Toxicological evaluation and concentration of airborne PM0.1 in high air pollution period in Guangzhou, China.

The emissions and exposure limits for airborne PM0.1 are lacking, with limited scientific data for toxicity. Therefore, we continuously monitored and calculated the number and mass concentrations of airborne PM0.1 in December 2017, January 2018 and March 2018 during the high pollution period in Guangzhou. We collected PM0.1 from the same period and analyzed their chemical components. A549, THP-1 and A549/THP-1 co-cultured cells were selected for exposure to PM0.1, and evaluated for toxicological responses. Our aims are to 1) measure and analyze the number and mass concentrations, and chemical components of PM0.1; 2) evaluate and compare PM0.1 toxicity to different airway cells models at different time points. Guangzhou had the highest mass concentration of PM0.1 in December 2017, while the number concentration was the lowest. Chemical components in PM0.1 vary significantly at different time periods, and the correlation between the chemical composition or source of PM0.1 and the mass and number concentration of PM0.1 was dissimilar. Exposure to PM0.1 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 PM0.1 at different times exhibited variations across different types of cells. PM0.1 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 PM0.1 throughout all seasons annually, as conventional toxicological experiments and the internal components of PM0.1 may not effectively reveal the health damages caused by elevated number levels of PM0.1.

Sources, chemical components, and toxicological responses of size segregated urban air PM samples in high air pollution season in Guangzhou, China.

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 (PM10-2.5, PM2.5-1, PM1-0.2, PM0.2) 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 PM10-2.5 and PM1-0.2 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 PM10-2.5 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 PM1-0.2 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.

Winter and spring variation in sources, chemical components and toxicological responses of urban air particulate matter samples in Guangzhou, China.

The sources and chemical components of urban air particles exhibit seasonal variations that may affect their hazardousness to human health. Our aims were to investigate winter and spring variation in particulate matter (PM) sources, components and toxicological responses of different PM size fractions from samples collected in Guangzhou, China. Four size-segregated PM samples (PM10-2.5, PM2.5-1, PM1-0.2, and PM0.2) were collected separately during winter (December 2017 and January 2018) and spring (March 2018). All PM samples were analyzed for chemical components and characterized by source. RAW 264.7 macrophages were exposed to four doses of PM samples for 24 h. Cytotoxicity, oxidation, cell cycle, genotoxicity and inflammatory parameters were tested. PM concentrations were higher in the winter samples and caused more severe cytotoxicity and oxidative damage than to PM in the spring samples. PM in winter and spring led to increases in cell cycle and genotoxicity. The trends of size-segregated PM components were consistent in winter and spring samples. Metallic elements and PAHs were found in the largest concentrations in winter PM, but ions were found in the largest concentrations in spring PM. metallic elements, PAHs and ions in size-segregated PM samples were associated with most toxicological endpoints. Soil dust and biomass burning were the main sources of PM in winter, whereas traffic exhaust and biomass burning was the main source with of spring PM. Our results suggest that the composition of PM samples from Guangzhou differed during winter and spring, which led to strong variations in toxicological responses. The results demonstrate the importance of examining a different particle sizes, compositions and sources across different seasons, for human risk assessment.

Fine and ultrafine airborne PM influence inflammation response of young adults and toxicological responses in vitro.

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 PM2.5, PM1, PM0.5 and number concentrations of ambient PM0.1 were measured. RAW 264.7 macrophages were exposed to PM (PM10-2.5, PM2.5-1, PM1-0.2, PM0.2) 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 PM2.5, PM1, PM0.5 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; PM10-2.5 induced the greatest TNF-α and macrophage inflammatory protein 2 (MIP-2) productions and oxidative damage. PM1-0.2 and PM0.2 induced more significant dose-dependent increases of cell cycle and genotoxic response. In the component concentrations of PM samples, metal elements were PM10-2.5 > PM2.5-1 > PM0.2 ≥ PM1-0.2; ions and polycyclic aromatic hydrocarbons (PAHs) were PM0.2 > PM1-0.2 > PM2.5-1 > PM10-2.5. 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.

Short-Term Effects of Particle Size and Constituents on Blood Pressure in Healthy Young Adults in Guangzhou, China.

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 (PM2.5), ≤1.0 µm (PM1.0), ≤0.5 µm (PM0.5), ≤0.2 µm (PM0.2), 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 PM2.5 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. PM0.2 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/m3) at lag 0 to 24 hours. For PM2.5 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.

Short-Term Effects of Particle Sizes and Constituents on Blood Biomarkers among Healthy Young Adults in Guangzhou, China.

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 (PM2.5), PM1, and PM0.5 and number concentrations of particles with aerodynamic diameters ≤ 200 nm (PN0.2) and PN0.1 were measured. We used linear mixed-effect models to explore the associations of size-fractionated particulate matter and PM2.5 constituents with five blood biomarkers 0-5 days prior to blood collection. We found that an interquartile range (45.9 µg/m3) increase in PM2.5 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 PM1, PM0.5, PN0.2, and PN0.1. For PM2.5 constituents, consistent positive associations were observed between F- and sVCAM-1 and CRP and between NH4+ and MCP-1, and negative associations were found between Na+ and MCP-1 and ET-1, between Cl- and MCP-1, and between Mg2+ and sVCAM-1. Our results suggested that both particle size and constituent exposure are significantly associated with circulating biomarkers among healthy Chinese adults. Particularly, PN0.1 at a 5-day lag and F- and NH4+ are the most associated with these blood biomarkers.

Associations of Particulate Matter Sizes and Chemical Constituents with Blood Lipids: A Panel Study in Guangzhou, China.

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 (PM2.5), ≤1.0 µm (PM1.0), and ≤0.5 µm (PM0.5) as well as number concentrations of particulate matter with diameters ≤ 0.2 µm (PN0.2) and ≤0.1 µm (PN0.1). We applied linear mixed-effect models to assess the associations between short-term exposure to different PM size fractions and PM2.5 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 PM2.5 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.

Influence of wood species on toxicity of log-wood stove combustion aerosols: a parallel animal and air-liquid interface cell exposure study on spruce and pine smoke.

BACKGROUND: Wood combustion emissions have been studied previously either by in vitro or in vivo models using collected particles, yet most studies have neglected gaseous compounds. Furthermore, a more accurate and holistic view of the toxicity of aerosols can be gained with parallel in vitro and in vivo studies using direct exposure methods. Moreover, modern exposure techniques such as air-liquid interface (ALI) exposures enable better assessment of the toxicity of the applied aerosols than, for example, the previous state-of-the-art submerged cell exposure techniques. METHODS: We used three different ALI exposure systems in parallel to study the toxicological effects of spruce and pine combustion emissions in human alveolar epithelial (A549) and murine macrophage (RAW264.7) cell lines. A whole-body mouse inhalation system was also used to expose C57BL/6 J mice to aerosol emissions. Moreover, gaseous and particulate fractions were studied separately in one of the cell exposure systems. After exposure, the cells and animals were measured for various parameters of cytotoxicity, inflammation, genotoxicity, transcriptome and proteome. RESULTS: We found that diluted (1:15) exposure pine combustion emissions (PM1 mass 7.7 ± 6.5 mg m- 3, 41 mg MJ- 1) contained, on average, more PM and polycyclic aromatic hydrocarbons (PAHs) than spruce (PM1 mass 4.3 ± 5.1 mg m- 3, 26 mg MJ- 1) emissions, which instead showed a higher concentration of inorganic metals in the emission aerosol. Both A549 cells and mice exposed to these emissions showed low levels of inflammation but significantly increased genotoxicity. Gaseous emission compounds produced similar genotoxicity and a higher inflammatory response than the corresponding complete combustion emission in A549 cells. Systems biology approaches supported the findings, but we detected differing responses between in vivo and in vitro experiments. CONCLUSIONS: Comprehensive in vitro and in vivo exposure studies with emission characterization and systems biology approaches revealed further information on the effects of combustion aerosol toxicity than could be achieved with either method alone. Interestingly, in vitro and in vivo exposures showed the opposite order of the highest DNA damage. In vitro measurements also indicated that the gaseous fraction of emission aerosols may be more important in causing adverse toxicological effects. Combustion aerosols of different wood species result in mild but aerosol specific in vitro and in vivo effects.

The role of influenza vaccination in mitigating the adverse impact of ambient air pollution on lung function in children: New insights from the Seven Northeastern Cities Study in China.

BACKGROUND: 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. METHODS: 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 (NO2) and particulate matter with an aerodynamic diameter <1 µm (PM1), <2.5 µm (PM2.5) and <10 µm (PM10). 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. RESULTS: 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 (pinteraction = 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 PM1 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 PM1 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 PM1 and impaired FVC: 2.33 (95%CI: 1.79, 3.03) vs 1.65 (95%CI: 1.20, 2.28); OR for PM2.5 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. CONCLUSION: 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.

Air quality intervention during the Nanjing youth olympic games altered PM sources, chemical composition, and toxicological responses.

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 (PM2.5) 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 PM0.2.

Ambient Airborne Particulates of Diameter ≤1 µm, a Leading Contributor to the Association Between Ambient Airborne Particulates of Diameter ≤2.5 µm and Children's Blood Pressure.

Evidence on the associations between airborne particulates of diameter ≤1 µm (PM1) and airborne particulates of diameter ≤2.5 µm (PM2.5) 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 PM1 and PM2.5 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/m3 greater PM1 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]). PM1 appears to play an important role in associations reported between PM2.5 exposure and BP, and we found that the ambient PM1/PM2.5 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 PM1 is associated with hypertension in children, and that PM1 might be a leading contributor to the hypertensive effect of PM2.5. Researchers and policy makers should pay closer attention to the potential health impacts of PM1.

Benefits of influenza vaccination on the associations between ambient air pollution and allergic respiratory diseases in children and adolescents: New insights from the Seven Northeastern Cities study in China.

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 (NO2) and particulate matter with aerodynamic diameters ≤1 µm (PM1), ≤2.5 µm (PM2.5) and ≤10 µm (PM10)] 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 PM1 and PM2.5 were significantly higher than the corresponding ORs among the vaccinated group [For PM1, 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 PM2.5, 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 PM1-related and PM2.5-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.

Greenness around schools associated with lower risk of hypertension among children: Findings from the Seven Northeastern Cities Study in China.

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 (PM1) concentrations were estimated by spatiotemporal models and nitrogen dioxide (NO2) 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 PM1 and NO2 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.

Association between community greenness and obesity in urban-dwelling Chinese adults.

Living in greener places may protect against obesity, but epidemiological evidence is inconsistent and mainly comes from developed nations. We aimed to investigate the association between greenness and obesity in Chinese adults and to assess air pollution and physical activity as mediators of the association. We recruited 24,845 adults from the 33 Communities Chinese Health Study in 2009. Central and peripheral obesity were defined by waist circumference (WC) and body mass index (BMI), respectively, based on international obesity standards. The Normalized Difference Vegetation Index (NDVI) was used to quantify community greenness. Two-level logistic and generalized linear mixed regression models were used to evaluate the association between NDVI and obesity, and a conditional mediation analysis was used also performed. In the adjusted models, an interquartile range increase in NDVI500-m was significantly associated with lower odds of peripheral 0.80 (95% confidence interval [CI]: 0.74-0.87) and central obesity 0.88 (95% CI: 0.83-0.93). Higher NDVI values were also significantly associated with lower BMI. Age, gender, and household income significantly modified associations between greenness and obesity, with stronger associations among women, older participants, and participants with lower household incomes. Air pollution mediated 2.1-20.8% of the greenness-obesity associations, but no mediating effects were observed for physical activity. In summary, higher community greenness level was associated with lower odds of central and peripheral obesity, especially among women, older participants, and those with lower household incomes. These associations were partially mediated by air pollutants. Future well-designed longitudinal studies are needed to confirm our findings.

Association of Breastfeeding and Air Pollution Exposure With Lung Function in Chinese Children.

Importance: Breastfeeding and exposure to ambient air pollutants have been found to be independently associated with respiratory health in children; however, previous studies have not examined the association of breastfeeding as a potential moderator of the association. Objective: To assess associations of breastfeeding and air pollution with lung function in children. Design, Setting, and Participants: Using a cross-sectional study design, children were recruited from 62 elementary and middle schools located in 7 Chinese cities from April 1, 2012, to October 31, 2013. Data analyses were conducted from November 1, 2018, to March 31, 2019. Exposures: Long-term concentrations of airborne particulate matter with a diameter of 1 µm or less (PM1), airborne particulate matter with a diameter of 2.5 µm or less (PM2.5), airborne particulate matter with a diameter of 10 µm or less (PM10), and nitrogen dioxide were estimated using a spatial statistical model matched to children's geocoded home addresses, and concentrations of PM10, sulfur dioxide, nitrogen dioxide, and ozone were measured by local air monitoring stations. Main Outcomes and Measures: Breastfeeding was defined as maternal report of having mainly breastfed for longer than 3 months. Lung function was measured using portable electronic spirometers. Using previously published predicted spirometric values for children in Northeast China as the reference, lung impairment was defined as forced vital capacity (FVC) less than 85%, forced expiratory volume in the first second of expiration less than 85%, peak expiratory flow less than 75%, or maximum midexpiratory flow less than 75%. Results: Participants included 6740 children (mean [SD] age, 11.6 [2.1] years; 3382 boys [50.2%]). There were 4751 children (70.5%) who were breastfed. Mean (SD) particulate matter concentrations ranged from 46.8 (6.5) µg/m3 for PM1 to 95.6 (9.8) µg/m3 for PM10. The prevalence of lung function impairment ranged from 6.8% for peak expiratory flow to 11.3% for FVC. After controlling for age, sex, and other covariates, 1-interquartile range greater concentration of pollutants was associated with higher adjusted odds ratios (AORs) for lung function impairment by FVC among children who were not breastfed compared with those who were (PM1: AOR, 2.71 [95% CI, 2.02-3.63] vs 1.20 [95% CI, 0.97-1.48]; PM2.5: AOR, 2.27 [95% CI, 1.79-2.88] vs 1.26 [95% CI, 1.04-1.51]; and PM10: AOR, 1.93 [95% CI, 1.58-2.37] vs 1.46 [95% CI, 1.23-1.73]). Younger age (<12 years) was associated with lower lung function impairment among the children who had been breastfed. In children from elementary schools, 1-interquartile range greater concentration of pollutants was associated with higher AORs for lung function impairment by FVC among children who had not been breastfed compared with those who had (PM1: AOR, 6.43 [95% CI, 3.97-10.44] vs 1.89 [95% CI, 1.28-2.80]; PM2.5: AOR, 3.83 [95% CI, 2.63-5.58] vs 1.50 [95% CI, 1.12-2.01]; and PM10: AOR, 2.61 [95% CI, 1.90-3.57] vs 1.52 [95% CI, 1.19-1.95]). Results from linear regression models also showed associations of air pollution with worse lung function among children who were not breastfed compared with their counterparts who were breastfed, especially for FVC (PM1: ß, -240.46 [95% CI, -288.71 to -192.21] vs -38.21 [95% CI, -69.27 to -7.16] mL) and forced expiratory volume in the first second of expiration (PM1: ß, -201.37 [95% CI, -242.08 to -160.65] vs -30.30 [95% CI, -57.66 to -2.94] mL). Conclusions and Relevance: In this study, breastfeeding was associated with lower risk of lung function impairment among children in China exposed to air pollution, particularly among younger children.

Association of Long-term Exposure to Ambient Air Pollutants With Risk Factors for Cardiovascular Disease in China.

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.

PM2.5 concentration and composition in the urban air of Nanjing, China: Effects of emission control measures applied during the 2014 Youth Olympic Games.

Industrial processes, coal combustion, biomass burning (BB), and vehicular transport are important sources of atmospheric fine particles (PM2.5) 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 PM2.5 concentration and composition. PAHs, OPAHs, hopanes, n­alkanes, heavy metals, and several other inorganic elements were measured. PM2.5 and potassium concentrations were the highest in May-June 2014 indicating the prevalence of BB plumes in Nanjing. Emission controls substantially reduced concentrations of PM2.5 (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, 1,8­naphthalic anhydride, and 9,10­anthracenedione in all campaigns. Carbon preference index and the contribution of wax n­alkanes indicated mainly biogenic sources of n­alkanes 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 PM2.5 may also change considerably due to emission control measures.

Is smaller worse? New insights about associations of PM1 and respiratory health in children and adolescents.

BACKGROUND AND OBJECTIVES: Little is known about PM1 effects on respiratory health, relative to larger size fractions (PM2.5). To address this literature gap, we assessed associations between PM1 exposure and asthmatic symptoms in Chinese children and adolescents, compared with PM2.5. 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. PM1 and PM2.5 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/m3 increase for PM1 and PM2.5 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/m3 increase in PM1 was 1.71 (95% CI: 1.60-1.83), which was stronger than in their counterparts (1.46; 1.37-1.56) (pfor interaction < 0.05). CONCLUSIONS: This study indicated that long-term exposure to PM1 may increase the risk of asthma and asthma-related symptoms, especially among boys and those with allergic predisposition. Furthermore, these positive associations for PM1 were very similar to those for PM2.5.

Emissions and atmospheric processes influence the chemical composition and toxicological properties of urban air particulate matter in Nanjing, China.

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. PM10-2.5 and PM0.2 caused the greatest toxicological responses for different endpoints, illustrating that particles with differing size and chemical composition activate distinct toxicological pathways in A549 cells. PM10-2.5 displayed the greatest oxidative stress and genotoxic responses; both were higher for the August samples compared with October. In contrast, PM0.2 and PM2.5-1.0 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 PM1.0-0.2 compared to PM0.2 and PM2.5-1.0 indicate diminished toxicological effects likely due to aerosol aging and lower proportion of fresh emission particles rich in highly reactive chemical components in the PM1.0-0.2 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.

Ambient air pollution in relation to diabetes and glucose-homoeostasis markers in China: a cross-sectional study with findings from the 33 Communities Chinese Health Study.

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 ß-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 [PM10], sulphur dioxide, nitrogen dioxide, and ozone) and a spatial statistical model (PM with an aerodynamic diameter of 1 µm or less [PM1] and 2·5 µm or less [PM2·5]). 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 PM1, PM2·5, and PM10 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.