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Fine particulate matter (PM 2.5 ) can cause brain damage and diseases. Of note, ultrafine particles (UFPs) with an aerodynamic diameter less than or equal to 100 nm are a growing concern. Evidence has suggested toxic effects of PM 2.5 and UFPs on the brain and links to neurological diseases. However, the underlying mechanism has not yet been fully illustrated due to the variety of the study models, different endpoints, etc. The adverse outcome pathway (AOP) framework is a pathway-based approach that could systematize mechanistic knowledge to assist health risk assessment of pollutants. Here, we constructed AOPs by collecting molecular mechanisms in PM-induced neurotoxicity assessments. We chose particulate matter (PM) as a stressor in the Comparative Toxicogenomics Database (CTD) and identified the critical toxicity pathways based on Ingenuity Pathway Analysis (IPA). We found 65 studies investigating the potential mechanisms linking PM 2.5 and UFPs to neurotoxicity, which contained 2, 675 genes in all. IPA analysis showed that neuroinflammation signaling and glucocorticoid receptor signaling were the common toxicity pathways. The upstream regulator analysis (URA) of PM 2.5 and UFPs demonstrated that the neuroinflammation signaling was the most initially triggered upstream event. Therefore, neuroinflammation was recognized as the MIE. Strikingly, there is a clear sequence of activation of downstream signaling pathways with UFPs, but not with PM 2.5 . Moreover, we found that inflammation response and homeostasis imbalance were key cellular events in PM 2.5 and emphasized lipid metabolism and mitochondrial dysfunction, and blood-brain barrier (BBB) impairment in UFPs. Previous AOPs, which only focused on phenotypic changes in neurotoxicity upon PM exposure, we for the first time propose AOP framework in which PM 2.5 and UFPs may activate pathway cascade reactions, resulting in adverse outcomes associated with neurotoxicity. Our toxicity pathway-based approach not only advances risk assessment for PM-induced neurotoxicity but shines a spotlight on constructing AOP frameworks for new chemicals., 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 © 2024 Elsevier B.V. All rights reserved.)

Introduction: Air pollution is a significant contributor to morbidity and mortality globally and has been linked to an increased risk of dementia. Previous studies within the Betula cohort in Northern Sweden have demonstrated associations between air pollution and dementia, as well as distinctive metabolomic profiles in dementia patients compared to controls. This study aimed to investigate whether air pollution is associated with quantitative changes in metabolite levels within this cohort, and whether future dementia status would modify this association., Methods: Both short-term and long-term exposure to air pollution were evaluated using high spatial resolution models and measured data. Air pollution from vehicle exhaust and woodsmoke were analyzed separately. Metabolomic profiling was conducted on 321 participants, including 58 serum samples from dementia patients and a control group matched for age, sex, and education level, using nuclear magnetic resonance spectroscopy., Results: No statistically significant associations were found between any metabolites and any measures of short-term or long-term exposure to air pollution. However, there were trends potentially suggesting associations between both long-term and short-term exposure to air pollution with lactate and glucose metabolites. Notably, these associations were observed despite the lack of correlation between long-term and short-term air pollution exposure in this cohort. There were also tendencies for associations between air pollution from woodsmoke to be more pronounced in participants that would later develop dementia, suggesting a potential effect depending on urban/rural factors., Discussion: While no significant associations were found, the trends observed in the data suggest potential links between air pollution exposure and changes in lactate and glucose metabolites. These findings provide some new insights into the link between air pollution and metabolic markers in a low-exposure setting. However, addressing existing limitations is crucial to improve the robustness and applicability of future research in this area. The pronounced associations in participants who later developed dementia may indicate an influence of urban/rural factors, warranting further investigation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The author(s) declared that they were an editorial board member of Frontiers, at the time of submission. This had no impact on the peer review process and the final decision., (Copyright © 2024 Raza, Öhman, Kanninen, Jalava, Zeng, de Crom, Ikram and Oudin.)

Objectives: Evidence on the link between long-term ambient particulate matter (PM) exposures and childhood sleep disorders were scarce. We examined the associations between long-term exposures to PM 2.5 and PM 1 (PM with an aerodynamic equivalent diameter <2.5 μm and <1 μm, respectively) with sleep disorders in children., Methods: We performed a population-based cross-sectional survey in 177,263 children aged 6 to 18 years in 14 Chinese cities during 2012-2018. A satellite-based spatiotemporal model was employed to estimate four-year annual average PM 2.5 and PM 1 exposures at residential and school addresses. Parents or guardians completed a checklist using the Sleep Disturbance Scale for Children. We estimated the associations using generalized linear mixed models with adjustment for characteristics of children, parents, and indoor environments., Results: Long-term PM 2.5 and PM 1 exposures were positively associated with odds of sleep disorders for almost all domains. For example, increments in PM 2.5 and PM 1 per 10 μg/m 3 were associated with odds ratios of global sleep disorder of 1.24 (95 % confidence interval [CI]: 1.14, 1.35) and 1.31 (95 %CI: 1.18, 1.46), respectively. Similar results were observed for subtypes of sleep disorder. These associations were heterogeneous regionally, with stronger associations among children residing in southeast region than in northeast and northwest regions. Moreover, larger estimates of PM 1 were found than that of PM 2.5 in southeast region., Conclusion: Long-term PM 2.5 and PM 1 exposures are independently associated with higher risks of childhood sleep disorders, and these associations vary by geographical region., 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 © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Exposure to PM 2.5 has been linked to neurodegenerative diseases, with limited understanding of constituent-specific contributions., Objectives: To explore the associations between long-term exposure to PM 2.5 constituents and neurodegenerative diseases., Methods: We recruited 148,274 individuals aged ≥ 60 from four cities in the Pearl River Delta region, China (2020 to 2021). We calculated twenty-year average air pollutant concentrations (PM 2.5 mass, black carbon (BC), organic matter (OM), ammonium (NH 4 + ), nitrate (NO 3 - ) and sulfate (SO 4 2- )) at the individuals' home addresses. Neurodegenerative diseases were determined by self-reported doctor-diagnosed Alzheimer's disease (AD) and Parkinson's disease (PD). Generalized linear mixed models were employed to explore associations between pollutants and neurodegenerative disease prevalence., Results: PM 2.5 and all five constituents were significantly associated with a higher prevalence of AD and PD. The observed associations generally exhibited a non-linear pattern. For example, compared with the lowest quartile, higher quartiles of BC were associated with greater odds for AD prevalence (i.e., the adjusted odds ratios were 1.81; 95% CI, 1.45-2.27; 1.78; 95% CI, 1.37-2.32; and 1.99; 95% CI, 1.54-2.57 for the second, third, and fourth quartiles, respectively)., Conclusions: Long-term exposure to PM 2.5 and its constituents, particularly combustion-related BC, OM, and SO 4 2- , was significantly associated with higher prevalence of AD and PD in Chinese individuals., Environmental Implication: PM 2.5 is a routinely regulated mixture of multiple hazardous constituents that can lead to diverse adverse health outcomes. However, current evidence on the specific contributions of PM 2.5 constituents to health effects is scarce. This study firstly investigated the association between PM 2.5 constituents and neurodegenerative diseases in the moderately to highly polluted Pearl River Delta region in China, and identified hazardous constituents within PM 2.5 that have significant impacts. This study provides important implications for the development of targeted PM 2.5 prevention and control policies to reduce specific hazardous PM 2.5 constituents., 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 © 2024 Elsevier B.V. All rights reserved.)

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.)

Objective: To evaluate the association of long-term ambient fine particulate matters (PM(2.5)) exposure with elevated blood pressure in children. Methods: From April 2012 to June 2013, we used cluster randomized sampling method to investigate 9 354 children aged 5-17 years old from 68 primary and middle schools in the seven Northeastern Cities (Shenyang, Dalian, Fushun, Anshan, Benxi, Liaoyang and Dandong) in Liaoning Province, and measured their blood pressure (BP). A spatial statistical model nested by aerosol optical depth (AOD) was used to inverse PM(2.5) concentrations. Generalized additive model was used to quantify the association between PM(2.5) exposure and blood pressure in children. To examine the associations, two-level regression model was used to evaluate individual characteristics' modifying effect on the health influence of PM(2.5). Results: The prevalence of hypertension in children was 13.78% (1 289/9 354). The results showed that there was an associations between hypertension and pollutants, and the multivariable regression analysis indicated that the increase in mean systolic blood pressure (SBP), diastolic blood pressure (DBP), and the OR of hypertension associated with a 10 μg/m(3) increase for PM(2).5 were 3.12 (95 %CI : 2.71-3.54) mmHg (1 mmHg=0.133 kPa), 1.45 (95 %CI :1.12-1.78) mmHg, and 1.55 (95 %CI : 1.10-2.19), respectively. Compared with non-breastfeeding children ( OR= 2.10, 95 %CI : 1.39-3.17), children who were breastfeeding ( OR= 1.49, 95 %CI : 1.00-2.20) exhibited consistently weaker effects, and the interaction effect of P value was 0.002. Conclusion: Study findings indicate that long-term exposure to PM(2.5) is associated with increased arterial BP and hypertension among the children. Breastfeeding may reduce this association.

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.

Children can be considered as a high-risk population to environmental stress since some of the organ systems including the immune system and respiratory system are still in development during childhood. During childhood, the impact of environmental pollutants exposure may program child growth and development that have long-term consequences on later health and disease risk. Considering the rapid economic growth in recent decades in China, the impact of ambient air pollution on children health causes concerns. Therefore, we aimed to review the current epidemiological evidence on the effects of air pollution exposure on adverse health outcome, including respiratory diseases, lung function, high blood pressure, cognitive disorder, and obesity in childhood in China. We believe that the findings summarized in our review demonstrate an unequivocal relationship between air pollutants exposure and Chinese children health and these results have large public health influences.

Background: Little information exists regarding the effect of interaction of obesity and long-term air pollution exposure on children's blood pressure and hypertension in areas with high levels of air pollution. The aim of this study is to assess effect modification by obesity on the association between exposure and blood pressure in Chinese children., Methods: We studied 9,354 Chinese children, ages 5-17 years old, from 24 elementary schools and 24 middle schools in the Seven Northeastern Cities during 2012-2013. Four-year average concentrations of particles with an aerodynamic diameter ≤10 µm (PM10), sulfur dioxide, nitrogen dioxides, and ozone (O3) were measured at the monitoring stations in the 24 districts. We used generalized additive models and two-level logistic regression models to examine the health effects., Results: Consistent interactions were found between exposure and obesity on blood pressure and hypertension. The association between exposure and hypertension was consistently larger for overweight/obese children than for children with normal-weight, with odds ratios for hypertension ranging from 1.16 per 46.3μg/m for O3 (95% confidence interval [CI] = 1.12, 1.20) to 2.91 per 30.6μg/m for PM10 (95% CI = 2.32, 3.64), and estimated increases in mean systolic and diastolic blood pressure ranging from 0.57 mmHg (95% CI = 0.36, 0.78) and 0.63 mmHg (95% CI = 0.46, 0.81) per 46.3 μg/m for O3 to 4.04 mmHg (95% CI = 3.00, 5.09) and 2.02 mmHg (95% CI = 1.14, 2.89) per 23.4 μg/m for sulfur dioxide., Conclusions: Obesity amplifies the association of long-term air pollution exposure with blood pressure and hypertension in Chinese children.