Search

Abstract: A recurrent problem in applications that build on environmental sensor networks is that of sensor data organization and interpretation. Organization focuses on, for instance, resolving the syntactic and semantic heterogeneity of sensor data. The distinguishing factor between organization and interpretation is the abstraction from sensor data with information acquired from sensor data. Such information may be situational knowledge for environmental phenomena. We discuss a generic software framework for the organization and interpretation of sensor data and demonstrate its application to data of a large scale sensor network for the monitoring of atmospheric phenomena. The results show that software support for the organization and interpretation of sensor data is valuable to scientists in scientific computing workflows. Explicitly represented situational knowledge is also useful to client software systems as it can be queried, integrated, reasoned, visualized, or annotated. [Copyright &y& Elsevier]

The health risks of air pollutants and ambient particulate matter (PM) are widely known. PM composition and toxicity have shown substantial spatiotemporal variability. Yet, the connections between PM composition and toxicological and health effects are vaguely understood. This is a crucial gap in knowledge that needs to be addressed in order to establish air quality guidelines and limit values that consider the chemical composition of PM instead of the current assumption of equal toxicity per inhaled dose. Here, we demonstrate further evidence for varying toxicological effects of urban PM at equal mass concentrations, and estimate how PM composition and emission source characteristics influenced this variation. We exposed a co-culture model mimicking alveolar epithelial cells and macrophages with size-segregated urban ambient PM collected before, during, and after the Nanjing Youth Olympic Games 2014. We measured the release of a set of cytokines, cell cycle alterations, and genotoxicity, and assessed the spatiotemporal variations in these responses by factorial multiple regression analysis. Additionally, we investigated how a previously identified set of emission sources and chemical components affected these variations by mixed model analysis. PM-exposure induced cytokine signaling, most notably by inducing dose-dependent increases of macrophage-regulating GM-CSF and proinflammatory TNFα, IL-6, and IL-1β concentrations, modest dose-dependent increase for cytoprotective VEGF-A, but very low to no responses for anti-inflammatory IL-10 and immunoregulatory IFNγ, respectively. We observed substantial differences in proinflammatory cytokine production depending on PM sampling period, location, and time of day. The proinflammatory response correlated positively with cell cycle arrest in G1/G0 phase and loss of cellular metabolic activity. Furthermore, PM 0.2 caused dose-dependent increases in sub-G1/G0 cells, suggesting increased DNA degradation and apoptosis. Variations in traffic and oil/fuel combustion emissions contributed substantially to the observed spatiotemporal variations of toxicological responses. • Co-culture model of alveolar epithelial cells and macrophages was exposed to PM. • PM-induced cytokines, cell cycle alterations, and genotoxicity were measured. • We observed spatio-temporal variability in the toxicological responses. • Traffic, oil/fuel combustion showed greatest influence on toxicological variation. • Coal combustion and industrial emissions are also highly influential in PM toxicity. [ABSTRACT FROM AUTHOR]

Epidemiological evidence has shown the association between exposure to ambient fine particulate matter (PM) and increased susceptibility to bacterial and viral respiratory infections. However, to date, the underlying mechanisms of immunomodulatory effects of PM remain unclear. Our objective was to explore how exposure to relatively low doses of urban air PM alters innate responses to bacterial and viral stimuli in vitro. We used secondary alveolar epithelial cell line along with monocyte-derived macrophages to replicate innate lung barrier in vitro. Co-cultured cells were first exposed for 24 h to PM 2.5-1 (particle aerodynamic diameter between 1 and 2.5 μm) and subsequently for an additional 24 h to lipopolysaccharide (TLR4), polyinosinic-polycytidylic acid (TLR3), and synthetic single-stranded RNA oligoribonucleotides (TLR7/8) to mimic bacterial or viral stimulation. Toxicological endpoints included pro-inflammatory cytokines (IL-8, IL-6, and TNF-α), cellular metabolic activity, and cell cycle phase distribution. We show that cells exposed to PM 2.5-1 produced higher levels of pro-inflammatory cytokines following stimulation with bacterial TLR4 ligand than cells exposed to PM 2.5-1 or bacterial ligand alone. On the contrary, PM 2.5-1 exposure reduced pro-inflammatory responses to viral ligands TLR3 and TLR7/8. Cell cycle analysis indicated that viral ligands induced cell cycle arrest at the G2-M phase. In PM-primed co-cultures, however, they failed to induce the G2-M phase arrest. Contrarily, bacterial stimulation caused a slight increase in cells in the sub-G1 phase but in PM 2.5-1 primed co-cultures the effect of bacterial stimulation was masked by PM 2.5-1. These findings indicate that PM 2.5-1 may alter responses of immune defense differently against bacterial and viral infections. Further studies are required to explain the mechanism of immune modulation caused by PM in altering the susceptibility to respiratory infections. • Exposure to ambient PM increases susceptibility to respiratory infections. • Fine PM increased inflammatory response against bacterial stimulation in vitro. • Inflammatory response against viral stimulation was suppressed in PM treated cells. • Fine PM also altered the capacity of viral ligand to induce G2-M cell-cycle arrest. [ABSTRACT FROM AUTHOR]

• Long-term PM 1 and PM 2.5 exposure can lead to decreased lung function in children. • Association of PM 1 with children's lung function are larger than PM 2.5. • PM 1 and PM 2.5 are associated with children's large/small airways in early/late life. 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. [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]

Ambient particulate matter (PM) is a leading global environmental health risk. Current air quality regulations are based on airborne mass concentration. However, PM from different sources have distinct chemical compositions and varied toxicity. Connections between emission control measures, air quality, PM composition, and toxicity remain insufficiently elucidated. The current study assessed the composition and toxicity of PM collected in Nanjing, China before, during, and after an air quality intervention for the 2014 Youth Olympic Games. A co-culture model that mimics the alveolar epithelium with the associated macrophages was created using A549 and THP-1 cells. These cells were exposed to size-segregated inhalable PM samples. The composition and toxicity of the PM samples were influenced by several factors including seasonal variation, emission sources, and the air quality intervention. For example, we observed a size-dependent shift in particle mass concentrations during the air quality intervention with an emphasized proportion of smaller particles (PM 2.5) present in the air. The roles of industrial and fuel combustion and traffic emissions were magnified during the emission control period. Our analyses revealed that the PM samples demonstrated differential cytotoxic potencies at equal mass concentrations between sampling periods, locations, and time of day, influenced by variations in the predominant emission sources. Coal combustion and industrial emissions were the most important sources affecting the toxicological responses and displayed the least variation in emission contributions between the sampling periods. In conclusion, emission control mitigated cytotoxicity and oxidative stress for particles larger than 0.2 μm, but there was inadequate evidence to determine if it was the key factor reducing the harmful effects of PM 0.2. • Air quality intervention reduced PM 10 mass concentrations by over 50%. • In addition, it altered the PM composition and emission source contributions. • Changes in PM composition caused varied cytotoxicity at equal mass concentrations. • Coal and industrial combustion showed the greatest influence on cytotoxicity of PM. • Changes of PM 0.2 cytotoxicity not attributable only to intervention. [ABSTRACT FROM AUTHOR]

The emissions and exposure limits for airborne PM 0.1 are lacking, with limited scientific data for toxicity. Therefore, we continuously monitored and calculated the number and mass concentrations of airborne PM 0.1 in December 2017, January 2018 and March 2018 during the high pollution period in Guangzhou. We collected PM 0.1 from the same period and analyzed their chemical components. A549, THP-1 and A549/THP-1 co-cultured cells were selected for exposure to PM 0.1 , and evaluated for toxicological responses. Our aims are to 1) measure and analyze the number and mass concentrations, and chemical components of PM 0.1 ; 2) evaluate and compare PM 0.1 toxicity to different airway cells models at different time points. Guangzhou had the highest mass concentration of PM 0.1 in December 2017, while the number concentration was the lowest. Chemical components in PM 0.1 vary significantly at different time periods, and the correlation between the chemical composition or source of PM 0.1 and the mass and number concentration of PM 0.1 was dissimilar. Exposure to PM 0.1 disrupted cell membranes, impaired mitochondrial function, promoted the expression of inflammatory mediators, and interfered with DNA replication in the cell cycle. The damage caused by exposure to PM 0.1 at different times exhibited variations across different types of cells. PM 0.1 in March 2018 stimulated co-cultured cells to secrete more inflammatory mediators, and CMA was significantly related to the expression of them. Our study indicates that it is essential to monitor both the mass and number concentrations of PM 0.1 throughout all seasons annually, as conventional toxicological experiments and the internal components of PM 0.1 may not effectively reveal the health damages caused by elevated number levels of PM 0.1 ., 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. Published by Elsevier B.V.)

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.)

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.

Evidence of the effects of various particle sizes and constituents on blood biomarkers is limited. We performed a panel study with five repeated measurements in 88 healthy college students in Guangzhou, China between December 2017 and January 2018. Mass concentrations of particles with aerodynamic diameters ≤ 2.5 μm (PM 2.5 ), PM 1 , and PM 0.5 and number concentrations of particles with aerodynamic diameters ≤ 200 nm (PN 0.2 ) and PN 0.1 were measured. We used linear mixed-effect models to explore the associations of size-fractionated particulate matter and PM 2.5 constituents with five blood biomarkers 0-5 days prior to blood collection. We found that an interquartile range (45.9 μg/m 3 ) increase in PM 2.5 concentration was significantly associated with increments of 16.6, 3.4, 12.3, and 8.8% in C-reactive protein (CRP), monocyte chemoattractant protein-1 (MCP-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and endothelin-1(ET-1) at a 5-day lag, respectively. Similar estimates were observed for PM 1 , PM 0.5 , PN 0.2 , and PN 0.1 . For PM 2.5 constituents, consistent positive associations were observed between F - and sVCAM-1 and CRP and between NH 4 + and MCP-1, and negative associations were found between Na + and MCP-1 and ET-1, between Cl - and MCP-1, and between Mg 2+ and sVCAM-1. Our results suggested that both particle size and constituent exposure are significantly associated with circulating biomarkers among healthy Chinese adults. Particularly, PN 0.1 at a 5-day lag and F - and NH 4 + are the most associated with these blood biomarkers.

Existing evidence is scarce concerning the various effects of different PM sizes and chemical constituents on blood lipids. A panel study that involved 88 healthy college students with five repeated measurements (440 blood samples in total) was performed. We measured 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 ) as well as number concentrations of particulate matter with diameters ≤ 0.2 μm (PN 0.2 ) and ≤0.1 μm (PN 0.1 ). We applied linear mixed-effect models to assess the associations between short-term exposure to different PM size fractions and PM 2.5 constituents and seven lipid metrics. We found significant associations of greater concentrations of PM in different size fractions within 5 days before blood collection with lower high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A (ApoA1) levels, higher apolipoprotein B (ApoB) levels, and lower ApoA1/ApoB ratios. Among the PM 2.5 constituents, we observed that higher concentrations of tin and lead were significantly associated with decreased HDL-C levels, and higher concentrations of nickel were associated with higher HDL-C levels. Our results suggest that short-term exposure to PM in different sizes was deleteriously associated with blood lipids. Some constituents, especially metals, might be the major contributors to the detrimental effects.

Background: The adverse effects of air pollutants including particulate matter (PM) on the central nervous system is increasingly reported by epidemiological, animal and post-mortem studies in the last decade. Oxidative stress and inflammation are key consequences of exposure to PM although little is known of the exact mechanism. The association of PM exposure with deteriorating brain health is speculated to be driven by PM entry via the olfactory system. How air pollutants affect this key entry site remains elusive. In this study, we investigated effects of urban size-segregated PM on a novel cellular model: primary human olfactory mucosal (hOM) cells., Results: Metabolic activity was reduced following 24-h exposure to PM without evident signs of toxicity. Results from cytometric bead array suggested a mild inflammatory response to PM exposure. We observed increased oxidative stress and caspase-3/7 activity as well as perturbed mitochondrial membrane potential in PM-exposed cells. Mitochondrial dysfunction was further verified by a decrease in mitochondria-dependent respiration. Transient suppression of the mitochondria-targeted gene, neuronal pentraxin 1 (NPTX1), was carried out, after being identified to be up-regulated in PM 2.5-1 treated cells via RNA sequencing. Suppression of NPTX1 in cells exposed to PM did not restore mitochondrial defects resulting from PM exposure. In contrast, PM-induced adverse effects were magnified in the absence of NPTX1, indicating a critical role of this protein in protection against PM effects in hOM cells., Conclusion: Key mitochondrial functions were perturbed by urban PM exposure in a physiologically relevant cellular model via a mechanism involving NPTX1. In addition, inflammatory response and early signs of apoptosis accompanied mitochondrial dysfunction during exposure to PM. Findings from this study contribute to increased understanding of harmful PM effects on human health and may provide information to support mitigation strategies targeted at air pollution.

Evidence suggests that residential greenness may be protective of high blood pressure, but there is scarcity of evidence on the associations between greenness around schools and blood pressure among children. We aimed to investigate this association in China. Our study included 9354 children from 62 schools in the Seven Northeastern Cities Study. Greenness around each child's school was measured by NDVI (Normalized Difference Vegetation Index) and SAVI (Soil-Adjusted Vegetation Index). Particulate matter ≤ 1 μm (PM 1 ) concentrations were estimated by spatiotemporal models and nitrogen dioxide (NO 2 ) concentrations were collected from air monitoring stations. Associations between greenness and blood pressure were determined by generalized linear and logistic mixed-effect models. Mediation by air pollution was assessed using mediation analysis. Higher greenness was consistently associated with lower blood pressure. An increase of 0.1 in NDVI corresponded to a reduction in SBP of 1.39 mmHg (95% CI: 1.86, -0.93) and lower odds of hypertension (OR = 0.76, 95% CI: 0.69, 0.82). Stronger associations were observed in children with higher BMI. Ambient PM 1 and NO 2 mediated 33.0% and 10.9% of the association between greenness and SBP, respectively. In summary, greater greenness near schools had a beneficial effect on blood pressure, particularly in overweight or obese children in China. The associations might be partially mediated by air pollution. These results might have implications for policy makers to incorporate more green space for both aesthetic and health benefits., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Background: Little information exists on interaction effects between air pollution and influenza vaccination on allergic respiratory diseases. We conducted a large population-based study to evaluate the interaction effects between influenza vaccination and long-term exposure to ambient air pollution on allergic respiratory diseases in children and adolescents., Methods: A cross-sectional study was investigated during 2012-2013 in 94 schools from Seven Northeastern Cities (SNEC) in China. Questionnaires surveys were obtained from 56 137 children and adolescents aged 2-17 years. Influenza vaccination was defined as receipt of the influenza vaccine. We estimated air pollutants exposure [nitrogen dioxide (NO 2 ) and particulate matter with aerodynamic diameters ≤1 μm (PM 1 ), ≤2.5 μm (PM 2.5 ) and ≤10 μm (PM 10 )] using machine learning methods. We employed two-level generalized linear mix effects model to examine interactive effects between influenza vaccination and air pollution exposure on allergic respiratory diseases (asthma, asthma-related symptoms and allergic rhinitis), after controlling for important covariates., Results: We found statistically significant interactions between influenza vaccination and air pollutants on allergic respiratory diseases and related symptoms (doctor-diagnosed asthma, current wheeze, wheeze, persistent phlegm and allergic rhinitis). The adjusted ORs for doctor-diagnosed asthma, current wheeze and allergic rhinitis among the unvaccinated group per interquartile range (IQR) increase in PM 1 and PM 2.5 were significantly higher than the corresponding ORs among the vaccinated group [For PM 1 , doctor-diagnosed asthma: OR: 1.89 (95%CI: 1.57-2.27) vs 1.65 (95%CI: 1.36-2.00); current wheeze: OR: 1.50 (95%CI: 1.22-1.85) vs 1.10 (95%CI: 0.89-1.37); allergic rhinitis: OR: 1.38 (95%CI: 1.15-1.66) vs 1.21 (95%CI: 1.00-1.46). For PM 2.5 , doctor-diagnosed asthma: OR: 1.81 (95%CI: 1.52-2.14) vs 1.57 (95%CI: 1.32-1.88); current wheeze: OR: 1.46 (95%CI: 1.21-1.76) vs 1.11 (95%CI: 0.91-1.35); allergic rhinitis: OR: 1.35 (95%CI: 1.14-1.60) vs 1.19 (95%CI: 1.00-1.42)]. The similar patterns were observed for wheeze and persistent phlegm. The corresponding p values for interactions were less than 0.05, respectively. We assessed the risks of PM 1 -related and PM 2.5 -related current wheeze were decreased by 26.67% (95%CI: 1.04%-45.66%) and 23.97% (95%CI: 0.21%-42.08%) respectively, which was attributable to influenza vaccination (both p for efficiency <0.05)., Conclusions: Influenza vaccination may play an important role in mitigating the detrimental effects of long-term exposure to ambient air pollution on childhood allergic respiratory diseases. Policy targeted at increasing influenza vaccination may yield co-benefits in terms of reduced allergic respiratory diseases., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

Industrial processes, coal combustion, biomass burning (BB), and vehicular transport are important sources of atmospheric fine particles (PM 2.5 ) and contribute to ambient air concentrations of health-hazardous species, such as heavy metals, polycyclic aromatic hydrocarbons (PAH), and oxygenated-PAHs (OPAH). In China, emission controls have been implemented to improve air quality during large events, like the Youth Olympic Games (YOG) in August 2014 in Nanjing. In this work, six measurement campaigns between January 2014 and August 2015 were undertaken in Nanjing to determine the effects of emission controls and meteorological factors on PM 2.5 concentration and composition. PAHs, OPAHs, hopanes, n‑alkanes, heavy metals, and several other inorganic elements were measured. PM 2.5 and potassium concentrations were the highest in May-June 2014 indicating the prevalence of BB plumes in Nanjing. Emission controls substantially reduced concentrations of PM 2.5 (31%), total PAHs (59%), OPAHs (37%), and most heavy metals (44-89%) during the YOG compared to August 2015. In addition, regional atmospheric transport and meteorological parameters partly explained the observed differences between the campaigns. The most abundant PAHs and OPAHs were benzo[b,k]fluoranthenes, fluoranthene, pyrene, chrysene, 1,8‑naphthalic anhydride, and 9,10‑anthracenedione in all campaigns. Carbon preference index and the contribution of wax n‑alkanes indicated mainly biogenic sources of n‑alkanes in May-June 2014 and anthropogenic sources in the other campaigns. Hopane indexes pointed to vehicular transport as the major source of hopanes, but contribution of coal combustion was detected in winter 2015. The results provide evidence to the local government of the impacts of the air protection regulations. However, differences between individual components were observed, e.g., concentrations of potentially more harmful OPAHs decreased less than concentrations of PAHs. The results suggest that the proportions of hazardous components in the PM 2.5 may also change considerably due to emission control measures., (Copyright © 2018 Elsevier B.V. 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.)

Ambient inhalable particulate matter (PM) is a serious health concern worldwide, but especially so in China where high PM concentrations affect huge populations. Atmospheric processes and emission sources cause spatial and temporal variations in PM concentration and chemical composition, but their influence on the toxicological characteristics of PM are still inadequately understood. In this study, we report an extensive chemical and toxicological characterization of size-segregated urban air inhalable PM collected in August and October 2013 from Nanjing, and assess the effects of atmospheric processes and likely emission sources. A549 human alveolar epithelial cells were exposed to day- and nighttime PM samples (25, 75, 150, 200, 300 μg/ml) followed by analyses of cytotoxicity, genotoxicity, cell cycle, and inflammatory response. PM 10-2.5 and PM 0.2 caused the greatest toxicological responses for different endpoints, illustrating that particles with differing size and chemical composition activate distinct toxicological pathways in A549 cells. PM 10-2.5 displayed the greatest oxidative stress and genotoxic responses; both were higher for the August samples compared with October. In contrast, PM 0.2 and PM 2.5-1.0 samples displayed high cytotoxicity and substantially disrupted cell cycle; August samples were more cytotoxic whereas October samples displayed higher cell cycle disruption. Several components associated with combustion, traffic, and industrial emissions displayed strong correlations with these toxicological responses. The lower responses for PM 1.0-0.2 compared to PM 0.2 and PM 2.5-1.0 indicate diminished toxicological effects likely due to aerosol aging and lower proportion of fresh emission particles rich in highly reactive chemical components in the PM 1.0-0.2 fraction. Different emission sources and atmospheric processes caused variations in the chemical composition and toxicological responses between PM fractions, sampling campaigns, and day and night. The results indicate different toxicological pathways for coarse-mode particles compared to the smaller particle fractions with typically higher content of combustion-derived components. The variable responses inside PM fractions demonstrate that differences in chemical composition influence the induced toxicological responses., (Copyright © 2018 The Authors. Published by Elsevier B.V. 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.)