Role In PM2 Research Articles

The mechanisms for lung cancer risk of PM2.5 : Induction of epithelial-mesenchymal transition and cancer stem cell properties in human non-small cell lung cancer cells.

Fine particulate matter (PM2.5 ) is a major component of air pollutions that are closely associated with increased risk of lung cancer. However, the role of PM2.5 in the etiology of lung cancer is largely unknown. In this study, we performed acute (24 hours) and chronic (five passages) exposure models to investigate the carcinogenetic mechanisms of PM2.5 by targeting the induction of epithelial-mesenchymal transition (EMT) and cancer stem cells (CSC) properties in human non-small cell lung cancer cell line A549. We found that both acute and chronic PM2.5 exposure enhanced cell migration and invasion, decreased mRNA expression of epithelial markers and increased mRNA expression of mesenchymal markers. Chronic PM2.5 exposure further induced notable EMT morphology and CSC properties, indicating the developing process of cell malignant behaviors from acute to chronic PM2.5 exposure. CSC properties induced by chronic PM2.5 exposure characterized with increased cell-surface markers (CD44, ABCG2), self-renewal genes (SOX2 and OCT4), side population cells and neoplastic capacity. Furthermore, the levels of three stemness-associated microRNAs, Let-7a, miR-16 and miR-34a, were found to be significantly downregulated by chronic PM2.5 exposure, with microarray data analysis from TCGA database showing their lower expression in human lung adenocarcinoma tissues than that in the adjacent normal lung tissues. These data revealed that the induction of EMT and CSC properties were involved in the lung cancer risk of PM2.5 , and implicated CSC properties and related microRNAs as possible biomarkers for carcinogenicity prediction of PM2.5 .

Atmospheric removal of PM2.5 by man-made Three Northern Regions Shelter Forest in Northern China estimated using satellite retrieved PM2.5 concentration

Atmospheric removal of PM2.5 by the Three Northern Regions Shelter Forest (TNRSF) – the so called Green Great Wall (GGW) in northern China through dry deposition process was estimated using a bulk big-leaf model and a vegetation collection model. Decadal trend of PM2.5 dry deposition flux from 1999 to 2010 was calculated from modeled dry deposition velocity and air concentration retrieved from the satellite remote sensing. Dry deposition velocities of PM2.5 calculated using the two deposition models increased in many places of the TNRSF over the last decade due to increasing vegetation coverage of the TNRSF. Both increasing deposition velocity due to forest expansion and PM2.5 atmospheric level contributed to the increasing deposition flux of PM2.5. The highest atmospheric deposition flux of PM2.5 was found in the Central-north region covering Beijing-Tianjin-Hebei area, followed by the Northwestern and the Northeastern regions of the TNRSF. While greater collection of PM2.5 by vegetation was identified in the Northeastern region of the TNRSF due to higher forest coverage over this region, the most significant incline of the PM2.5 atmospheric removal due to vegetation collection was discerned in the Central-north region because of the most rapid increase in the vegetation coverage in this region. A total mass of 2.85×107t PM2.5 was estimated to be removed from the atmosphere through dry deposition process over the TNRSF from 1999 to 2010. The two deposition models simulated similar magnitude and spatial patterns of PM2.5 dry deposition fluxes. Our results suggest that the TNRSF plays a moderate role in PM2.5 uptake, but enhances PM2.5 atmospheric removal by 30% in 2010 than in 1980.

PM2.5 exposure decreases viability, migration and angiogenesis in human umbilical vein endothelial cells and human microvascular endothelial cells.

Previous studies have confirmed that exposure to particulate matter with a diameter of ≤2.5 µm (PM2.5) is associated with inflammation. PM2.5 decreases cardiac cell viability and increases apoptosis through overproduction of reactive oxygen species (ROS). In the present study, the role of PM2.5 in ECs was investigated in vitro. Human umbilical vein endothelial cells and human microvascular endothelial cells (ECs) were incubated with PM2.5 (100–800 µg/ml) to investigate the effects of PM2.5 on EC viability, migration, tube formation and intracellular levels of ROS. Cell viability and cell apoptosis were determined by MTT assay and flow cytometry analysis. Cell migration was assessed using a Boyden chamber assay, and tube formation was determined by matrigel assay. Tumor necrosis factor-α and interleukin-8 levels were measured by ELISA, and ROS levels were assessed with 2′,7′-dichlorofluorescin diacetate. The results indicated that PM2.5 decreases EC viability and increases EC apoptosis in a concentration-dependent manner. PM2.5 also decreased EC tube formation in a dose-dependent manner. The results also demonstrated that PM2.5 suppresses adhesion to EC extracellular matrix proteins. Furthermore, PM2.5 exposure significantly induced ROS generation, indicative of oxidative stress. Finally, it was demonstrated that PM2.5 decreased angiogenesis in vivo. These results suggested that repeated exposure to PM2.5 induces vascular inflammation.

Outdoor Environment and Pediatric Asthma: An Update on the Evidence from North America.

Introduction. The evidence about the association between asthma and outdoor environmental factors has been inadequate for certain allergens. Even less is known about how these associations vary across seasons and climate regions. We reviewed recent literature from North America for research related to outdoor environmental factors and pediatric asthma, with attention to spatial-temporal variations of these associations. Method. We included indexed literature between years 2010 and 2015 on outdoor environmental factors and pediatric asthma, by searching PubMed. Results. Our search resulted in 33 manuscripts. Studies about the link between pediatric asthma and traffic-related air pollutants (TRAP) consistently confirmed the correlation between TRAP and asthma. For general air pollution, the roles of PM2.5 and CO were consistent across studies. The link between asthma and O3 varied across seasons. Regional variation exists in the role of SO2. The impact of pollen was consistent across seasons, whereas the role of polycyclic aromatic hydrocarbon was less consistent. Discussion. Recent studies strengthened the evidence about the roles of PM2.5, TRAP, CO, and pollen in asthma, while the evidence for roles of PM10-2.5, PM10, O3, NO2, SO2, and polycyclic aromatic hydrocarbon in asthma was less consistent. Spatial-temporal details of the environment are needed in future studies of asthma and environment.

Analysis of PM2.5 distribution and transfer characteristics in a car cabin

To investigate the transfer characteristics of PM2.5 in a car cabin, several experiments were performed featuring real-time online monitoring of the concentration of PM2.5 and CO2 in the cabin under different ventilation modes (circulation with outdoor air and recirculation without outdoor air), at a minimum of mechanical ventilation and matching experimental route conditions. We analyzed the PM2.5 concentration distribution characteristics and the ratio of inside-to-outside PM2.5 concentration (I/O). The ventilation rate was determined by the CO2 concentration change during the experiments, and it was used to analyze the transfer characteristics of PM2.5. The results showed that under the “circulation with outdoor air” condition, the average I/O was 0.6, while it was 0.25 under the “recirculation” condition. I/O value decreased with acceleration of driving speed. It could be concluded that the ventilation mode has a significant impact on the concentration of PM2.5 in the cabin, and plays a decisive role in PM2.5 levels. The quantitative evaluation of PM2.5 transfer characteristics under the “circulation with outdoor air” condition showed that the contributions of ventilation, penetration, and deposition to the cabin PM2.5 concentration accounted for 69.3%, 22.8%, and 7.9%, respectively; while under the “recirculation” condition, penetration accounted for 72.0% and deposition accounted for 28.0%.

DDAH1 plays dual roles in PM2.5 induced cell death in A549 cells

BackgroundDimethylarginine dimethylaminohydrolase 1 (DDAH1) is an enzyme that can degrade asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase (NOS) inhibitor. Emerging evidence suggests that alterations in the ADMA–DDAH1 pathway are involved in environmental pollution induced airway inflammation. However, the role of DDAH1 in protection against cytotoxicity of ambient airborne particulate matter is unclear. MethodsWe examined the influence of DDAH1 expression on oxidative stress and cell apoptosis in human type II alveolar epithelial A549 cells exposed to PM2.5 (particulate matter with an aerodynamic diameter less than 2.5μM). ResultsWe found that PM2.5 exposure for 48h significantly decreased DDAH1 expression. However, knockdown of DDAH1 prior to PM2.5 exposure actually attenuated the cytotoxicity of PM2.5. Cytoprotection in DDAH1 deficient cells was due to increased reactive oxygen species, activation of PI3K–AKT and mitogen-activated protein kinase (MAPK) pathways, subsequent activation of nuclear factor erythroid-2-related factor 2 (Nrf2) and this caused a subsequent reduction in PM2.5 induced oxidative stress relative to control. DDAH1 depletion also repressed the induction of inducible NOS (iNOS) in PM2.5-exposed cells and knockdown of iNOS protected cells against PM2.5 induced cell death. Interestingly, overexpression of DDAH1 also exerted a protective effect against the cytotoxicity of PM2.5 and this was associated with a reduction in oxidative stress and upregulation of the anti-apoptotic protein Bcl-2. ConclusionsOur data indicate that DDAH1 plays dual roles in protection against cytotoxicity of PM2.5 exposure, apparently by limiting PM2.5 induced oxidative stress. General significanceOur findings reveal new insights into the role(s) of the DDAH1/ADMA in pulmonary protection against airborne pollutants. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.

Integrative analysis of mRNA and microRNA expression of a human alveolar epithelial cell(A549) exposed to water and organic‐soluble extract from particulate matter (PM)2.5

MicroRNA (miRNA) is now attracting attention as a powerful negative regulator of messenger RNA(mRNA) levels, and is implicated in the modulation of important mRNA networks involved in toxicity. In this study, we assessed the effects of particulate matter 2.5 (PM2.5 ), one of the most significant air pollutants, on miRNA and target gene expression. We exposed human alveolar epithelial cell (A549) to two types of PM2.5 [water (W-PM2.5 ) and organic (O-PM2.5 ) soluble extracts] and performed miRNA microarray analysis. A total of 37 miRNAs and 62 miRNAs were altered 1.3-fold in W-PM2.5 and O-PM2.5 , respectively. Integrated analyses of miRNA and mRNA expression profiles identified negative correlations between miRNA and mRNA in both W-PM2.5 and O-PM2.5 exposure groups. Gene ontology and Kyoto encyclopedia of genes and genomes (KEGG) pathway analyses showed that the 35 W-PM2.5 target genes are involved in responses to nutrients, positive regulation of biosynthetic processes, positive regulation of nucleobase, nucleoside, and nucleotide, and nucleic acid metabolic processes; while the 69 O-PM2.5 target genes are involved in DNA replication, cell cycle processes, the M phase, and the cell cycle check point. We suggest that these target genes may play important roles in PM2.5 -induced respiratory toxicity by miRNA regulation. These results demonstrate an integrated miRNA-mRNA approach for identifying molecular events induced by environmental pollutants in an in vitro human model. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 302-310, 2017.

Effects of Urban Landscape Pattern on PM2.5 Pollution--A Beijing Case Study.

PM2.5 refers to particulate matter (PM) in air that is less than 2.5μm in aerodynamic diameter, which has negative effects on air quality and human health. PM2.5 is the main pollutant source in haze occurring in Beijing, and it also has caused many problems in other cities. Previous studies have focused mostly on the relationship between land use and air quality, but less research has specifically explored the effects of urban landscape patterns on PM2.5. This study considered the rapidly growing and heavily polluted Beijing, China. To better understand the impact of urban landscape pattern on PM2.5 pollution, five landscape metrics including PLAND, PD, ED, SHEI, and CONTAG were applied in the study. Further, other data, such as street networks, population density, and elevation considered as factors influencing PM2.5, were obtained through RS and GIS. By means of correlation analysis and stepwise multiple regression, the effects of landscape pattern on PM2.5 concentration was explored. The results showed that (1) at class-level, vegetation and water were significant landscape components in reducing PM2.5 concentration, while cropland played a special role in PM2.5 concentration; (2) landscape configuration (ED and PD) features at class-level had obvious effects on particulate matter; and (3) at the landscape-level, the evenness (SHEI) and fragmentation (CONTAG) of the whole landscape related closely with PM2.5 concentration. Results of this study could expand our understanding of the role of urban landscape pattern on PM2.5 and provide useful information for urban planning.

PM2.5 induces embryonic growth retardation: Potential involvement of ROS-MAPKs-apoptosis and G0/G1 arrest pathways.

Airborne fine particulate matter (PM2.5 ) is an "invisible killer" to human health. There is increasing evidence revealing the adverse effects of PM2.5 on the early embryonic development and pregnancy outcome, but the molecular mechanism underlying PM2.5 -induced embryotoxicity is largely unknown. Previous studies have documented that exposure to PM triggers ROS generation, leads to subsequent activation of MAPKs signaling, and results in corresponding cell biological changes including enhanced apoptosis and altered cell cycle in the cardiopulmonary system. Here, we investigated whether ROS-MAPKs-apoptosis/cell cycle arrest pathways play an important role in PM2.5 -induced embryotoxicity using the rat whole embryo culture system. The results showed that PM2.5 treatment led to embryonic growth retardation at concentrations of 50 μg/ml and above, as evidenced by the reduced yolk sac diameter, crown-rump length, head length and somite number. PM2.5 -induced embryonic growth retardation was accompanied by cell apoptosis and G0/G1 phase arrest. Furthermore, ROS generation and subsequent activation of JNK and ERK might be involved in PM2.5 -induced apoptosis and G0/G1 phase arrest by downregulating Bcl-2/Bax protein ratio and upregulating p15INK4B , p16INK4A , and p21WAF1/CIP1 transcription level. In conclusion, our results indicate that ROS-JNK/ERK-apoptosis and G0/G1 arrest pathways are involved in PM2.5 -induced embryotoxicity, which not only provides insights into the molecular mechanism of PM2.5 -induced embryotoxicity, but also may help to identify specific interventions to improve adverse pregnancy outcomes of PM2.5 . © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 2028-2044, 2016.

The toxic effects of indoor atmospheric fine particulate matter collected from allergic and non-allergic families in Wuhan on mouse peritoneal macrophages.

Recent studies have shown that fine particulate matter (PM2.5) is associated with multiple adverse health outcomes and PM2.5-induced oxidative stress is now commonly known as a proposed mechanism of PM2.5-mediated toxicity. However, the association between allergic symptoms in children and exposure to PM2.5 has not been fully elucidated, particularly the role of PM2.5 on the indoor environment involved in allergy or non-allergy is unknown. The aim of the present study was to explore whether indoor PM2.5 from the homes of children with allergic symptoms had more increased risks of allergy than that of healthy ones and then compare the toxicity and inflammatory response of them. In this study, indoor PM2.5 was collected from the homes of schoolchildren with allergic symptoms and those of healthy ones respectively, and components of PM2.5 were analyzed. PM2.5-mediated oxidative damage and inflammatory response were further evaluated in mouse peritoneal macrophages based on its effects on the levels of reactive oxygen species accumulation, lipid peroxidation, DNA damage or cytokine production. It seems that oxidative stress may contribute to PM2.5-induced toxicity, and PM2.5 from the allergic indoor environment produced more serious toxic effects and an inflammatory response on mouse peritoneal macrophages than that from a non-allergic indoor environment.

Maternal exposure to ambient PM2.5 and term low birthweight in the State of Georgia

A growing body of evidence suggests that ambient air pollution could be associated with low birthweight (LBW). In this study, we examined pregnancy exposure to ambient PM2.5 and the risk of LBW in the State of Georgia. The study population consisted of 48,172 full-term live births between 1 January 2004 and 31 December 2004 in nine counties of Georgia, which was obtained from the national natality dataset. County-level air quality index data obtained from the U.S. Environmental Protection Agency was used to estimate exposure to ambient levels of PM2.5. Multivariate logistic regression revealed that infants with maternal exposure to PM2.5 falling within 75 to < 95th percentiles were at increased risk of LBW (OR: 1.36; 95 % CI: 1.03, 1.79), after adjusting for potential confounders. This study provided more evidence on the role of PM2.5 in LBW. Reducing exposure for pregnant women would be necessary to improve the health of infants.

Study on Planning and Construction of Community Greenway for PM2.5 Reduction

In the developing process of urbanization in China, PM2.5 pollution has become a problem that must be faced. Greenway, especially those in the community, is the important green infrastructure to improve ecological environment in urban areas, which plays a crucial role in PM2.5 reduction. With basic cognitive analysis on definitions and characteristics of community greenway and PM2.5, this paper proposed the strategy on planning and construction for greenways in community to reduce PM2.5 from four aspects including subarea construction, construction elements, allocation of afforestation plants and injection of regional culture, hoping to benefit the construction of greenways in community.

Exposure to Elemental Carbon, Organic Carbon, Nitrate, and Sulfate Fractions of Fine Particulate Matter and Risk of Preterm Birth in New Jersey, Ohio, and Pennsylvania (2000-2005).

BackgroundParticulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) has been consistently associated with preterm birth (PTB) to varying degrees, but roles of PM2.5 species have been less studied.ObjectiveWe estimated risk differences (RD) of PTB (reported per 106 pregnancies) associated with change in ambient concentrations of elemental carbon (EC), organic carbon (OC), nitrates (NO3), and sulfates (SO4).MethodsFrom live birth certificates from three states, we constructed a cohort of singleton pregnancies at or beyond 20 weeks of gestation from 2000 through 2005 (n = 1,771,225; 8% PTB). We estimated mean species exposures for each week of gestation from monitor-corrected Community Multi-Scale Air Quality modeling data. RDs and 95% confidence intervals (CIs) for four PTB categories were estimated for each exposure using linear regression, adjusted for maternal race/ethnicity, marital status, education, age, smoking, maximum temperature, ozone, and season of conception. We also adjusted for other species in multi-species models.ResultsRDs varied by exposure window and outcome period. EC was positively associated with PTB after 27 and before 35 weeks of gestation. For example, for a 0.25-μg/m3 increase in EC exposure during gestational week 9, RD = 96 (95% CI: –20, 213) and RD = 145 (95% CI: –50, 341) for PTB during weeks 28–31 and 32–34, respectively. Associations with OCs were null or negative. RDs for NO3 were elevated with exposure in early weeks of gestation, and null in later weeks. RDs for SO4 exposure were positively associated with PTB, though magnitude varied across gestational weeks. We observed effect measure modification for associations between EC and PTB by race/ethnicity and smoking status.ConclusionEC and SO4 may contribute to associations between PM2.5 and PTB. Associations varied according to the timing of exposure and the timing of PTB.CitationRappazzo KM, Daniels JL, Messer LC, Poole C, Lobdell DT. 2015. Exposure to elemental carbon, organic carbon, nitrate, and sulfate fractions of fine particulate matter and risk of preterm birth in New Jersey, Ohio, and Pennsylvania (2000–2005). Environ Health Perspect 123:1059–1065; http://dx.doi.org/10.1289/ehp.1408953

Analysis of the PM2.5 Distribution and the Transfer Characteristic in a Car-Cabin

In order to investigate the transfer characteristics of PM2.5 in a car-cabin, several experiments were done through real-time online monitoring the concentration of PM2.5 and CO2 in the car-cabin under different ventilation modes (Circulation with the outdoor air and Recirculation without fresh air) under the minimum of mechanical ventilation and the same experimental route condition. PM2.5 concentration distribution characteristics and the ratio of inside to outside concentration I/O were analyzed. The ventilation rate was determined by the CO2 concentration change during the experiment and further was used to analyze the transfer characteristic of PM2.5. The results showed that under the circulation with the outdoor air condition, average I/O is 0.6, while it is 0.25 under recirculation condition. I/O value increases with the increase of the driving speed. It could be concluded that ventilation mode have a significant impact on the cabin concentration of PM2.5 and plays a decisive role in PM2.5 levels in the car-cabin. The quantitative evaluation PM2.5 transfer characteristic analysis under circulation with outdoor air condition shows that the ventilation, penetration and deposition accounted for 69.3%, 22.8%, and 7.9%, respectively. While under recirculation condition, penetration accounted for 72%, and deposition accounted for 28%.

Airborne particulate matter (PM2.5) and the prevalence of allergic conjunctivitis in Japan

ObjectiveExposure to particulate matter less than 2.5μm in diameter (PM2.5) is associated with asthma and respiratory symptoms, but little is known about the influence of PM2.5 on allergic conjunctivitis. The purpose of this study was to examine the association of PM2.5 with outpatient attendance for allergic conjunctivitis. MethodsWe conducted a time-series analysis of the association between outpatient attendance for allergic conjunctivitis and PM2.5 levels from May to July (non-pollen season) and from August to October (the autumnal pollen season) in 2012. Air pollution data (including the levels of PM2.5, oxidants, nitric oxide, nitrogen dioxide, nitrogen oxide, carbon monoxide, methane, non-methane hydrocarbons, and total hydrocarbons) and data on the daily weather conditions (temperature, wind speed, and humidity) were collected at a centrally located monitoring station in Tokyo. We calculated weekly average values for the daily number of outpatient visits, as well as the air pollution and weather data, and used the weekly average values for analysis. ResultsThere was a significant association between the number of outpatient visits for allergic conjunctivitis and the PM2.5 level (r=0.62, p=0.0177) from May to July, while no correlation was found between the number of outpatient visits and any variable assessed from August to November. Multivariate analysis also showed that PM2.5 was a significant predictor of the number of outpatient visits from May to July (odds ratio=9.05, p=0.0463), while there were no significant predictors of the number of outpatient visits from August to October. From May to July, PM2.5 showed a negative correlation with humidity (r=−0.53, p=0.0499). ConclusionsThese findings suggest a possible role of PM2.5 in the development of allergic conjunctivitis during the non-pollen season. This association between PM2.5 and allergic conjunctivitis may have broad public health implications in relation to allergic diseases.

A Synergistic Vascular Effect of Airborne Particulate Matter and Nickel in a Mouse Model

Both epidemiological and empirical studies have indicated that nickel (Ni) may play an important role in PM2.5 exposure-induced adverse cardiovascular effects. However, the underlying mechanism remains unclear. In the present study, we exposed mice to concentrated ambient PM2.5 (CAP), Ni, or coexposure to both CAP + Ni in a specially designed whole-body exposure system for a duration of 3 months and investigated their effects on vascular function, oxidative stress, and vascular inflammation. CAP + Ni exposure induced greater endothelial dysfunction compared with CAP or Ni alone. Ni exposure decreased endothelial nitric oxide synthase (eNOS) dimers in the aorta, which was potentiated by coexposure with CAP. CAP alone did not reduce NOS dimers but was more effective than Ni in decreasing phosphorylation of eNOS (S1177) and Akt (T308). Ni had minimal effects on the expression of vascular inflammatory genes but synergized with CAP in marked upregulation of tumor necrosis factor-alpha and monocyte chemotactic protein-1. The effects of Ni on NOS monomer formation in endothelial cells were redox dependent as evidenced by attenuation of effects by Tiron in cultured endothelial cells. Ni synergized with lipopolysaccharide, another bioactive component of CAP in reducing eNOS dimerization in cultured endothelial cells. Ni exposure induces endothelial dysfunction through oxidative stress-dependent inhibition of eNOS dimerization. Its interaction with other components of CAP may significantly contribute to the adverse cardiovascular effects of CAP exposure.

Fine Scale Modeling of Agricultural Air Quality over the Southeastern United States Using Two Air Quality Models. Part II. Sensitivity Studies and Policy Implications

ABSTRACTSensitivity simulations using CMAQ at various grid resolutions are evaluated. Compared with the simulations at 12- and 4-km, the 1.33-km simulation shows large improvement in most meteorological predictions in July and some chemical predictions in January and July 2002. Limited improvements at 1.33-km and 4-km are attributed to current limitations in meteorological parameterizations and lack of accurate data for land use and emissions at a fine scale. NH3 plays an important role in PM2.5 formation, but the emission control strategies focus only on SO2 and NOx in the southeastern U.S. To understand the impact of NH3, NH3 to NH4+ conversion and the chemical regimes of PM2.5 formation are examined. The conversion rates of NH3 to NH4+ from CMAQ and CAMx simulations are 10–60% in January and 10–50% in July at and near major sources. The eastern North Carolina and northeastern Georgia are NH3-rich and the remaining areas are NH3-neutral in both months. To further assess the impact of NH3 emission reductions, the sensitivity of CMAQ to emission reductions is evaluated for four emission scenarios: reducing emissions of SO2, NOx, agricultural livestock-NH3 (AL-NH3) by 50%, respectively and collectively. The largest reductions of PM2.5 are by up to 19.2% in January and 18.3% in July when all these emissions are reduced by 50%. AL-NH3 reductions result in the largest decrease in January by up to 16%, dominated by a reduction in NH4NO3, while SO2 reductions result in the largest decrease in July (up to 11%) due to decreases in NH4+ and SO42–. This indicates that reducing AL-NH3 emissions together with SO2 and NOx emissions can reduce PM2.5 concentrations more than reducing emissions of SO2 and NOx alone, particularly in winter. Future emission control strategies for PM2.5 controlling should consider the reduction of NH3 emissions, in addition to the emissions of SO2 and NOx.

PM2.5 source apportionment in the southeastern U.S.: Spatial and seasonal variations during 2001–2005

The seasonal and spatial variations of source contributions of 112 composite fine particulate matter (PM2.5) samples collected in the Southeastern Aerosol Research and Characterization Study (SEARCH) monitoring network during 2001–2005 using molecular marker‐based chemical mass balance (CMB‐MM) model were determined. The lowest PM2.5 concentration occurs in January with higher values in warm months (maxima in July at four inland sites versus October at the coastal sites). Sulfate shows a similar pattern and plays a primary role in PM2.5 seasonality. Carbonaceous material (organic matter plus EC) exhibits less seasonality, but more spatial variations between the inland and coastal sites. Compared with the data at coastal sites, source attributions of diesel exhaust, gasoline exhaust, other organic matter (other OM), secondary sulfate, nitrate, and ammonium in PM2.5 mass at inland sites are higher. The difference in source attributions of wood combustion, meat cooking, vegetative detritus, and road dust among the eight sites is not significant. Contributions of eight primary sources to fine OC are wood burning (17 ± 19%), diesel exhaust (9 ± 4%), gasoline exhaust (5 ± 7%), meat cooking (5 ± 5%), road dust (2 ± 3%), vegetative detritus (2 ± 2%), cigarette smoke (2 ± 2% at four urban sites), and coke production (2 ± 1% only at BHM). Primary and secondary sources explain 82–100% of measured PM2.5 mass at the eight sites, including secondary ionic species (SO42−, NH4+, and NO3−; 41.4 ± 5.7%), identified OM (24.9 ± 11.3%), “other OM” (unexplained OM, 23.3 ± 10.3%), and “other mass” (11.4 ± 9.6%). Vehicle exhaust from both diesel and gasoline contributes the lowest fraction to PM2.5 mass in July and higher fractions at BHM and JST than other sites. Wood combustion, in contrast, contributes significantly to a larger fraction in winter than in summer. Road dust shows relatively high levels in July and April across the eight sites, while minor sources such as meat cooking and other sources (e.g., vegetative detritus, coke production, and cigarette smoke) show relatively small seasonal and spatial variations in the SEARCH monitoring network.

PM 2.5 COMPONENTS EXPOSURES AND CARDIAC AUTONOMIC FUNCTION: A PANEL STUDY OF TAXI DRIVERS

Background and Aims: Carbonaceous and metallic components of particles have been shown to play a role in particles’ effects on cardiac autonomic function as measured by heart rate variability (HRV). We previously reported the association of HRV with marked changes in traffic-related particulate air pollution around the Beijing 2008 Olympic Games in a panel of taxi drivers (Wu et al., 2010). We further investigated the relationship between exposures to the carbonaceous and metallic components of traffic-related particles and HRV in the same population. Methods: Repeated measurements of in-car exposures to particulate matter ≤2.5 µm in aerodynamic diameter (PM2.5) and carbon monoxide were conducted in a group of 14 taxi drivers for one work shift in four study periods around the Beijing 2008 Olympics. The quantities of organic/elemental carbons and 27 elements of the traffic-related PM2.5 mass were determined laboratorially. Linear mixed-effects models were used to evaluate the impact of exposures to different PM2.5 components on HRV while controlling for potential confounders. Results: Taxi drivers’ exposures to traffic-related PM2.5 components showed dramatic changes across the four study periods around the Beijing 2008 Olympics. Differences in associations of traffic-related PM2.5 components with HRV were found. An interquartile range (IQR: 917.9 ng/m3) increase in calcium was associated with a 5.48 milliseconds [95% confidence interval (CI): 0.71, 10.24] increase in standard deviations of normal-to-normal (SDNN) intervals, whereas an IQR (4.1 ng/m3) increase in nickel was associated with a 1.53 milliseconds (95% CI: 0.14, 2.92) increase in SDNN index. Additionally, a decline of 8.11 milliseconds (95% CI: -15.26, -0.97) in SDNN per IQR (481.4 ng/m3) increase in iron was also found. Conclusions: Our results support associations of PM2.5 metallic components with cardiac autonomic function in the study population. Future studies are needed to clarify the interaction among different PM2.5 components or the role of PM2.5 mixtures.

Characterization of Major Chemical Components of Fine Particulate Matter in North Carolina

This paper presents measurements of daily sampling of fine particulate matter (PM2.5) and its major chemical components at three urban and one rural locations in North Carolina during 2002. At both urban and rural sites, the major insoluble component of PM2.5 is organic matter, and the major soluble components are sulfate (SO4 2−), ammonium (NH4 +), and nitrate (NO3 −). NH4 + is neutralized mainly by SO4 2− rather than by NO3 −, except in winter when SO4 2− concentration is relatively low, whereas NO3 − concentration is high. The equivalent ratio of NH4 + to the sum of SO4 2− and NO3 − is <1, suggesting that SO4 2−and NO3 −are not completely neutralized by NH4 +. At both rural and urban sites, SO4 2−concentration displays a maximum in summer and a minimum in winter, whereas NO3 −displays an opposite seasonal trend. Mass ratio of NO3 − to SO4 2−is consistently <1 at all sites, suggesting that stationary source emissions may play an important role in PM2.5 formation in those areas. Organic carbon and elemental carbon are well correlated at three urban sites although they are poorly correlated at the agriculture site. Other than the daily samples, hourly samples were measured at one urban site. PM2.5 mass concen trations display a peak in early morning, and a second peak in late afternoon. Back trajectory analysis shows that air masses with lower PM2.5 mass content mainly originate from the marine environment or from a continental environment but with a strong subsidence from the upper troposphere. Air masses with high PM2.5 mass concentrations are largely from continental sources. Our study of fine particulate matter and its chemical composition in North Carolina provides crucial information that may be used to determine the efficacy of the new National Ambient Air Quality Standard (NAAQS) for PM fine. Moreover, the gas-to-particle conversion processes provide improved prediction of long-range transport of pollutants and air quality.