Abstract  The volatile organic compound isoprene is produced by many plant species, and provides protection against biotic and abiotic stresses1. Globally, isoprene emissions from plants are estimated to far exceed anthropogenic emissions of volatile organic compounds2. Once in the atmosphere, isoprene reacts rapidly with hydroxyl radicals3 to form peroxy radicals, which can react with nitrogen oxides to form ground-level ozone4. Here, we use canopy-scale measurements of isoprene fluxes from two tropical ecosystems in Malaysia—a rainforest and an oil palm plantation—and three models of atmospheric chemistry to explore the effects of isoprene fluxes on ground-level ozone. We show that isoprene emissions in these ecosystems are under circadian control on the canopy scale, particularly in the oil palm plantation. As a result, these ecosystems emit less isoprene than present emissions models predict. Using local-, regional- and global-scale models of atmospheric chemistry and transport, we show that accounting for circadian control of isoprene emissions brings model predictions of ground-level ozone into better agreement with measurements, especially in isoprene-sensitive regions of the world.

Abstract  RATIONALE: Several studies have linked long-term exposure to particulate air pollution with increased cardiopulmonary mortality; only two have also examined incident circulatory disease. OBJECTIVES: To examine associations of individualized long-term exposures to particulate and gaseous air pollution with incident myocardial infarction (MI) and stroke, as well as all-cause and cause-specific mortality. METHODS: We estimated long-term residential air pollution exposure for over 100,000 participants in the California Teachers Study, a prospective cohort of female public school professionals. We linked geocoded residential addresses with inverse distance-weighted monthly pollutant surfaces for two measures of particulate matter and for several gaseous pollutants. We examined associations between exposure to these pollutants and risks of incident MI and stroke, and of all-cause and cause-specific mortality, using Cox proportional hazards models. MEASUREMENTS AND MAIN RESULTS: We found elevated hazard ratios linking long-term exposure to fine particulate matter (PM2.5, scaled to an increment of 10 µg/m3) with mortality from ischemic heart disease (IHD) (1.20, 95% C.I. 1.02-1.41) and, particularly among post-menopausal women, incident stroke (1.19, 95% C.I. 1.02-1.38). Long-term exposure to particulate matter less than 10 µm aerodynamic diameter (PM10) was associated with elevated risks for IHD mortality (1.06, 95% C.I. 0.99-1.14) and incident stroke 1.06 (95% CI: 1.00-1.13), while nitrogen oxides were associated with elevated risks for cardiovascular as well as IHD mortality. CONCLUSIONS: Long-term exposures to PM2.5 and PM10 were associated with increased risks of incident stroke and death from IHD; exposures to nitrogen oxides were associated with all cardiovascular as well as IHD mortality.

Abstract  BACKGROUND: The fractional concentration of nitric oxide in exhaled air (FeNO) potentially detects airway inflammation related to air pollution exposure. Existing studies have not yet provided conclusive evidence on FeNO's association with traffic-related pollution (TRP). OBJECTIVES: To evaluate the association of FeNO with residential TRP exposure in a large cohort of children. METHODS: We related FeNO measured on 2,143 children (ages 7-11) who participated in the Southern California Children's Health Study (CHS) to five classes of metrics of residential TRP: distances to freeways and major roads; length of all and local roads within circular buffers around the home; traffic densities within buffers; annual average line source dispersion modeled NOx from freeways and non-freeway roads; and predicted annual average NO, NO2, and NOx from a model based on intra-community sampling in the CHS. RESULTS: In children with asthma, length of roads was positively associated with FeNO, with stronger associations in smaller buffers (46.7% (95% confidence interval (CI): 14.3, 88.4), 12.4% (95% CI: -8.8, 38.4), and 4.1% (95% CI: -14.6, 26.8) higher FeNO for 100-, 300-, and 1000-m increases in the length of all roads in 50-, 100-, and 200-m buffers, respectively). Other TRP metrics were not significantly associated with FeNO, even though the study design was powered to detect exposures explaining as little as 0.4% of the variation in natural log transformed FeNO (R2 = 0.004). CONCLUSION: Length of road was the only indicator of residential TRP exposure associated with airway inflammation in children with asthma, as measured by FeNO.

Abstract  Background: Air pollution exposure during pregnancy might have trimester specific effects on fetal growth. Objective: We prospectively evaluated the associations of maternal air pollution exposure with fetal growth characteristics and adverse birth outcomes in 7772 subjects in the Netherlands. Methods: PM10 and NO2 levels were estimated using dispersion modelling at the home address. Fetal head circumference, length and weight were estimated in each trimester by ultrasound. Information on birth outcomes was obtained from medical records. Results: In cross-sectional analyses, NO2 levels were inversely associated with fetal femur length in second and third trimester, and PM10 and NO2 levels both were associated with smaller fetal head circumference in third trimester (-0.18 mm, 95% confidence interval (CI) -0.24, -0.12 and -0.12 mm, 95% CI -0.17, -0.06 per 1-μg/m3 increase in PM10 and NO2, respectively). Average PM10 and NO2 levels during pregnancy were not associated with head circumference and length at birth or neonatally, but were inversely associated with birth weight (-3.6g, 95% CI -6.7, -0.4 and -3.4g, 95% CI -6.2, -0.6, respectively). Longitudinal analyses showed similar patterns for head circumference and weight, but no associations with length. The third and fourth quartiles of PM10 exposure were associated with preterm birth (odds ratio (OR) 1.40, 95% CI 1.03, 1.89, and OR 1.32, 95% CI 0.96, 1.79, relative to the first quartile). The third quartile of PM10 exposure, but not the fourth, was associated with small size for gestational age at birth (OR 1.38, 95% CI 1.00, 1.90). No consistent associations were observed for NO2 levels and adverse birth outcomes. Conclusions: Results suggest that maternal air pollution exposure is inversely associated with fetal growth during the second and third trimester and with weight at birth. PM10 exposure was positively associated with preterm birth and small size for gestational age at birth.

Abstract  Both classical and Berkson exposure measurement errors as encountered in environmental epidemiology data can result in biases in fitted exposure-response relationships that are large enough to affect the interpretation and use of the apparent exposure-response shapes in risk assessment applications. A variety of sources of potential measurement error exist in the process of estimating individual exposures to environmental contaminants, and the authors review the evaluation in the literature of the magnitudes and patterns of exposure measurement errors that prevail in actual practice. It is well known among statisticians that random errors in the values of independent variables (such as exposure in exposure-response curves) may tend to bias regression results. For increasing curves, this effect tends to flatten and apparently linearize what is in truth a steeper and perhaps more curvilinear or even threshold-bearing relationship. The degree of bias is tied to the magnitude of the measurement error in the independent variables. It has been shown that the degree of bias known to apply to actual studies is sufficient to produce a false linear result, and that although nonparametric smoothing and other error-mitigating techniques may assist in identifying a threshold, they do not guarantee detection of a threshold. The consequences of this could be great, as it could lead to a misallocation of resources towards regulations that do not offer any benefit to public health.

Abstract  Rate constants for the reactions of 2-methoxy-6-(trifluoromethyl)pyridine, diethylamine, and 1,1,3,3,3-pentamethyldisiloxan-1-ol with OH radicals have been measured at 298 +/- 2 K using a relative rate method. The measured rate constants (cm(3) molecule(-1) s(-1)) are (1.54 +/- 0.21) x 10(-12) for 2-methoxy-6-(trifluoromethyl)pyridine, (1.19 +/- 0.25) x 10(-10) for diethylamine, and (1.76 +/- 0.38) x 10(-12) for 1,1,3,3,3-pentamethyldisiloxan-1-ol, where the indicated errors are the estimated overall uncertainties including those in the rate constants for the reference compounds. No reaction of 2-methoxy-6-(trifluoromethyl)pyridine with gaseous nitric acid was observed, and an upper limit to the rate constant for the reaction of 1,1,3,3,3-pentamethyldisiloxan-1-ol with O(3) of <7 x 10(-20) cm(3) molecule(-1) s(-1) was determined. Using a 12-h average daytime OH radical concentration of 2 x 10(6) molecule cm(-3), the lifetimes of the volatile organic compounds studied here with respect to reaction with OH radicals are 7.5 days for 2-methoxy-6-(trifluoromethyl) pyridine, 1.2 h for diethylamine, and 6.6 days for 1,1,3,3,3-pentamethyldisiloxan-1-ol. Likely reaction mechanisms are discussed. (C) 2011 Wiley Periodicals, Inc. Int J Chem Kinet 43: 631-638, 2011

Abstract  Susceptibility to the respiratory effects of air pollution varies between individuals. Although some evidence suggests higher susceptibility for subjects carrying variants of antioxidant genes, findings from gene-pollution interaction studies conflict in terms of the presence and direction of interactions. The authors conducted a systematic review on antioxidant gene-pollution interactions which included 15 studies, with 12 supporting the presence of interactions. For the glutathione S-transferase M1 gene (GSTM1) (n = 10 studies), only 1 study found interaction with the null genotype alone, although 5 observed interactions when GSTM1 was evaluated jointly with other genes (mainly NAD(P)H dehydrogenase [quinone] 1 (NQO1)). All studies on the glutathione S-transferase P1 (GSTP1) Ile105Val polymorphism (n = 11) provided some evidence of interaction, but findings conflicted in terms of risk allele. Results were negative for glutathione S-transferase T1 (GSTT1) (n = 3) and positive for heme oxygenase 1 (HMOX-1) (n = 2). Meta-analysis could not be performed because there were insufficient data available for any specific gene-pollutant-outcome combination. Overall the evidence supports the presence of gene-pollution interactions, although which pollutant interacts with which gene is unclear. However, issues regarding multiple testing, selective reporting, and publication bias raise the possibility of false-positive findings. Larger studies with greater accuracy of pollution assessment and improved quality of conduct and reporting are required.

Abstract  In this study we aimed to evaluate the relationship between individual total exposure to air pollution (AP) and airways changes in a group of 51 wheezing children. Respiratory status was assessed four times (January 2006, June 2006, January 2007, June 2007) during one week, through a standardized questionnaire, spirometry, FeNO and pH in EBC. Concentrations of PM10, O3, NO2 and volatile organic compounds were estimated through direct measurements with an ad hoc device or AP modelling in the children's schools and at their homes in the same 4 weeks of the study. For each child, total exposure to the different air pollutants was estimated as a function of pollutants concentrations and daily activity patterns. Increasing total exposure to PM10, NO2, benzene, toluene and ethylbenzene was associated significantly with a decrease of FEV1 and with an increase of ΔFEV1. Increasing exposure to NO2 and benzene was also related to a significant decrease of FEV1/FVC. Increasing exposure to PM10, NO2, benzene and ethylbenzene was associated with acidity of EBC. This study suggests an association in wheezing children between airways changes and total exposure to air pollutants as estimated by taking into account the concentrations in the various microenvironments attended by the children.

Abstract  OBJECTIVES: The internal thoracic artery (ITA) is the preferred conduit for coronary artery bypass graft (CABG) surgery. The authors investigated whether thoracic epidural anesthesia (TEA) as an adjunct to general anesthesia (GA) can increase the blood flow of the ITA.

DESIGN: A prospective randomized study.

SETTING: A university hospital.

PARTICIPANTS: Patients with ischemic heart disease.

INTERVENTIONS: Thirty patients scheduled for elective CABG surgery were randomized to receive either GA (n = 15) or GA + TEA (n = 15) after receiving institutional review board approval. Demographics showed similarity between the groups. The epidural catheter was inserted in the thoracic region between T1 and T5 levels. In the GA + TEA group, the patients received a 20-mg bolus of 0.25% bupivacaine through epidural catheters 1 hour before surgery, and this was followed by the infusion (20 mg/h) of 0.25% bupivacaine. In all patients, ITA free blood flow was measured before cardiopulmonary bypass and without the administration of any vasodilatory agent. A short segment of ITA was excised for histologic examination; immunocytochemistry analysis was performed using antirabbit polyclonal VEGF antibody, rabbit polyclonal inducible nitric oxide synthase (i-NOS) antibody, and adenosine anti-A2B receptor antibody. The immunoreactivity rates then were evaluated.

MAIN RESULTS: The mean ITA free flow in the GA + TEA group was significantly higher than in the GA group (56.0 ± 9.0 mL/min v 39.6 ± 14 mL/min, p = 0.001). Immunostaining intensity in the sections after incubation with each primary antibody increased in the GA + TEA group compared with the GA group.

CONCLUSIONS: The results of this study indicated that TEA increased ITA free blood flow significantly via increased VEGF, i-NOS, and adenosine-A2B receptor expressions. Therefore, the use of TEA as an adjunct to GA might be considered as an alternative to vasoactive agents for increasing ITA flow in CABG surgery.

Abstract  We examined the preventive effect of human recombinant erythropoietin (HrEPO) on nitric oxide (NO)-mediated toxicity to neurons and cysteine protease release into cytoplasm, which is attributed to neuronal death in brain ischemia. Focal cerebral ischemia was induced by permanent occlusion of middle cerebral artery in two sets of rat. The first set was used to monitor NO concentration and cathepsin activity, while the second was used for histological examination with hematoxylin and eosin, and TUNEL staining. A group in both set was administered human recombinant erythropoietin (HrEPO). NO content, cathepsins B and L activity increased significantly in the post-ischemic cerebral tissue (p<0.05). HrEPO treatment reduced NO concentration and cathepsin activity to control level (p>0.05). A significant increase in the number of necrotic and apoptotic neurons was observed in the post-ischemic cerebral cortex (p<0.05). HrEPO treatment was markedly lowered both of these (p<0.05). It is concluded that HrEPO prevents neuronal death by protecting neuronal liposomes from NO-mediated toxicity and suppressing the release of cathepsins.

Abstract  The solution method was used to create polysulfone/carbon nanotubes composites. The effect of three solvents (NMP, DMF, and THF), treatments (nitric acid and ethanol) and surfactants (ODA and OCA) on CNT/solvent stability was investigated. NMP and DMF resulted in improved stability compared to THF, and all CNT treatments improved stability. Four composites were produced with CNT loadings of 0-5 wt%: as-received CNT and nitric acid treated in THF, as-received CNT and OCA surfactant CNT in NMP. Optical, TEM, and electrical percolation measurements confirmed the role of CNT/solvent stability on the final composite dispersion. Tensile testing and thermal analysis confirmed the presence of residual solvent in all samples.

Abstract  A 30 kW bench-scale rig of pulverized anthracite combustion preheated by a circulating fluidized bed (CFB) was developed. The CFB riser has a diameter of 90 mm and a height of 1,500 mm. The down-fired combustion chamber (DFCC) has a diameter of 260 mm and a height of 3,000 mm. Combustion experiments were carried out using pulverized anthracite with 6.74% volatile content. This low volatile coal is difficult to ignite and burn out. Therefore, it requires longer burnout time and higher combustion temperature, which results in larger NO(x) emissions. In the current study, important factors that influence the combustion characteristics and NO(x) emissions were investigated such as excess air ratio, air ratio in the reducing zone, and fuel residence time in the reducing zone. Pulverized anthracite can be quickly preheated up to 800 degrees C in CFB when the primary air is 24% of theoretical air for combustion, and the temperature profile is uniform in DFCC. The combustion efficiency is 94.2%, which is competitive with other anthracite combustion technologies. When the excess air ratio ranges from 1.26 to 1.67, the coal-N conversion ratio is less than 32% and the NO(x) emission concentration is less than 371 mg/m(3) (@6% O(2)). When the air ratio in the reducing zone is 0.12, the NO(x) concentration is 221 mg/m(3) (@6% O(2)), and the coal-N conversion ratio is 21%, which is much lower than that of other boilers.

Abstract  The article focus on the isomerization of nitrous acid HONO to hydrogen nitryl HNO(2). Density functional (B3LYP) and MP2 methods, and a wide variety of basis sets, have been chosen to investigate the mechanism of this reaction. The results clearly show that there are two possible paths: 1) Uncatalysed isomerisation, trans-HONO --> HNO(2), involving 1,2-hydrogen shift and characterized by a large energetic barrier 49.7 divided by 58.9 kcal/mol, 2) Catalysed double hydrogen transfer process, trans-HONO + cis-HONO --> HNO(2) + cis-HONO, which displays a significantly lower energetic barrier in a range of 11.6 divided by 18.9 kcal/mol. Topological analysis of the Electron Localization Function (ELF) shows that the hydrogen transfer for both studied reactions takes place through the formation of a 'dressed' proton along the reaction path. Use of a wide variety of basis sets demonstrates a clear basis set dependence on the ELF topology of HNO(2). Less saturated basis sets yield two lone pair basins, V(1)(N), V(2)(N), whereas more saturated ones (for example aug-cc-pVTZ and aug-cc-pVQZ) do not indicate a lone pair on the nitrogen atom. Topological analysis of the Electron Localizability Indication (ELI-D) at the CASSCF (12,10) confirms these findings, showing the existence of the lone pair basins but with decreasing populations as the basis set becomes more saturated (0.35e for the cc-pVDZ basis set to 0.06e for the aug-cc-pVTZ). This confirms that the choice of basis set not only can influence the value of the electron population at the particular atom, but can also lead to different ELF topology.

Abstract  Multiple demands are placed on farming systems today. Society, national legislation and market forces seek what could be seen as conflicting outcomes from our agricultural systems, e.g. food quality, affordable prices, a healthy environmental, consideration of animal welfare, biodiversity etc., Many of these demands, or desirable outcomes, are interrelated, so reaching one goal may often compromise another and, importantly, pose a risk to the economic viability of the farm. SIMS(DAIRY), a farm-scale model, was used to explore this complexity for dairy farm systems. SIMS(DAIRY) integrates existing approaches to simulate the effect of interactions between farm management, climate and soil characteristics on losses of nitrogen, phosphorus and carbon. The effects on farm profitability and attributes of biodiversity, milk quality, soil quality and animal welfare are also included. SIMS(DAIRY) can also be used to optimise fertiliser N. In this paper we discuss some limitations and strengths of using SIMS(DAIRY) compared to other modelling approaches and propose some potential improvements. Using the model we evaluated the sustainability of organic dairy systems compared with conventional dairy farms under non-optimised and optimised fertiliser N use. Model outputs showed for example, that organic dairy systems based on grass-clover swards and maize silage resulted in much smaller total GHG emissions per l of milk and slightly smaller losses of NO(3) leaching and NO(x) emissions per l of milk compared with the grassland/maize-based conventional systems. These differences were essentially because the conventional systems rely on indirect energy use for 'fixing' N compared with biological N fixation for the organic systems. SIMS(DAIRY) runs also showed some other potential benefits from the organic systems compared with conventional systems in terms of financial performance and soil quality and biodiversity scores. Optimisation of fertiliser N timings and rates showed a considerable scope to reduce the (GHG emissions per l milk too).

Abstract  The incidence of allergic respiratory diseases and bronchial asthma appears to be increasing worldwide, and people living in urban areas more frequently experience these conditions than those living in rural areas. One of the several causes of the rise in morbidity associated with allergic respiratory diseases is the increased presence of outdoor air pollutants resulting from more intense energy consumption and exhaust emissions from cars and other vehicles. Urban air pollution is now a serious public health hazard. Laboratory studies confirm epidemiologic evidence that air pollution adversely affects lung function in asthmatics. Damage to airway mucous membranes and impaired mucociliary clearance caused by air pollution may facilitate access of inhaled allergens to the cells of the immune system, thus promoting sensitization of the airway. Consequently, a more severe immunoglobulin (Ig) E-mediated response to aeroallergens and airway inflammation could account for increasing prevalence of allergic respiratory diseases in polluted urban areas. The most abundant components of urban air pollution in urban areas with high levels of vehicle traffic are airborne particulate matter, nitrogen dioxide, and ozone. In addition, the earth's temperature is increasing, mainly as a result of anthropogenic factors (e.g., fossil fuel combustion and greenhouse gas emissions from energy supply, transport, industry, and agriculture), and climate change alters the concentration and distribution of air pollutants and interferes with the seasonal presence of allergenic pollens in the atmosphere by prolonging these periods.

Abstract  The organ toxicity of lanthanides (Ln) on organisms had been recognized, but very little is known about the oxidative injury of brain caused by Ln. In order to study the mechanisms underlying the effects of Ln on the brain, ICR mice were injected with a single 20 mg/kg body weight dose of LaCl(3), CeCl(3), and NdCl(3) into the abdominal cavity daily for 14 days. We then examined the coefficient of the brain, the brain pathological changes and oxidative stress-mediated responses, and the accumulation of Ln and levels of neurochemicals in the brain. The results showed that CeCl(3) and NdCl(3) could induce some neurons to turn inflammatory cells and slight edema but did not observe the brain pathological changes from LaCl(3)-treated group. The concentrations of La, Ce, and Nd in the brain were significantly different and ranked in the order of Ce, Nd, and La. The injury of the brain and oxidative stress occurred as Ln appeared to trigger a cascade of reactions such as lipid peroxidation, the decreases of the total antioxidation capacity and activities of antioxidative enzymes, the excessive release of nitric oxide, the increase of glutamic acid, and the downregulated level of acetylcholinesterase activities. Furthermore, both Ce(3+) and Nd(3+) exhibited higher oxidative stress and toxicity on brain than La(3+), and Ce(3+) caused more severe brain injuries and oxidative stress than Nd(3+), implying that the differences in the brain injuries caused by Ln might be related to the number of 4f electrons of Ln.

Abstract  Policies to control emissions of criteria pollutants in China may have conflicting impacts on public health, soil acidification, and climate. Two scenarios for 2020, a base case without anticipated control measures and a more realistic case including such controls, are evaluated to quantify the effects of the policies on emissions and resulting environmental outcomes. Large benefits to public health can be expected from the controls, attributed mainly to reduced emissions of primary PM and gaseous PM precursors, and thus lower ambient concentrations of PM2.5. Approximately 4% of all-cause mortality in the country can be avoided (95% confidence interval: 1-7%), particularly in eastern and north-central China, regions with large population densities and high levels of PM2.5. Surface ozone levels, however, are estimated to increase in parts of those regions, despite NOX reductions. This implies VOC-limited conditions. Even with significant reduction of SO2 and NOX emissions, the controls will not significantly mitigate risks of soil acidification, judged by the exceedance levels of critical load (CL). This is due to the decrease in primary PM emissions, with the consequent reduction in deposition of alkaline base cations. Compared to 2005, even larger CL exceedances are found for both scenarios in 2020, implying that PM control may negate any recovery from soil acidification due to SO2 reductions. Noting large uncertainties, current polices to control emissions of criteria pollutants in China will not reduce climate warming, since controlling SO2 emissions also reduces reflective secondary aerosols. Black carbon emission is an important source of uncertainty concerning the effects of Chinese control policies on global temperature change. Given these conflicts, greater consideration should be paid to reconciling varied environmental objectives, and emission control strategies should target not only criteria pollutants but also species such as VOCs and CO2.

Abstract  In the present work, graphene sheets (GS) and multiwall carbon nanotubes (MWCNTs) were dispersed in the mixed solution of cyclodextrin (CD) and cyclodextrin prepolymer (pre-CD) and were used as modifier to fabricate chemical modified electrode to simultaneous detect dopamine (DA), ascorbic acid (AA) and nitrite (NO(2)(-)). CD cross-linked pre-CD (CDP) displays excellent film forming ability, which made the electrode stable. Comparing with CDP-GS, CDP-MWCNTs and CDP-GS-MWCNTs modified electrodes, the CDP-GS-MWCNTs displays higher catalytic activity and selectivity toward the oxidation of DA, AA and NO(2)(-), revealing that MWCNTs effectively inhibited the stacking of individual GS and enhanced the utilization of GS based composites. The host-guest chemical reaction ability of CD and π-π stacking interaction between detected molecules and GS-MWCNTs surface were considered as the main reasons of the successfully simultaneous detection of DA, AA and NO(2)(-). Cyclic voltammetry (CV), scanning electron microscopy (SEM) and different pulse voltammetry (DPV) were employed to characterize the biosensor. The linear response range for AA, DA and NO(2)(-) were 5μM-0.48mM, 0.15-21.65μM and 5μM-6.75mM, respectively and the detection limits were 1.65μM, 0.05μM and 1.65μM.

Abstract  The study is to explore the toxicity of organic extracts and water-soluble fraction of fine particles on human umbilical vein endothelial cells (HUVECs). The exposure doses were 100, 200 and 400 μg/ml, respectively, for two kinds of fractions. Moreover, atorvastatin was used for intervention study. HUVECs were stimulated by 400 μg/ml organic and water soluble extracts, respectively, immediately followed by treatment with atorvastatin in concentrations of 0.1 μmol/L, 1 μmol/L and 10 μmol/L, respectively. Cell viability, malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), reactive oxygen species (ROS) and the expression of interleukin-6 beta (IL-6), tumor necrosis factor-α (TNF-α), endothelin-1 and P-selectin were determined in cells. The results showed that MDA and ROS increased in HUVECs after exposed to organic extracts and water-soluble fraction, whereas cell viability, NO and SOD decreased. The mRNA expression of IL-6, TNF-α, endothelin-1 (ET-1) and P-selectin increased after exposed to different fractions. Meanwhile, at the same exposure dose, water-soluble fraction caused more significant increase of MDA, IL-6, TNF-α and P-selectin and decrease of cell viability and NO when compared to organic extracts. Compared to no atorvastatin group, the levels of MDA, ROS and the expression of IL-6, TNF-α, ET-1 and P-selectin decreased in HUVECs in adding atorvastatin group, but cell viability, NO and SOD increased, which indicated that atorvastatin attenuated fine particle-induced inflammatory response, oxidative stress and endothelial damage. The results hinted that the inflammatory response, oxidative stress and endothelial dysfunction might be the mechanisms of cardiovascular injury induced by different fractions of ambient fine particles.

Abstract  Chemical functionalization of graphene provides a promising route to improve its solubility in water and organic solvents as well as modify its electronic properties, thus significantly expanding its potential applications. In this article, by using density functional theory (DFT) methods, we have studied the effects of the chemical functionalization of graphenes via aryne cycloaddition on its properties. We found that the adsorption of an isolated aryne group on the graphene sheet is very weak with the adsorption energy of -0.204 eV, even though two new single C-C interactions are formed between the aryne group and the graphene. However, the interaction of graphene with the aryne group can be greatly strengthened by (i) substituting the H-atoms in aryne group with F-, Cl-, -NO(2) (electron-withdrawing capability), or CH(3)-group (electron-donating capability), and (ii) increasing the coverage of the adsorbed aryne groups on the graphene sheet. As expected, the strongest bonding is found on the graphene edges, in which the adsorbed aryne groups prefer to be far away from each other. Interestingly, chemical functionalization with aryne groups leads to an opening of the band gap of graphene, which is dependent on the coverage of the adsorbed aryne groups. The present work provides an insight into the modifications of graphene with aryne groups in experiment.

Abstract  BACKGROUND: A number of epidemiological studies have examined the adverse effect of air pollution on mortality and morbidity. Also, several studies have investigated the associations between air pollution and specific-cause diseases including arrhythmia, myocardial infarction, and heart failure. However, little is known about the relationship between air pollution and the onset of hypertension. OBJECTIVE: To explore the risk effect of particulate matter air pollution on the emergency hospital visits (EHVs) for hypertension in Beijing, China. METHODS: We gathered data on daily EHVs for hypertension, fine particulate matter less than 2.5 microm in aerodynamic diameter (PM(2.5)), particulate matter less than 10 microm in aerodynamic diameter (PM(10)), sulfur dioxide, and nitrogen dioxide in Beijing, China during 2007. A time-stratified case-crossover design with distributed lag model was used to evaluate associations between ambient air pollutants and hypertension. Daily mean temperature and relative humidity were controlled in all models. RESULTS: There were 1,491 EHVs for hypertension during the study period. In single pollutant models, an increase in 10 microg/m(3) in PM(2.5) and PM(10) was associated with EHVs for hypertension with odds ratios (overall effect of five days) of 1.084 (95% confidence interval (CI): 1.028, 1.139) and 1.060% (95% CI: 1.020, 1.101), respectively. CONCLUSION: Elevated levels of ambient particulate matters are associated with an increase in EHVs for hypertension in Beijing, China.

Abstract  Background Determinants of exhaled nitric oxide (FeNO) need to be understood better to maximize the value of FeNO measurement in clinical practice and research. Our aim was to identify significant predictors of FeNO in an initial cross-sectional survey of southern California schoolchildren, part of a larger longitudinal study of asthma incidence. Methods During one school year, we measured FeNO at 100 ml/sec flow, using a validated offline technique, in 2568 children of age 7–10 yr. We estimated online (50 ml/sec flow) FeNO using a prediction equation from a separate smaller study with adjustment for offline measurement artifacts, and analyzed its relationship to clinical and demographic characteristics. Results FeNO was lognormally distributed with geometric means ranging from 11 ppb in children without atopy or asthma to 16 ppb in children with allergic asthma. Although effects of atopy and asthma were highly significant, ranges of FeNO for children with and without those conditions overlapped substantially. FeNO was significantly higher in subjects aged > 9, compared to younger subjects. Asian-American boys showed significantly higher FeNO than children of all other sex/ethnic groups; Hispanics and African-Americans of both sexes averaged slightly higher than non-Hispanic whites. Increasing height-for-age had no significant effect, but increasing weight-for-height was associated with decreasing FeNO. Conclusion FeNO measured offline is a useful biomarker for airway inflammation in large population-based studies. Further investigation of age, ethnicity, body-size, and genetic influences is needed, since they may contribute to substantial variation in FeNO.

Abstract  OBJECTIVE: To assess the association between daily exposure to air pollution and lung function in school children. METHODS: Panel study with a random sample of 118 students (between 6 and 15 years of age), enrolled in a public school of the city of Rio de Janeiro, state of Rio de Janeiro, and living within 2 km of the study site. Data on students' characteristics were obtained with a questionnaire, including the International Study of Asthma and Allergies in Childhood - ISAAC. Daily peak expiratory flow measurements were taken to measure lung function. Daily data on PM10, SO2, O3, NO2 and CO levels, temperature and humidity were provided by a portable monitor. Repeated measurements of lung function were associated with pollutant levels with a multilevel model adjusted for time trend, temperature, air humidity, exposure to smoking at home, presence of asthma, height, sex, weight and age of children. RESULTS: Mean peak expiratory flow was 243.5 l/m (sd=58.9). The lowest mean peak expiratory flow was 124 l/m, and the highest, 450 l/m. For the 10 microg/m(3) increase in PM10, there was a 0.34 l/min decrease in mean peak flow on the third day. For the 10 microg/m(3) increase in NO2, there was a decrease between 0.23 l/min and 0.28 l/min in mean peak flow after exposure. CO and SO2 effects on students' peak flow were not statistically significant. O3 showed a protective result: an increase in 10 microg/m(3) of O3 would be associated, after a day of exposure, with a 0.2 l/min increase in mean lung function. CONCLUSIONS: Even within acceptable levels most of the time, air pollution, especially PM10 and NO2, was associated with a decrease in lung function in children living in the city of Rio de Janeiro.

Abstract  Sequential exposures to inhaled environmental pollutants may result in injuries/responses not predicted by evaluating exposures to an individual toxicant. This may indicate that the lung is damaged or primed by earlier events, so exposure to a nontoxic dose of an environmental pollutant may be sufficient to trigger adverse responses. The present study was designed to test the hypothesis that stimulating lung epithelial damage or inflammatory cell activation followed by a second stimulus leads to responses not seen after individual exposures in the postnatal lung. C57Bl/6 mice ages 4, 10, and 56 days were exposed to either a 10-minute inhalation of lipopolysaccharide (LPS), with an estimated deposited dose of 26 EU, followed immediately by 2.5 PPM ozone for 4 hours, or to 2.5 PPM ozone for 4 hours followed immediately by a 10-minute inhalation of LPS and examined 2 hours post exposure. Abundance of proinflammatory cytokine messages was measured by RNase protection assay. Exposure to LPS followed by ozone induced an inflammatory response in 4-day-old mice, which was not detected after LPS or ozone exposure alone. This exposure sequence also generated a synergistic increase in interleukin (IL)-6 mRNA abundance in 10- and 56-day-old mice but not in 4-day-old mice. Exposure to ozone followed by LPS inhibited IL-1alpha and IL-1beta responses in 4-, 10-, and 56-day-old mice; furthermore, this inhibitory effect was observed after 1.0 and 0.5 PPM ozone exposures. These results demonstrate that preexposure to LPS, which primarily activates inflammatory cell recruitment, can cause sensitization to a secondary stimulus. However, preexposure to ozone, which primarily damages the epithelium, inhibited proinflammatory responses. Thus it was concluded that sequential exposures to ozone and LPS resulted in responses not predicted by evaluating individual exposures during postnatal lung development.

Abstract  The aerosol distribution in Europe was simulated with the Community Multiscale Air Quality (CMAQ) model system version 4.5 for the years 2000 and 2001. The results were compared with daily averages of PM10 measurements taken in the framework of EMEP and with aerosol optical depth (AOD) values measured within AERONET. The modelled total aerosol mass is typically about 30-60% lower than the corresponding measurements. However a comparison of the chemical composition of the aerosol revealed a considerably better agreement between the modelled and the measured aerosol components for ammonium, nitrate and sulfate, which are on average only 15-20% underestimated. Sligthly worse agreement was determined for sea salt, that was only avaliable at two sites. The largest discrepancies result from the aerosol mass which was not chemically specified by the measurements. The agreement between measurements and model is better in winter than in summer. The modelled organic aerosol mass is higher in summer than in winter but it is significantly underestimated by the model. This could be one of the main reasons for the discrepancies between measurements and model results. The other is that primary coarse particles are underestimated in the emissions. The probability distribution function of the PM10 measurements follows a log-normal distribution at most sites. The model is only able to reproduce this distribution function at non-coastal low altitude stations. The AOD derived from the model results is 20-70% lower than the values observed within AERONET. This is mainly attributed to the missing aerosol mass in the model. The day-to-day variability of the AOD and the log-normal distribution functions are quite well reproduced by the model. The seasonality on the other hand is underestimated by the model results because better agreement is achieved in winter. ABSTRACT FROM AUTHOR Copyright of Atmospheric Chemistry & Physics is the property of European Geosciences Union and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts)