questionnaire developed by the American Thoracic Society. PM 1 and PM 2.5 concentrations were estimated using a spatial statistical model matched to the children's geocoded home addresses. To examine the associations, mixed models with school/kindergarten as random intercept were used, controlling for covariates., Results: Odds ratios (ORs) of doctor-diagnosed asthma associated with a 10-μg/m 3 increase for PM 1 and PM 2.5 were 1.56 (95% CI: 1.46-1.66) and 1.50 (1.41-1.59), respectively, and similar pattern were observed for other outcomes. Interaction analyses indicated that boys and the individuals with an allergic predisposition may be vulnerable subgroups. For example, among children with allergic predisposition, the ORs for doctor diagnosed asthma per 10 μg/m 3 increase in PM 1 was 1.71 (95% CI: 1.60-1.83), which was stronger than in their counterparts (1.46; 1.37-1.56) (p for interaction  < 0.05)., Conclusions: This study indicated that long-term exposure to PM 1 may increase the risk of asthma and asthma-related symptoms, especially among boys and those with allergic predisposition. Furthermore, these positive associations for PM 1 were very similar to those for PM 2.5 ., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Background: Health effects of air pollution on diabetes have been scarcely studied in developing countries. We aimed to explore the associations of long-term exposure to ambient particulate matter (PM) and gaseous pollutants with diabetes prevalence and glucose-homoeostasis markers in China., Methods: Between April 1 and Dec 31, 2009, we recruited a total of 15 477 participants aged 18-74 years using a random number generator and a four-staged, stratified and cluster sampling strategy from a large cross-sectional study (the 33 Communities Chinese Health Study) from three cities in Liaoning province, northeastern China. Fasting and 2 h insulin and glucose concentrations and the homoeostasis model assessment of insulin resistance index and β-cell function were used as glucose-homoeostasis markers. Diabetes was defined according to the American Diabetes Association's recommendations. We calculated exposure to air pollutants using data from monitoring stations (PM with an aerodynamic diameter of 10 μm or less [PM 10 ], sulphur dioxide, nitrogen dioxide, and ozone) and a spatial statistical model (PM with an aerodynamic diameter of 1 μm or less [PM 1 ] and 2·5 μm or less [PM 2·5 ]). We used two-level logistic regression and linear regression analyses to assess associations between exposure and outcomes, controlling for confounders., Findings: All the studied pollutants were significantly associated with increased diabetes prevalence (eg, the adjusted odds ratios associated with an increase in IQR for PM 1 , PM 2·5 , and PM 10 were 1·13, 95% CI 1·04-1·22; 1·14, 1·03-1·25; and 1·20, 1·12-1·28, respectively). These air pollutants were also associated with higher concentrations of fasting glucose (0·04-0·09 mmol/L), 2 h glucose (0·10-0·19 mmol/L), and 2 h insulin (0·70-2·74 μU/L). No association was observed for the remaining biomarkers. Stratified analyses indicated greater effects on the individuals who were younger (<50 years) or overweight or obese., Interpretation: Long-term exposure to air pollution was associated with increased risk of diabetes in a Chinese population, particularly in individuals who were younger or overweight or obese., Funding: The National Key Research and Development Program of China, the National Natural Science Foundation of China, the Fundamental Research Funds for the Central Universities, the Guangdong Province Natural Science Foundation, the Career Development Fellowship of Australian National Health and Medical Research Council, and the Early Career Fellowship of Australian National Health and Medical Research Council., (Copyright © 2018 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

As the world's second-largest economy, China is going on suffering from environmental pollution, especially for ambient air pollution, which has become a major threat to public health; public awareness of the detrimental effects of air pollution on health is increasing-particularly in relation to haze days. Considering the nonlinear relationship of ambient air pollution exposure and health impacts, and the differences in specific sources of air pollution with those in North America and Europe, conducting health impact assessments of ambient air pollution in China has thus become an urgent task for public health practitioners. Systematic review of the health effects of exposure to ambient air pollution from quantitative studies conducted in Chinese could provide vital information for epidemiology-based health impact assessments and the implementation of a national environmental protection policy.

The rapid economic growth in China is coupled with a severe ambient air pollution, which poses a huge threat to human health and the sustainable development of social economy. The rapid urbanization and industrialization over the last three decades have placed China as one of countries with the greatest disease burden in world. Notably, the prevalence rate of chronic noncommunicable diseases (CND), including respiratory diseases, CVD, and stroke, in 2010 reaches 16.9%. The continuous growth of the incidence of CND urgent needs for effective regulatory action for health protection. This study aims to evaluate the impact of rapid urbanization on status of ambient air pollution and associated adverse health effects on the incidence and the burden of CND and risk assessment. Our findings would be greatly significant in the prediction of the risk of ambient air pollution on CND and for evidence-based policy making and risk management in China.

Elevated heart rate (HR) can be hypothesized to be involved in the pathways by which ambient air pollution, especially fine particulate matter (PM2.5), causes cardiovascular morbidity and mortality. However, evidence concerning long-term PM2.5 exposure and HR is still limited. Therefore, in this study, we assessed the associations of PM2.5 with HR levels and tachycardia prevalence and explored potential modifiers of the associations. We used baseline data of 1,802,207 adults from the Kashgar Prospective Cohort Study (KPCS). PM2.5 exposure was assessed based on satellite sensing data, meteorological factors, multi-resolution emission inventory, and measurements from ground-based surface monitors measurements. HR was measured using a calibrated electronic sphygmomanometer, and tachycardia was defined as resting heart rate (RHR) equal to or greater than 80 beats per minute. Linear regression and logistic regression models were employed to evaluate the associations of PM2.5 levels with RHR levels and tachycardia prevalence, respectively. Stratified analyses by sex, age, ethnicity, smoking status, alcohol use, and physical activity were also performed. The mean (standard deviation) age of the study participants was 39.4 (15.5) years old. In the adjusted models, an interquartile range (8.8 µg/m3) increase in PM2.5 levels was associated with 0.515 (95% confidence interval: 0.503–0.526) bpm increase in RHR levels and with 1.062-fold (95% confidence interval: 1.059–1.064) increase in the odds of tachycardia. The results were robust against several sensitivity analyses. In addition, we observed the above associations were stronger in participants that were men, of Uyghur ethnicity, smoking cigarettes, drinking alcohol, and having physical inactivity, compared to their counterparts. In summary, our findings indicate that long-term exposure to ambient PM2.5 may be hazardously associated with HR, and women, Uyghur people, and those with unhealthy lifestyles may be more vulnerable to the hazardous effects. [ABSTRACT FROM AUTHOR]

Introduction: There is growing interest in the impact of greenness exposure on airway diseases, but the impact of greenness on lung function in children is limited. We aimed to investigate the associations between greenness surrounding schools and lung function in children and whether these associations are modified by air pollution exposure.Methods: Between 2012 and 2013, a cross-sectional survey and spirometry were performed among 6740 school children. Lung function patterns were determined as obstructive forced expiratory volume 1 s/forced vital capacity (FEV1/FVC <0.8) or restrictive (FEV1/FVC ≥0.8 but FVC <80% of predicted). School greenness was defined by Normalized difference vegetation index (NDVI) and soil-adjusted vegetation index. Nitrogen dioxide, sulphur dioxide and particular matter concentrations were assessed using a spatiotemporal model and national monitoring data. Two-level generalised linear models were used to investigate associations and interactions.Results: Overall, an IQR in NDVI within 500 m was associated with higher FEV1 (+57 mL 95% CI 44 to 70) and FVC (+58 mL 95% CI 43 to 73). NDVI was similarly associated with 25% reduced odds of spirometric restriction (OR: 0.75, 95% CI 0.65 to 0.86). However, among children exposed to the highest compared with the lowest quartile of particulate matter, increasing NDVI was paradoxically associated with lower -40 mL FVC (95% CI -47 to -33, p interaction <0.05).Discussion: Our findings suggest that, in this study population, greening urban areas may promote lung health in low-moderate pollution areas but not in high air pollution areas. If the findings are replicated in other moderate-to-high pollution settings, this highlights a need to have a flexible green policy. [ABSTRACT FROM AUTHOR]

Ambient air pollutants exposures may lead to aggravated Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD). However, there is still a scarcity of empirical studies that have rigorously estimated this association, especially in regions where air pollution is severe. To fill in the literature gap, we conducted a cross-sectional study involving 2711,207 adults living in five regions of southern Xinjiang Uyghur Autonomous Region in 2021. Using a Space-Time Extra-Trees model, we assessed the four-year (2017–2020) average concentrations of particulate matter with aerodynamic diameter ≤1 µm (PM 1), particulate matter with aerodynamic diameter ≤2.5 µm (PM 2.5), particulate matter with aerodynamic diameter ≤10 µm (PM 10), ozone (O 3), sulfur dioxide (SO 2), and carbon monoxide (CO), and then assigned these values to the participants. Generalized linear mixed models were employed to examine the relationships between air pollutants and the prevalence of MAFLD, with adjustment for multiple confounding factors. The odds ratios and 95% confidence intervals of MAFLD were 2.002 (1.826–2.195), 1.133 (1.108–1.157), 1.034 (1.027–1.040), 1.077 (1.023–1.134), 2.703 (2.322–3.146) and 1.033 (1.029–1.036) per 10 µg/m3 increase in the 4-year average PM 1 , PM 2.5 , PM 10 , O 3 , SO 2 and CO exposures, respectively. The robustness of the findings was confirmed by a series of sensitivities. In summary, long-term exposure to ambient air pollutants was associated with increased odds of MAFLD, particularly in males and individuals with unhealthy lifestyles. • Evidence concerning ambient air pollution and MAFLD is limited. • Exposure to air pollutants was related to higher odds of MAFLD. • The association between gaseous pollutants and MAFLD is more pronounced in males. • A healthy lifestyle may mitigate the adverse effects of air pollution on MAFLD. [ABSTRACT FROM AUTHOR]

Background: Recent studies suggest that household endotoxin and allergens can modify the impact of air pollutants on development of asthma; however, epidemiological evidence is limited and conflicting. Objectives: To investigate whether pet ownership modified the association between ambient air pollution and asthma in children. Methods: We conducted a population‐based cross‐sectional study, the Seven Northeast Cities Study in China and recruited a total of 59,754 children from 94 schools during 2012–2013. Long‐term air pollutant concentrations, including airborne particulate matter with a diameter of 1 μm or less (PM1), PM2.5, PM10, and nitrogen dioxide (NO2) from 2009 to 2012 were estimated using a random forest model. We collected information of respiratory health in children using the Epidemiologic Standardization Project Questionnaire of the American Thoracic Society (ATS‐DLD‐78‐A). Regression models were used to evaluate associations between pet ownership and air pollution on asthma after adjusting for potential covariates. Results: Exposure to increasing levels of air pollutants was associated with higher prevalence of asthma, but associations were significantly attenuated in children who owned pets. For example, compared to children without pets, those who owned pets did not have an increased risk of symptoms of asthma (odds ratio, 1.01, 95% confidence interval: 0.78, 1.30), wheeze (0.96, 95% confidence interval [CI]: 0.76, 1.21), and cough (1.01, 95% CI: 0.87, 1.18) for each 10 µg/m3 increase in PM1 (P‐int < 0.05). Similar trends were observed for other air pollutants. Dog and bird ownership decreased the associations of asthma and cough with air pollutant exposure. The main findings were consistent with a series of sensitivity analyses. Conclusion: Current pet ownership may reduce the adverse impact of long‐term air pollution on childhood asthma. Longitudinal studies are needed to confirm this finding which could have important implications for public health. [ABSTRACT FROM AUTHOR]

Abstract Background Little information exists on the lipidemic effects of air pollution, particularly in developing countries. We aimed to investigate the associations of long-term exposure to ambient air pollutants with lipid levels and dyslipidemias in China. Methods In 2009, a total of 15,477 participants aged 18–74 years were recruited from the 33 Communities Chinese Health Study conducted in three Northeastern China cities. Total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) were measured in participants' blood specimens. Three year (2006–08) average air pollution concentrations were assessed using data from 33 communities (particles with diameters ≤1.0 μm (PM 1) and ≤2.5 μm (PM 2.5) were predicted using a spatial statistical model) or 11 air monitoring stations (particles with diameters ≤10 μm (PM 10), sulfur dioxide (SO 2), nitrogen dioxide (NO 2), and ozone (O 3)). Associations were evaluated by two-level logistic and generalized linear regression models. Results We detected many significant associations between exposure to air pollutants (especially for PM 1 and PM 2.5) and blood lipid levels. Most of the associations suggested deleterious effects on blood lipid markers (e.g., a 10 μg/m3 increase in PM 1 was associated with 1.6% (95% confidence interval (CI): 1.1, 2.0), 2.9% (95% CI: −3.3, 9.3), and 3.2% (95% CI: 2.6, 3.9) higher levels of TC, TG, and LDL-C, respectively, but 1.4% (95% CI: −1.8, −0.9) lower HDL-C levels), although beneficial associations were found for O 3. In analysis with dyslipidemias, all the observed associations suggested deleterious lipidemic effects of air pollutants, and no significant beneficial association was observed for O 3. Stratified analyses showed that the associations were stronger in overweight or obese participants; sex and age modified the associations, but the pattern of effects was mixed. Conclusions Long-term ambient air pollution was associated with both altered lipid profiles and dyslipidemias, especially among overweight or obese participants. Highlights • Little information exists on the lipidemic effects of ambient air pollution. • We conducted a cross-sectional study among 15,477 Chinese adults. • Associations between ambient air pollution and blood lipids were examined. • Long-term ambient air pollution may have deleterious effects on lipid profiles. [ABSTRACT FROM AUTHOR]

Little evidence exists about the effects of long-term exposure to ambient air pollution on metabolic syndrome (MetS). This study aimed to determine the association between long-term ambient air pollution and MetS in China. A total of 15,477 adults who participated in the 33 Communities Chinese Health Study (33CCHS) in 2009 were evaluated. MetS was defined based on the recommendation by the Joint Interim Societies. Exposure to air pollutants was assessed using data from monitoring stations and a spatial statistical model (including particles with diameters ≤ 1.0 µm (PM 1 ), ≤ 2.5 µm (PM 2.5 ), and ≤ 10 µm (PM 10 ), sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), and ozone (O 3 )). Two-level logistic regression analyses were utilized to assess the associations between air pollutants and MetS. The prevalence of MetS was 30.37%. The adjusted odds ratio of MetS per 10 µg/m 3 increase in PM 1 , PM 2.5 , PM 10 , SO 2 , NO 2 , and O 3 were 1.12 (95% CI = 1.00–1.24), 1.09 (95% CI = 1.00–1.18), 1.13 (95% CI = 1.08–1.19), 1.10 (95% CI = 1.02–1.18), 1.33 (95% CI = 1.12–1.57), and 1.10 (95% CI = 1.01–1.18), respectively. Stratified analyses indicated that the above associations were stronger in participants with the demographic variables of males, < 50 years of age, and higher income, as well as with the behavioral characteristics of smoking, drinking, and consuming sugar-sweetened soft drinks frequently. This study indicates that long-term exposure to ambient air pollutants may increase the risk of MetS, especially among males, the young to middle aged, those of low income, and those with unhealthy lifestyles. [ABSTRACT FROM AUTHOR]

Although numerous studies have investigated the association of ambient air pollution with hypertension and blood pressure (BP), the results were inconsistent. We performed a comprehensive systematic review and meta-analysis of these studies. Seven international and Chinese databases were searched for studies examining the associations of particulate (diameter<2.5 μm (PM 2.5 ), 2.5–10 μm (PM 2.5-10 ) or >10 μm (PM 10 )) and gaseous (sulfur dioxide (SO 2 ), nitrogen dioxide (NO 2 ), nitrogen oxides (NO x ), ozone (O 3 ), carbon monoxide (CO)) air pollutants with hypertension or BP. Odds ratios (OR), regression coefficients (β) and their 95% confidence intervals were calculated to evaluate the strength of the associations. Subgroup analysis, sensitivity analysis, and meta-regression analysis were also conducted. The overall meta-analysis showed significant associations of long-term exposures to PM 2.5 with hypertension (OR = 1.05), and of PM 10 , PM 2.5 , and NO 2 with DBP (β values: 0.47–0.86 mmHg). In addition, short-term exposures to four (PM 10 , PM 2.5 , SO 2 , NO 2 ), two (PM 2.5 and SO 2 ), and four air pollutants (PM 10 , PM 2.5 , SO 2 , and NO 2 ), were significantly associated with hypertension (ORs: 1.05–1.10), SBP (β values: 0.53–0.75 mmHg) and DBP (β values: 0.15–0.64 mmHg), respectively. Stratified analyses showed a generally stronger relationship among studies of men, Asians, North Americans, and areas with higher air pollutant levels. In conclusion, our study indicates a positive association between ambient air pollution and increased BP and hypertension. Geographical and socio-demographic factors may modify the pro-hypertensive effects of air pollutants. [ABSTRACT FROM AUTHOR]

Particulate matter (PM) exposure is associated to the adverse change in blood lipids. Vitamin D is beneficial to lipid metabolism, but whether vitamin D levels modifies the impact of air pollutants on lipids is unclear. The purpose of the study was to investigate if vitamin D modifies the associations of PM and serum lipids in young healthy people. From December 2017 to January 2018, a panel study with five once weekly follow-ups was conducted on 88 healthy adults aged 21.09 (1.08) (mean (SD)) years on average in Guangzhou, China. We measured serum lipids, serum 25-hydroxyvitamin D (25(OH)D) concentrations (440 blood samples in total), mass concentrations of particulate matter with diameters ≤2.5 μm (PM 2.5), ≤1.0 μm (PM 1.0), and ≤0.5 μm (PM 0.5), and number concentrations of particulate matter with diameters ≤0.2 μm (PN 0.2) and ≤0.1 μm (PN 0.1) at each follow-up. Linear mixed-effect models were applied to assess the interaction of vitamin D and size-fractionated PM short-term exposure on four lipid metrics. We found the interactions between 25(OH)D and size-fractionated PM exposure on blood lipids in different lags (lag 3 days and 4 days). An interquartile range increase in PM 2.5 , PM 1.0 , PM 0.5 were significantly associated with increments of 12.30%, 12.99%, and 13.66% in triglycerides (TGs) at lag 4 days at vitamin D levels <15 ng/mL group, respectively. Similar results were found for PN 0.2 , PN 0.1 and low-density lipoprotein cholesterol (LDL-C). All the associations between size-fractionated PM and blood lipids were found null statistically significant in vitamin D levels ≥15 ng/mL group. [Display omitted] • Vitamin D modified the association between particulate matter (PM) and blood lipids. • PM 2.5 , PM 10 , PM 0.5 are associated with increments of TGs at vitamin D < 15 ng/mL group. • PN 0.2 and PN 0.1 are associated with increments of LDL-C at vitamin D < 15 ng/mL group. • No association is observed between PM and blood lipids at vitamin D ≥ 15 ng/mL group. [ABSTRACT FROM AUTHOR]

• Maternal PM and NO 2 exposure was associated with higher odds of CHD. • The first trimester might be the critical exposure window of air pollution for CHD. • Pattern of the associations of air pollutants with CHD subtypes was mixed. Evidence of maternal exposure to ambient air pollution on congenital heart defects (CHD) has been mixed and are still relatively limited in developing countries. We aimed to investigate the association between maternal exposure to air pollution and CHD in China. This longitudinal, population-based, case-control study consecutively recruited fetuses with CHD and healthy volunteers from 21 cities, Southern China, between January 2006 and December 2016. Residential address at delivery was linked to random forests models to estimate maternal exposure to particulate matter with an aerodynamic diameter of ≤ 1 µm (PM 1), ≤2.5 µm, and ≤10 µm as well as nitrogen dioxides, in three trimesters. The CHD cases were evaluated by obstetrician, pediatrician, or cardiologist, and confirmed by cardia ultrasound. The CHD subtypes were coded using the International Classification Diseases. Adjusted logistic regression models were used to assess the associations between air pollutants and CHD and its subtypes. A total of 7055 isolated CHD and 6423 controls were included in the current analysis. Maternal air pollution exposures were consistently higher among cases than those among controls. Logistic regression analyses showed that maternal exposure to all air pollutants during the first trimester was associated with an increased odds of CHD (e.g., an interquartile range [13.3 µg/m3] increase in PM 1 was associated with 1.09-fold ([95% confidence interval, 1.01–1.18]) greater odds of CHD). No significant associations were observed for maternal air pollution exposures during the second trimester and the third trimester. The pattern of the associations between air pollutants and different CHD subtypes was mixed. Maternal exposure to greater levels of air pollutants during the pregnancy, especially the first trimester, is associated with higher odds of CHD in offspring. Further longitudinal well-designed studies are warranted to confirm our findings. [ABSTRACT FROM AUTHOR]

Evidence concerning exposure to air pollution and visual impairment is scarce. We evaluated the associations of ambient air pollution with visual impairment and visual acuity levels in Chinese schoolchildren. We recruited 61,995 children from 7 provinces/municipalities across China. Concentrations of air pollutants (i.e., particulate matter with an aerodynamic diameter of ≤ 1.0 µm [PM 1 ], ≤ 2.5 µm [PM 2.5 ], and 10 µm [PM 10 ] as well as nitrogen dioxides [NO 2 ]) were measured using machine learning methods. Visual acuity levels were measured using standard protocols. We used SAS PROC SURVEYLOGISTIC to assess the association between air pollution and visual impairment. An interquartile range increase in PM 1 , PM 2.5 , PM 10 , and NO 2 was associated with a 1.133- (95% CI, 1.035-1.240), 1.267- (95% CI, 1.082-1.484), 1.142- (95% CI, 1.019-1.281), and 1.276-fold (95% CI, 1.173-1.388) increased odds of visual impairment, and the associations were stronger in children being boys, older, living in rural areas, and born to parents who had a lower educational level or smoked, compared to their counterparts. These results suggest that exposure to air pollution were positively associated with the odds of visual impairment, and the association may be modified by children's age, sex, and residential area as well as parental education level and cigarette smoking. ga1 • A total of 61,995 Children from 7 Chinese provinces/municipalities were recruited. • Visual acuity was measured according to standard protocol. • Concentrations of four air pollutants were measured using machine-learning methods. • Air pollution was significantly associated with higher odds of visual impairment. • The association may be modified by both demographic and lifestyle factors. [ABSTRACT FROM AUTHOR]

Evidence concerning effects of ambient air pollution on homocysteine (HCY) metabolism is scarce. We aimed to explore the associations between ambient particulate matter (PM) exposure and the HCY metabolism markers and to evaluate effect modifications by folate, vitamin B 12 , and methylenetetrahyfrofolate reductase (MTHFR) C677T gene polymorphism. Between December 1, 2017 and January 5, 2018, we conducted a panel study in 88 young college students in Guangzhou, China, and received 5 rounds of health examinations. Real-time concentrations of PMs with aerodynamic diameter ≤2.5 (PM 2.5), ≤1.0 (PM 1.0), and ≤0.1 (PM 0.1) were monitored, and the serum HCY metabolism markers (i.e., HCY, S-Adenosylhomocysteine [SAH], and S-Adenosylmethionine [SAM]) were repeatedly measured. We applied linear mixed effect models combined with a distributed lag model to evaluate the associations of PMs with the HCY metabolism markers. We also explored effect modifications of folate, vitamin B 12 , and the MTHF R C677T polymorphism on the associations. We observed that higher concentrations of PM 2.5 and PM 1.0 were associated with higher serum levels of HCY, SAH, SAM, and SAM/SAH ratio (e.g., a 10 μg/m3 increase in PM 2.5 during lag 0 day and lag 5 day was significantly associated with 1.3–19.4%, 1.3–28.2%, 6.2–64.4%, and 4.8–28.2% increase in HCY, SAH, SAM, and SAM/SAH ratio, respectively). In addition, we observed that the associations of PM 2.5 with the HCY metabolism markers were stronger in participants with lower B vitamins levels. This study demonstrated that short-term exposure to PM 2.5 and PM 1.0 was deleteriously associated with the HCY metabolism markers, especially in people with lower B vitamins levels. Image 1 • PM 2.5 and PM 1.0 exposures were associated with HCY metabolism markers. • B vitamins modified the associations of PMs with HCY metabolism markers. • MTHFR genotype did not modify the associations of PMs with HCY metabolism markers. Short-term exposures to PM 2.5 and PM 1.0 were deleteriously associated with the HCY metabolism markers, and the associations were modified by B vitamins. [ABSTRACT FROM AUTHOR]

Elevated blood homocysteine (Hcy) is an independent risk factor for cardiovascular disease. A growing number of studies have evaluated the link between air pollution and blood Hcy levels, but the results are inconsistent. To date, no systematic review of the published studies has been conducted yet. We aimed to provide a comprehensive overview of these studies. We systematically searched three international databases (PubMed, Web of Science, and Embase) and four Chinese databases (Wanfang, CNKI, CBM, and VIP) for peer-reviewed epidemiological studies investigating associations between ambient air pollutants and Hcy levels published before December 2019. We screened literature, extracted data, assessed methodological quality, and evaluated the risk of bias of the included studies. Of 1157 identified articles, 10 were finally included in this systematic review. Most were cross-sectional studies and were performed in developed countries. Particulate matter with aerodynamic diameters less than 2.5 μm (PM 2.5) and/or 10 μm (PM 10) were investigated in all of the included studies. Overall, the evidence generally supports a positive association between higher PM concentrations and elevated Hcy levels. However, high heterogeneity in terms of study participants, study design, exposure duration, and particle components and sources, low methodological quality and probable high risk of bias in some studies, and limited literature number precluded us from drawing a robust conclusion. Associations between Hcy and gaseous pollutants were explored in only one or two studies, and the results were inconclusive. Additional, well-designed studies remain required to validate the association between air pollution and Hcy. [ABSTRACT FROM AUTHOR]

Ambient air pollution exposure and influenza virus infection have been documented to be independently associated with reduced lung function previously. Influenza vaccination plays an important role in protecting against influenza-induced severe diseases. However, no study to date has focused on whether influenza vaccination may modify the associations between ambient air pollution exposure and lung function. We undertook a cross-sectional study of 6740 children aged 7–14 years into Seven Northeast Cities (SNEC) Study in China during 2012–2013. We collected information from parents/guardians about sociodemographic factors and influenza vaccination status in the past three years. Lung function was measured using portable electronic spirometers. Machine learning methods were used to predict 4-year average ambient air pollutant exposures to nitrogen dioxide (NO 2) and particulate matter with an aerodynamic diameter <1 μm (PM 1), <2.5 μm (PM 2.5) and <10 μm (PM 10). Two-level linear and logistic regression models were used to assess interactions between influenza vaccination and long-term ambient air pollutants exposure on lung function reduction, controlling for potential confounding factors. Ambient air pollution were observed significantly associated with reductions in lung function among children. We found significant interactions between influenza vaccination and air pollutants on lung function, suggesting greater vulnerability to air pollution among unvaccinated children. For example, an interaction (p interaction = 0.002) indicated a −283.44 mL (95% CI: −327.04, −239.83) reduction in forced vital capacity (FVC) per interquartile range (IQR) increase in PM 1 concentrations among unvaccinated children, compared with the −108.24 mL (95%CI: −174.88, −41.60) reduction in FVC observed among vaccinated children. Results from logistic regression models also showed stronger associations between per IQR increase in PM 1 and lung function reduction measured by FVC and peak expiratory flow (PEF) among unvaccinated children than the according ORs among vaccinated children [i.e., Odds Ratio (OR) for PM 1 and impaired FVC: 2.33 (95%CI: 1.79, 3.03) vs 1.65 (95%CI: 1.20, 2.28); OR for PM 2.5 and impaired PEF: 1.45 (95%CI: 1.12,1.87) vs 1.04 (95%CI: 0.76,1.43)]. The heterogeneity of the modification by influenza vaccination of the associations between air pollution exposure and lung function reduction appeared to be more substantial in girls than in boys. Our results suggest that influenza vaccination may moderate the detrimental effects of ambient air pollution on lung function among children. This study provides new insights into the possible co-benefits of strengthening and promoting global influenza vaccination programs among children. Image 1 • No study on interactions between flu vaccine and air pollution on lung function. • Flu vaccine may mitigate the detrimental effects of air pollution on lung function. • The interactions appeared to be more substantial in girls than in boys. [ABSTRACT FROM AUTHOR]

• Few studies have examined association between greenness and metabolic syndrome. • We explored the topic in 15,477 Chinese urban dwellers. • Higher greenness levels were associated with lower odds of metabolic syndrome. • Stronger association was observed in people aged 65 years or younger and those with higher household income. • Air pollution partly mediated the greenness-metabolic syndrome association. Residing in greener areas has several health benefits, but no study to date has examined the effects of greenness on metabolic syndrome (MetS). We aimed to assess associations between residential greenness and MetS prevalence in China, and to explore whether air pollution and physical activity mediated any observed associations. We analyzed data from 15,477 adults who participated in the 33 Communities Chinese Health Study during 2009. We defined MetS according to standard guidelines for Chinese populations. Residential greenness was estimated using the Normalized Difference Vegetation Index (NDVI), the Soil Adjusted Vegetation Index (SAVI), and the Vegetation Continuous Field (VCF). We used generalized linear mixed models to assess the associations between greenness and MetS, and mediation analyses to explore potential mechanisms underlying the associations. Higher greenness levels were associated with lower odds of MetS [e.g., for every interquartile range increase of NDVI 500-m , SAVI 500-m , and VCF 500-m , the adjusted odds ratio of MetS was 0.81 (95% confidence interval: 0.70–0.93), 0.80 (95% confidence interval: 0.69–0.93), and 0.91 (95% confidence interval: 0.83–1.00), respectively]. The direction and the magnitude of the associations persisted in several sensitivity analyses. Stratified analyses showed that age and household income modified the associations, with greater effect estimates observed in participants younger than 65 years old or those with higher household income. Particulate matter with an aerodynamic diameter ≤10 μm, nitrogen dioxide, and ozone mediated 2.1–20.3% of the associations between greenness and MetS; no evidence of mediation was observed for physical activity. Our findings suggest a beneficial association for residential greenness and MetS in Chinese urban dwellers, especially for participants younger than 65 years old and those with higher household income. Particulate matter with an aerodynamic diameter ≤10 μm, nitrogen dioxide and ozone, but not physical activity, may only partially mediate the association. [ABSTRACT FROM AUTHOR]

Air pollutants are suggested to be related to type 2 diabetes (T2D). Since several high quality papers on air pollutants and T2D have been published beyond the last reviews, an extended systematic review is highly warranted. We review epidemiological studies to quantify the association between air pollutants and T2D, and to answer if diabetes patients are more vulnerable to air pollutants. We systematically reviewed the databases of PubMed and Web of Science based on the guidelines of the Preferred Reporting Items for Systematic review and Meta-analysis (PRISMA). We calculated odds ratios (OR) or hazard ratios (HR) and their 95% confidence intervals (CI) to assess the strength of the associations between air pollutants [e.g., particulate matter with diameter ≤ 2.5 μm (PM 2.5), particulate matter with diameter ≤ 10 μm (PM 10), and nitrogen dioxide (NO 2)] and T2D. We evaluated the quality and risk of bias of the included studies and graded the credibility of the pooled evidence using several recommended tools. We also performed sensitivity analysis, meta-regression analysis, and publication bias test. Out of 716 articles identified, 86 were used for this review and meta-analysis. Meta-analyses showed significant associations of PM 2.5 with T2D incidence (11 studies; HR = 1.10, 95% CI = 1.04–1.17 per 10 μg/m3 increment; I2 = 74.4%) and prevalence (11 studies; OR = 1.08; 95% CI = 1.04–1.12 per 10 μg/m3 increment; I2 = 84.3%), of PM 10 with T2D prevalence (6 studies; OR = 1.10; 95% CI = 1.03–1.17 per 10 μg/m3 increment; I2 = 89.5%) and incidence (6 studies; HR = 1.11; 95% CI = 1.00–1.22 per μg/m3 increment; I2 = 70.6%), and of NO 2 with T2D prevalence (11 studies; OR = 1.07; 95% CI = 1.04–1.11 per 10 μg/m3 increment; I2 = 91.1%). The majority of studies on glucose-homoeostasis markers also showed increased risks with higher air pollutants levels, but the studies were too heterogeneous for meta-analysis. Overall, patients with diabetes might be more vulnerable to PM. Recent publications strengthened the evidence for adverse effects of ambient air pollutants exposure (especially for PM) on T2D and that diabetic patients might be more vulnerable to air pollutants exposure. • Evidence on ambient air pollution and diabetes is still inconsistent. • We reviewed 86 studies on air pollution and diabetes and its traits. • We meta-analyzed 29 studies for PM and NO2 with diabetes. • Air pollutants (e.g., PM and NO2) are associated with higher odds of diabetes. • Air pollution is associated with dysregulation of glucose metabolism. [ABSTRACT FROM AUTHOR]

Ambient air pollution increases the risk of respiratory mortality and morbidity, but evidence concerning effects of air pollution on chronic bronchitis (CB) is scarce. This study aimed to evaluate the associations of a set of air pollutants with the burden of CB, and to explore potential modifiers on the associations. In 2020, a total of 6,556,440 adults living in the Northwestern region of China were recruited. The Space-Time Extra-Trees model was employed to assess the annual average concentrations of six air pollutants for the three years (2017-2019) before 2020 , and subsequently allocated to the participants based on the latitude and longitude of their home addresses. We investigated the associations between the levels of various air pollutants and the odds of CB using generalized linear mixed models, and conducted multiple sensitivity analyses and subgroup analyses. The odds of CB displays an approximately linear association with particulate matter with aerodynamic diameter ≤2.5 μm (PM 2.5), particulate matter with aerodynamic diameter ≤10 μm (PM 10), while it shows a non-linear relationship with gaseous pollutants. In the adjusted model, the odds ratios and 95% confidence intervals for CB per 10 μg/m3 increase in PM 2.5 , PM 10 , and sulfur dioxide (SO 2) were 1.297 (1.262–1.332), 1.072 (1.064–1.080), and 2.587 (2.186–3.063), respectively. Furthermore, several additional sensitivity analyses demonstrated the stability of these associations. Subgroup analyses found that the aforementioned associations were greater among participants aged below 50 years old and those who smoked and had no leisure time exercise. Long-term exposure to ambient air pollutants may increase the odds of CB, especially among younger people and those with unhealthy lifestyles. [Display omitted] • Evidence concerning ambient air pollution and chronic bronchitis (CB) is limited. • We examined the association between air pollution and CB in northwestern China. • Exposure to particulate and gaseous pollutants was related to higher odds of CB. • Our findings may help develop individual-and population-level interventions to reduce CB burden. [ABSTRACT FROM AUTHOR]

This study sought to clarify the correlation of individual exposure measurements and PM 2.5 measurements collected at regulatory monitoring sites in short-term panel study settings. To achieve this goal, 30 young, healthy adult participants were assigned to three groups with 4 samplers in each group to collect individual exposures during four weekends in March 2016. Participants also completed cardiopulmonary function tests during the same periods. For comparison, ambient air pollution data were obtained from the Air Pollution Surveillance Network in Guangzhou, China. The 8-h ambient pollutant averages and group sampler concentrations were used as separate indicators of air pollution exposure. Results showed that the 8-h mean concentration of personal PM 2.5 exposure was 65.09 ± 22.18 μg/m 3 , which was 24.34 μg/m 3 statistically higher than the ambient concentrations over the same period (p < 0.05). However, these concentrations were strongly correlated (Spearman's r = 0.937, p < 0.01). Separate mixed-effect models were fit for ambient and personal exposures to estimate their associations with cardiopulmonary outcomes. Higher PM 2.5 and PM 10 exposures were related to lower lung function of maximal mid-expiratory flow (MMEF). A 10 μg/m 3 higher PM was associated with 0.11 L/S to 0.52 L/S lower MMEF. No effects on cardiovascular function were found. In conclusion, personal PM 2.5 exposure might be higher than ambient concentrations. Young, healthy adults in urban areas may experience reduced lung function (lower MMEF), even after just 8 h of exposure to PM 2.5 and PM 10 . [ABSTRACT FROM AUTHOR]

Low haemoglobin (Hb) concentrations and anaemia in children have adverse effects on development and functioning, some of which may have consequences in later life. Exposure to ambient air pollution is reported to be associated with anaemia, but there is little evidence specific to low- and middle-income countries (LMICs), where childhood anaemia prevalence is greatest. We aimed to determine if long-term ambient fine particulate matter (≤2.5 μm in aerodynamic diameter [PM 2.5 ]) exposure was associated with Hb levels and the prevalence of anaemia in children aged <5 years living in 36 LMICs. We used Demographic and Health Survey data, collected between 2010 and 2019, which included blood Hb measurements. Satellite-derived estimates of annual average PM 2.5 was the main exposure variable, which was linked to children's area of residence. Anaemia was defined according to standard World Health Organization guidelines (Hb < 11 g/dL). The association of PM 2.5 with Hb levels and anaemia prevalence was examined using multivariable linear and logistic regression models, respectively. We examined whether the effects of ambient PM 2.5 were modified by a child's sex and age, household wealth index, and urban/rural place of residence. Models were adjusted for relevant covariates, including other outdoor pollutants and household cooking fuel. The study included 154,443 children, of which 89,904 (58.2%) were anaemic. The country-level prevalence of anaemia ranged from 15.8% to 87.9%. Mean PM 2.5 exposure was 33.0 (±21.6) μg/m3. The adjusted model showed that a 10 μg/m3 increase in annual PM 2.5 concentration was associated with greater odds of anaemia (OR = 1.098 95% CI: 1.087, 1.109). The same increase in PM 2.5 was associated with a decrease in average Hb levels of 0.075 g/dL (95% CI: 0.081, 0.068). There was evidence of effect modification by household wealth index and place of residence, with greater adverse effects in children from lower wealth quintiles and children in rural areas. Exposure to annual PM 2.5 was cross-sectionally associated with decreased blood Hb levels, and greater risk of anaemia, in children aged <5 years living in 36 LMICs. [Display omitted] • PM 2.5 exposure may be associated with anaemia and haemoglobin levels in children. • This study found that anaemia prevalence in children aged <5 years was 58%. • PM 2.5 was associated with decreased haemoglobin levels and greater odds of anaemia. • Greater effects were observed in children from lower wealth index and rural areas. [ABSTRACT FROM AUTHOR]

[Display omitted] • High number concentration and toxicity of ultrafine particles cannot be ignored. • Monitoring the number concentrations of small particles is important. • Mono-culture exposure to PM may underestimate the true PM toxicity. Epidemiological and toxicological evidence show that PM 1 is a key driver of PM 2.5. However, the particle sizes that play the major damaging role in PM 1 is unclear. Our aims were to (1) explore the concentration and chemical composition of ultrafine particles in PM 1 ; (2) evaluate and compare the differences in toxicity of PM 1-0.2 and PM 0.2 to different airway cell models. We collected PM 1-0.2 and PM 0.2 in Guangzhou in December 2017, monitored and detected their concentrations, size, and components. A549, THP-1 mono-cultures and A549/THP-1 co-cultured cells were exposed to PM 1-0.2 and PM 0.2 , and evaluated for toxicological responses. PM 0.2 contributed to15% PM 1 mass and 87.67% to particle number (PN). Most of PM 0.2 was PM 0.1 (exceed 75%). Structure of particles in PM 0.2 were mostly spherical, whereas in PM 1-0.2 they were more diverse. Within the same mass unit, PM 0.2 contained more chemical components than PM 1-0.2 ; within the same volume, a higher mass of components was found in PM 1-0.2. IL-6 and IL-8 were secreted by co-cultured cells in higher manner compared to mono cell cultures. PM 0.2 -induced higher toxicological responses compared to PM 1-0.2. Our findings suggest that high PN concentration and toxicity of ultrafine or PM 1 cannot be ignored. Mono-cell culture may underestimate the true PM toxicity. [ABSTRACT FROM AUTHOR]

Exposure to ambient air pollution is consistently associated with increased cardiovascular morbidity and mortality; however, the underlying pathophysiologic mechanisms remain unclear. High left ventricular voltage has been related to cardiac dysfunction.Therefore, this study aimed to investigate the association between longitudinal exposure to size-fractioned particulate matter (PM) and left ventricular voltage (assessed as the sum of the voltages of the R-wave in lead V5 [RV5] and S-wave in lead V1[SV1]) among 88 healthy, young Chinese adults. We collected weekly 12-lead electrocardiogram (ECG) and serum biomarkers from each participant five times over 35 days. The fixed point, real-time, mass concentrations of particles with aerodynamic diameters of ≤2.5 μm (PM 2.5), PM 1 , PM 0.5 , and number concentrations of particles with aerodynamic diameters of ≤0.2 μm (PNC 0.2), PNC 0.1 , and PNC 0.03 were monitored in the catchment area, and linear mixed-effect models were used to estimate the associations between the size-fractioned PM exposure and ECG indices. The results showed that there was a significant association between higher size-fractioned PM levels and higher RV5+SV1 voltage within 24 h of exposure. We detected increases in the RV5+SV1 voltage of 0.060, 0.058, 0.090, 0.084, and 0.077 mV per interquartile range (IQR) PM 2.5 (45.92 μg/m3; 95% confidence interval [CI] = 0.003, 0.117), PM 1 (43.51 μg/m3; 95% CI = 0.003, 0.113), PNC 0.2 (14.92 × 103 particles/cm3; 95% CI = 0.017, 0.163), PNC 0.1 (12.79 × 103 particles/cm3; 95% CI = 0.004, 0.163), and PNC 0.03 (5.43 × 103 particles/cm3; 95% CI = 0, 0.153), respectively. The associations between the RV5+SV1 voltage and size-fractioned PM exposure were stronger among participants with greater serum concentrations of monocyte chemoattractant protein-1, soluble CD40 ligand, plasminogen activator inhibitor-1, and total cholesterol, and lower high-density lipoprotein cholesterol levels. Exposure to various PM size fractions (PNC 0.03 -PNC 0.2 , and PM 0.5 -PM 2.5) may increase the left ventricular voltage among healthy young adults, and the effects may be modified by inflammation, coagulation, and lipid biomarkers. [Display omitted] • The mechanisms for the relationship between PM and cardiac disease remain unclear. • Size-fractioned PM exposure increased left ventricular voltage, especially in men. • The smaller the particles size, the greater effects on left ventricular voltage. • The PM associations were modified by inflammation, coagulation and lipids biomarkers. [ABSTRACT FROM AUTHOR]

• A systematic review identified 22 studies from 10 countries of the world. • Short-term exposure to NO 2 was associated with an increased odds of depression. • Long-term PM 2.5 , PM 10 , and NO 2 exposure was not associated with depression. • Short-term PM 2.5 , PM 10 , SO 2 , and O 3 exposure was not associated with depression. Although epidemiological studies have evaluated the associations of ambient air pollution with depression, the results remained mixed. To clarify the nature of the association, we performed a comprehensive systematic review and meta-analysis with the Inverse Variance Heterogeneity (IVhet) model to estimate the effect of ambient air pollution on depression. Three English and four Chinese databases were searched for epidemiologic studies investigating associations of ambient particulate (diameter ≤ 2.5 μm (PM 2.5), ≤10 μm (PM 10)) and gaseous (nitric oxide (NO), nitrogen dioxide (NO 2), carbon monoxide (CO), sulfur dioxide (SO 2) and ozone (O 3)) air pollutants with depression. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were calculated to evaluate the strength of the associations. We identified 22 eligible studies from 10 countries of the world. Under the IVhet model, per 10 µg/m3 increase in long-term exposure to PM 2.5 (OR: 1.12, 95% CI: 0.97–1.29, I2 : 51.6), PM 10 (OR: 1.04, 95% CI: 0.88–1.25, I2 : 85.7), and NO 2 (OR: 1.05, 95% CI: 0.83–1.34, I2 : 83.6), as well as short-term exposure to PM 2.5 (OR: 1.01, 95% CI: 0.99–1.04, I2 : 51.6), PM 10 (OR: 1.01, 95% CI: 0.98–1.04, I2 : 86.7), SO 2 (OR: 1.03, 95% CI: 0.99–1.07, I2 : 71.2), and O 3 (OR: 1.01, 95% CI: 0.99–1.03, I2 : 82.2) was not significantly associated with depression. However, we observed significant association between short-term NO 2 exposure (per 10 µg/m3 increase) and depression (OR: 1.02, 95% CI: 1.00–1.04, I2 : 65.4). However, the heterogeneity was high for all of the pooled estimates, which reduced credibility of the cumulative evidence. Additionally, publication bias was detected for six of eight meta-estimates. In conclusion, short-term exposure to NO 2 , but not other air pollutants, was significantly associated with depression. Given the limitations, a larger meta-analysis incorporating future well-designed longitudinal studies, and investigations into potential biologic mechanisms, will be necessary for a more definitive result. [ABSTRACT FROM AUTHOR]