Vehicular exhaust particles promote allergic airway inflammation through an aryl hydrocarbon receptor-notch signaling cascade.

BACKGROUND: Traffic-related particulate matter (PM) has been linked to a heightened incidence of asthma and allergic diseases. However, the molecular mechanisms by which PM exposure promotes allergic diseases remain elusive. OBJECTIVE: We sought to determine the expression, function, and regulation of pathways involved in promotion of allergic airway inflammation by PM. METHODS: We used gene expression transcriptional profiling, in vitro culture assays, and in vivo murine models of allergic airway inflammation. RESULTS: We identified components of the Notch pathway, most notably Jagged 1 (Jag1), as targets of PM induction in human monocytes and murine dendritic cells. PM, especially ultrafine particles, upregulated TH cytokine levels, IgE production, and allergic airway inflammation in mice in a Jag1- and Notch-dependent manner, especially in the context of the proasthmatic IL-4 receptor allele Il4raR576. PM-induced Jag1 expression was mediated by the aryl hydrocarbon receptor (AhR), which bound to and activated AhR response elements in the Jag1 promoter. Pharmacologic antagonism of AhR or its lineage-specific deletion in CD11c(+) cells abrogated the augmentation of airway inflammation by PM. CONCLUSION: PM activates an AhR-Jag1-Notch cascade to promote allergic airway inflammation in concert with proasthmatic alleles.

Global perspective on the oxidative potential of airborne particulate matter: a synthesis of research findings.

An emerging hypothesis in the field of air pollution is that oxidative stress is one of the important pathways leading to adverse health effects of airborne particulate matter (PM). To advance our understanding of sources and chemical elements contributing to aerosol oxidative potential and provide global comparative data, we report here on the biological oxidative potential associated with size-segregated airborne PM in different urban areas of the world, measured by a biological (cell-based) reactive oxygen species (ROS) assay. Our synthesis indicates a generally greater intrinsic PM oxidative potential as well as higher levels of exposure to redox-active PM in developing areas of the world. Moreover, on the basis of our observations, smaller size fractions are generally associated with higher intrinsic ROS activity compared with larger PM size fractions. Another important outcome of our study is the identification of major species and sources that are associated with ROS activity. Water-soluble transition metals (e.g., Fe, Ni, Cu, Cr, Mn, Zn and V) and water-soluble organic carbon (WSOC) showed consistent correlations with the oxidative potential of airborne PM across different urban areas and size ranges. The major PM sources associated with these chemical species include residual/fuel oil combustion, traffic emissions, and secondary organic aerosol formation, indicating that these sources are major drivers of PM-induced oxidative potential. Moreover, comparison of ROS activity levels across different seasons indicated that photochemical aging increases the intrinsic oxidative potential of airborne PM.

Seasonal and spatial variation in dithiothreitol (DTT) activity of quasi-ultrafine particles in the Los Angeles Basin and its association with chemical species.

A year-long sampling campaign of quasi-ultrafine particles (dp < 0.25 µm) was conducted at 10 distinct sites representing source, urban and/or near-freeway, rural receptor and desert locations across the Los Angeles air basin. Redox activity of the PM samples was measured by means of the Dithiothreitol (DTT) assay and detailed chemical analysis was performed to measure the concentrations of chemical species. DTT activity per unit air volume and unit PM mass (expressed in nmol min(-1) m(-3) and nmol/min/µg PM, respectively) showed similar trends across sites and seasons. DTT activity was generally higher during cold seasons (winter and fall) compared to warm seasons (summer and spring). Noticeable peaks were observed at urban near-freeway locations representing "source" sites impacted by fresh traffic emissions. Regression analysis indicated strong association (R > 0.7) between the DTT activity and the concentrations of carbonaceous species (OC, EC, WSOC and WIOC) across all seasons and strong winter-time correlations with organic tracers of primary vehicular emissions including polycyclic aromatic hydrocarbons (PAHs), alkanes, hopanes and steranes. Strong correlations were also observed, particularly during winter, between DTT activity and transition metals (e.g., Cr, Mn, V, Fe, Cu, Cd and Zn), which share similar vehicular sources with primary organics. A multivariate linear regression analysis indicated that the variability in DTT activity is best explained by the variability in concentrations of WSOC, WIOC, EC and hopanes. Combined contributions from these species explained 88% of the DTT activity. The appearance of WSOC as a typical tracer of secondary organic aerosol, along with EC, WIOC and hopanes, all markers of emissions from primary combustion sources, emphasizes the contributions of both primary and secondary sources to the overall oxidative potential of quasi-ultrafine particles. Supplemental materials are available for this article. Go to the publisher's online edition of the Journal of Environmental Science and Health, Part A, to view the supplemental file.

Increased biomass burning due to the economic crisis in Greece and its adverse impact on wintertime air quality in Thessaloniki.

The recent economic crisis in Greece resulted in a serious wintertime air pollution episode in Thessaloniki. This air quality deterioration was mostly due to the increased price of fuel oil, conventionally used as a source of energy for domestic heating, which encouraged the residents to burn the less expensive wood/biomass during the cold season. A wintertime sampling campaign for fine particles (PM2.5) was conducted in Thessaloniki during the winters of 2012 and 2013 in an effort to quantify the extent to which the ambient air was impacted by the increased wood smoke emissions. The results indicated a 30% increase in the PM2.5 mass concentration as well as a 2-5-fold increase in the concentration of wood smoke tracers, including potassium, levoglucosan, mannosan, and galactosan. The concentrations of fuel oil tracers (e.g., Ni and V), on the other hand, declined by 20-30% during 2013 compared with 2012. Moreover, a distinct diurnal variation was observed for wood smoke tracers, with significantly higher concentrations in the evening period compared with the morning. Correlation analysis indicated a strong association between reactive oxygen species (ROS) activity and the concentrations of levoglucosan, galactosan, and potassium, underscoring the potential impact of wood smoke on PM-induced toxicity during the winter months in Thessaloniki.

Chemical characterization and source apportionment of fine and coarse particulate matter inside the refectory of Santa Maria Delle Grazie Church, home of Leonardo Da Vinci's "Last Supper".

The association between exposure to indoor particulate matter (PM) and damage to cultural assets has been of primary relevance to museum conservators. PM-induced damage to the "Last Supper" painting, one of Leonardo da Vinci's most famous artworks, has been a major concern, given the location of this masterpiece inside a refectory in the city center of Milan, one of Europe's most polluted cities. To assess this risk, a one-year sampling campaign was conducted at indoor and outdoor sites of the painting's location, where time-integrated fine and coarse PM (PM(2.5) and PM(2.5-10)) samples were simultaneously collected. Findings showed that PM(2.5) and PM(2.5-10) concentrations were reduced indoors by 88 and 94% on a yearly average basis, respectively. This large reduction is mainly attributed to the efficacy of the deployed ventilation system in removing particles. Furthermore, PM(2.5) dominated indoor particle levels, with organic matter as the most abundant species. Next, the chemical mass balance model was applied to apportion primary and secondary sources to monthly indoor fine organic carbon (OC) and PM mass. Results revealed that gasoline vehicles, urban soil, and wood-smoke only contributed to an annual average of 11.2 ± 3.7% of OC mass. Tracers for these major sources had minimal infiltration factors. On the other hand, fatty acids and squalane had high indoor-to-outdoor concentration ratios with fatty acids showing a good correlation with indoor OC, implying a common indoor source.

Diurnal trends in coarse particulate matter composition in the Los Angeles Basin.

To investigate the diurnal profile of the concentration and composition of ambient coarse particles, three sampling sites were set up in the Los Angeles Basin to collect coarse particulate matter (CPM) in four different time periods of the day (morning, midday, afternoon and overnight) in summer and winter. The samples were analyzed for total and water-soluble elements, inorganic ions and water-soluble organic carbon (WSOC). In summer, highest concentrations of CPM gravimetric mass, mineral and road dust, and WSOC were observed in midday and afternoon, when the prevailing onshore wind was stronger. In general, atmospheric dilution was lower in winter, contributing to the accumulation of air pollutants during stagnation conditions. Turbulences induced by traffic become a significant particle re-suspension mechanism, particularly during winter night time, when mixing height was lowest. This is evident by the high levels of CPM mass, mineral and road dust in winter overnight at the near-freeway sites located in urban Los Angeles, and to a lesser extent in Riverside. WSOC levels were higher in summer, with a similar diurnal profile with mineral and road dust, indicating that they either share common sources, or that WSOC may be adsorbed or absorbed onto the surfaces of these dust particles. In general, the contribution of inorganic ions to CPM mass was greater in the overnight sampling period at all sampling sites, suggesting that the prevailing meteorological conditions (lower temperature and higher relative humidity) favor the formation of these ions in the coarse mode. Nitrate, the most abundant CPM-bound inorganic species in this basin, is found to be predominantly formed by reactions with sea salt particles in summer. When the sea salt concentrations were low, the reaction with mineral dust particles and the condensation of ammonium nitrate on CPM surfaces also contributes to the formation of nitrate in the coarse mode.

Comparison of carcinogen, carbon monoxide, and ultrafine particle emissions from narghile waterpipe and cigarette smoking: Sidestream smoke measurements and assessment of second-hand smoke emission factors.

The lack of scientific evidence on the constituents, properties, and health effects of second-hand waterpipe smoke has fueled controversy over whether public smoking bans should include the waterpipe. The purpose of this study was to investigate and compare emissions of ultrafine particles (UFP, <100 nm), carcinogenic polyaromatic hydrocarbons (PAH), volatile aldehydes, and carbon monoxide (CO) for cigarettes and narghile (shisha, hookah) waterpipes. These smoke constituents are associated with a variety of cancers, and heart and pulmonary diseases, and span the volatility range found in tobacco smoke.Sidestream cigarette and waterpipe smoke was captured and aged in a 1 m(3) Teflon-coated chamber operating at 1.5 air changes per hour (ACH). The chamber was characterized for particle mass and number surface deposition rates. UFP and CO concentrations were measured online using a fast particle spectrometer (TSI 3090 Engine Exhaust Particle Sizer), and an indoor air quality monitor. Particulate PAH and gaseous volatile aldehydes were captured on glass fiber filters and DNPH-coated SPE cartridges, respectively, and analyzed off-line using GC-MS and HPLC-MS. PAH compounds quantified were the 5- and 6-ring compounds of the EPA priority list. Measured aldehydes consisted of formaldehyde, acetaldehyde, acrolein, methacrolein, and propionaldehyde.We found that a single waterpipe use session emits in the sidestream smoke approximately four times the carcinogenic PAH, four times the volatile aldehydes, and 30 times the CO of a single cigarette. Accounting for exhaled mainstream smoke, and given a habitual smoker smoking rate of 2 cigarettes per hour, during a typical one-hour waterpipe use session a waterpipe smoker likely generates ambient carcinogens and toxicants equivalent to 2-10 cigarette smokers, depending on the compound in question. There is therefore good reason to include waterpipe tobacco smoking in public smoking bans.

Nrf2-related gene expression and exposure to traffic-related air pollution in elderly subjects with cardiovascular disease: An exploratory panel study.

Gene expression changes are linked to air pollutant exposures in in vitro and animal experiments. However, limited data are available on how these outcomes relate to ambient air pollutant exposures in humans. We performed an exploratory analysis testing whether gene expression levels were associated with air pollution exposures in a Los Angeles area cohort of elderly subjects with coronary artery disease. Candidate genes (35) were selected from published studies of gene expression-pollutant associations. Expression levels were measured weekly in 43 subjects (≤ 12 weeks) using quantitative PCR. Exposures included gaseous pollutants O3, nitrogen oxides (NOx), and CO; particulate matter (PM) pollutants elemental and black carbon (EC, BC); and size-fractionated PM mass. We measured organic compounds from PM filter extracts, including polycyclic aromatic hydrocarbons (PAHs), and determined the in vitro oxidative potential of particle extracts. Associations between exposures and gene expression levels were analyzed using mixed-effects regression models. We found positive associations of traffic-related pollutants (EC, BC, primary organic carbon, PM 0.25-2.5 PAH and/or PM 0.25 PAH, and NOx) with NFE2L2, Nrf2-mediated genes (HMOX1, NQO1, and SOD2), CYP1B1, IL1B, and SELP. Findings suggest that NFE2L2 gene expression links associations of traffic-related air pollution with phase I and II enzyme genes at the promoter transcription level.

Effect of exposure to atmospheric ultrafine particles on production of free fatty acids and lipid metabolites in the mouse small intestine.

BACKGROUND: Exposure to ambient ultrafine particulate matter (UFP) is a well-recognized risk factor for cardiovascular and respiratory diseases. However, little is known about the effects of air pollution on gastrointestinal disorders. OBJECTIVE: We sought to assess whether exposure to ambient UFP (diameter < 180 nm) increased free fatty acids and lipid metabolites in the mouse small intestine. METHODS: Ldlr-null mice were exposed to filtered air (FA) or UFP collected at an urban Los Angeles, California, site that was heavily affected by vehicular emissions; the exposure was carried out for 10 weeks in the presence or absence of D-4F, an apolipoprotein A-I mimetic peptide with antioxidant and anti-inflammation properties on a high-fat or normal chow diet. RESULTS: Compared with FA, exposure to UFP significantly increased intestinal hydroxyeicosatetraenoic acids (HETEs), including 15-HETE, 12-HETE, 5-HETE, as well as hydroxyoctadecadienoic acids (HODEs), including 13-HODE and 9-HODE. Arachidonic acid (AA) and prostaglandin D2 (PGD2) as well as some of the lysophosphatidic acids (LPA) in the small intestine were also increased in response to UFP exposure. Administration of D-4F significantly reduced UFP-mediated increase in HETEs, HODEs, AA, PGD2, and LPA. Although exposure to UFP further led to shortened villus length accompanied by prominent macrophage and neutrophil infiltration into the intestinal villi, administration of D-4F mitigated macrophage infiltration. CONCLUSIONS: Exposure to UFP promotes lipid metabolism, villus shortening, and inflammatory responses in mouse small intestine, whereas administration of D-4F attenuated these effects. Our findings provide a basis to further assess the mechanisms underlying UFP-mediated lipid metabolism in the digestive system with clinical relevance to gut homeostasis and diseases.

Toxicity of aged gasoline exhaust particles to normal and diseased airway epithelia.

Particulate matter (PM) pollution is a leading cause of premature death, particularly in those with pre-existing lung disease. A causative link between particle properties and adverse health effects remains unestablished mainly due to complex and variable physico-chemical PM parameters. Controlled laboratory experiments are required. Generating atmospherically realistic aerosols and performing cell-exposure studies at relevant particle-doses are challenging. Here we examine gasoline-exhaust particle toxicity from a Euro-5 passenger car in a uniquely realistic exposure scenario, combining a smog chamber simulating atmospheric ageing, an aerosol enrichment system varying particle number concentration independent of particle chemistry, and an aerosol deposition chamber physiologically delivering particles on air-liquid interface (ALI) cultures reproducing normal and susceptible health status. Gasoline-exhaust is an important PM source with largely unknown health effects. We investigated acute responses of fully-differentiated normal, distressed (antibiotics-treated) normal, and cystic fibrosis human bronchial epithelia (HBE), and a proliferating, single-cell type bronchial epithelial cell-line (BEAS-2B). We show that a single, short-term exposure to realistic doses of atmospherically-aged gasoline-exhaust particles impairs epithelial key-defence mechanisms, rendering it more vulnerable to subsequent hazards. We establish dose-response curves at realistic particle-concentration levels. Significant differences between cell models suggest the use of fully-differentiated HBE is most appropriate in future toxicity studies.

Long-term source apportionment of ambient fine particulate matter (PM2.5) in the Los Angeles Basin: a focus on emissions reduction from vehicular sources.

Positive Matrix Factorization (PMF) was utilized to quantify sources of ambient PM2.5 in central Los Angeles (LA) and Rubidoux, using the Speciation Trends Network data, collected between 2002 and 2013. Vehicular emissions (including gasoline and diesel vehicles) were the second major contributor to PM2.5, following secondary aerosols, with about 20% contribution to total mass in both sites. Starting in 2007, several major federal, state, and local regulations on vehicular emissions were implemented. To assess the effect of these regulations, daily-resolved vehicular source contributions from 2002 to 2006 were pooled together and compared to the combination of 2008 to 2012 datasets. Compared to the 2002-2006 dataset, the median values of vehicular emissions in 2008-2012 statistically significantly decreased by 24 and 21% in LA and Rubidoux, respectively. These reductions were noted despite an overall increase or similarity in the median values of the daily flow of vehicles after 2007, at the sites.

Human brain derived cells respond in a type-specific manner after exposure to urban particulate matter (PM).

Exposure to particulate matter (PM), a component of urban air pollution, may cause adverse effects in the brain. Although the exact mechanisms involved are unknown, both oxidative and inflammatory responses have been reported. Since the main route of exposure to particulate matter is through inhalation, there is a potential for compounds to directly enter the brain and alter normal cellular function. Enhancement in both oxidative stress and neuroinflammatory markers has been observed in neurodegenerative disorders and PM-induced potentiation of these events may accelerate the disease process. The objective of this pilot study was to use normal human brain cells, a model system which has not been previously used, to assess cell-type-specific responses after exposure to ultrafine particles (UFP). Human microglia, neurons, and astrocytes were grown separately or as co-cultures and then exposed to aqueous UFP suspensions. Reactive Oxygen Species (ROS) formation and the proinflammatory cytokine tumor necrosis factor alpha (TNF-α) were measured as markers of oxidative stress or inflammation respectively. Our results revealed that after exposure to 2 µg/ml of particles, normal human neurons exhibit a decrease in ROS formation and an increase in TNF-α. The observed decrease in ROS formation persisted in the presence of glial cells, which contrasts previous studies done in rodent cells reporting that PM-induced microglial activation modulates neuronal responses. Our study indicates that human CNS cells may respond differently compared to rodent cells and that their use may be more predictive in risk assessment.

Dust episodes in Beirut and their effect on the chemical composition of coarse and fine particulate matter.

Particles captured during dust episodes in Beirut originated from both the African and Arabian deserts. This particular air mixture showed an increase, over non-dust episodes, in particle volume distribution which was mostly noticed for particles ranging in sizes between 2.25 and 5 µm. It also resulted in an increase in average mass concentration by 48.5% and 14.6%, for the coarse and fine fractions, respectively. Chemical analysis of major aerosol components accounted for 93% of fine PM and 71% of coarse PM. Crustal material (CM) dominated the coarse PM fraction, contributing to 39 ± 15% of the total mass. Sea salt (SS) (11 ± 10%) and secondary ions (SI) (11 ± 7%) were the second most abundant elements. In the fine fraction, SI (36 ± 14%) were the most abundant PM constituent, followed by organic matter (OM) (33 ± 7%) and CM (13 ± 2%). Enrichment factors (EF) and correlation coefficients show that biogenic and anthropogenic sources contribute to the elemental composition of particles during dust episodes. This study emphasizes on the role played by the long-range transport of aerosols in changing the chemical composition of the organic and inorganic constituents of urban coarse and fine PM. The chemical reactions between aged urban and dust aerosols are enhanced during transport, leading to the formation of organo-nitrogenated and -sulfonated compounds. Their oligomeric morphologies are further confirmed by SEM-EDX measurements.

Chemical characterization and source apportionment of indoor and outdoor fine particulate matter (PM(2.5)) in retirement communities of the Los Angeles Basin.

Concurrent indoor and outdoor measurements of fine particulate matter (PM2.5) were conducted at three retirement homes in the Los Angeles Basin during two separate phases (cold and warm) between 2005 and 2006. Indoor-to-outdoor relationships of PM2.5 chemical constituents were determined and sources of indoor and outdoor PM2.5 were evaluated using a molecular marker-based chemical mass balance (MM-CMB) model. Indoor levels of elemental carbon (EC) along with metals and trace elements were found to be significantly affected by outdoor sources. EC, in particular, displayed very high indoor-to-outdoor (I/O) mass ratios accompanied by strong I/O correlations, illustrating the significant impact of outdoor sources on indoor levels of EC. Similarly, indoor levels of polycyclic aromatic hydrocarbons (PAHs), hopanes, and steranes were strongly correlated with their outdoor components and displayed I/O ratios close to unity. On the other hand, concentrations of n-alkanes and organic acids inside the retirement communities were dominated by indoor sources (e.g. food cooking and consumer products), as indicated by their I/O ratios, which exceeded unity. Source apportionment results revealed that vehicular emissions were the major contributor to both indoor and outdoor PM2.5, accounting for 39 and 46% of total mass, respectively. Moreover, the contribution of vehicular sources to indoor levels was generally comparable to its corresponding outdoor estimate. Other water-insoluble organic matter (other WIOM), which accounts for emissions from uncharacterized primary biogenic sources, displayed a wider range of contributions, varying from 2 to 73% of PM2.5, across all sites and phases of the study. Lastly, higher indoor than outdoor contribution of other water-soluble organic matter (other WSOM) was evident at some of the sites, suggesting the production of secondary aerosols as well as direct emissions from primary sources (including cleaning or other consumer products) at the indoor environments.

Oxidative potential and chemical speciation of size-resolved particulate matter (PM) at near-freeway and urban background sites in the greater Beirut area.

To assess particle oxidative potential in the greater Beirut area, size-resolved PM10-2.5, PM2.5-0.25 and PM0.25 samples were collected at near-freeway and urban background sites. Metals and trace elements, including Mn, Cr, Cu, Ba, Mo and Sb, displayed increased levels and crustal enrichment factors at the roadway, indicating their vehicular origin. These elements in addition to Co, V, Ni and Zn were mostly distributed in PM2.5-0.25 and PM0.25 at both sites, with moderate-to-high water-solubility (>30%). The presence of these metals, mainly air toxics, in small size ranges constitutes an added health risk. Of particular concern are elements with strong correlations (R ≥ 0.70) with reactive oxygen species (ROS)-activity, measured by a cellular assay. In PM10-2.5, road dust component Mn and soil-related element Co were highly correlated with ROS-activity. In PM2.5-0.25, vehicular abrasion element Cu and soil-derived component Co were highly associated with ROS-activity. In PM0.25, V and Ni, originating from fuel oil combustion, strongly correlated with ROS formation. ROS-activity displayed a particle-size dependency, with lowest activity associated with PM10-2.5. On a per air volume basis, size-resolved ROS-activity was 1.5-2.8 times greater at the roadside than background location, indicating that exposure to redox-active species may be greatest near the freeway. Size-fractionated PM intrinsic activity (i.e. PM mass-normalized) was comparable at both sites, possibly suggesting a similarity in the sources of ROS-active species. Relative to other urban settings, while the intrinsic redox activity of PM10-2.5 in Beirut is comparable to that measured at an urban site in Los Angeles (LA), its PM0.25-induced ROS-activity is ~2.3-fold greater. Moreover, the intrinsic ROS-activity of ambient PM2.5 in Beirut is comparable to that reported in Milan-Italy, but 3.1-times PM2.5 activity in the heavily-polluted Lahore-Pakistan. Lastly, findings suggest a dominant role of transition metals in generating ROS compared to organic carbon in the LA area.

Particulate metals and organic compounds from electronic and tobacco-containing cigarettes: comparison of emission rates and secondhand exposure.

In recent years, electronic cigarettes have gained increasing popularity as alternatives to normal (tobacco-containing) cigarettes. In the present study, particles generated by e-cigarettes and normal cigarettes have been analyzed and the degree of exposure to different chemical agents and their emission rates were quantified. Despite the 10-fold decrease in the total exposure to particulate elements in e-cigarettes compared to normal cigarettes, specific metals (e.g. Ni and Ag) still displayed a higher emission rate from e-cigarettes. Further analysis indicated that the contribution of e-liquid to the emission of these metals is rather minimal, implying that they likely originate from other components of the e-cigarette device or other indoor sources. Organic species had lower emission rates during e-cigarette consumption compared to normal cigarettes. Of particular note was the non-detectable emission of polycyclic aromatic hydrocarbons (PAHs) from e-cigarettes, while substantial emission of these species was observed from normal cigarettes. Overall, with the exception of Ni, Zn, and Ag, the consumption of e-cigarettes resulted in a remarkable decrease in secondhand exposure to all metals and organic compounds. Implementing quality control protocols on the manufacture of e-cigarettes would further minimize the emission of metals from these devices and improve their safety and associated health effects.

Seasonal and spatial variation of trace elements and metals in quasi-ultrafine (PM0.25) particles in the Los Angeles metropolitan area and characterization of their sources.

Year-long sampling campaign of quasi-ultrafine particles (PM0.25) was conducted at 10 distinct locations across the Los Angeles south coast air basin and concentrations of trace elements and metals were quantified at each site using high-resolution inductively coupled plasma sector field mass spectrometry. In order to characterize sources of trace elements and metals, principal component analysis (PCA) was applied to the dataset. The major sources were identified as road dust (influenced by vehicular emissions as well as re-suspended soil), vehicular abrasion, residual oil combustion, cadmium sources and metal plating. These sources altogether accounted for approximately 85% of the total variance of quasi-ultrafine elemental content. The concentrations of elements originating from source and urban locations generally displayed a decline as we proceeded from the coast to the inland. Occasional concentration peaks in the rural receptor sites were also observed, driven by the dominant westerly/southwesterly wind transporting the particles to the receptor areas.

Seasonal and spatial variability in chemical composition and mass closure of ambient ultrafine particles in the megacity of Los Angeles.

Emerging toxicological research has shown that ultrafine particles (UFP, dp < 0.1­0.2 µm) may be more potent than coarse or fine particulate matter. To better characterize quasi-UFP (PM0.25, dp < 0.25 µm), we conducted a year-long sampling campaign at 10 distinct areas in the megacity of Los Angeles, including source, near-freeway, semi-rural receptor and desert-like locations. Average PM0.25 mass concentration ranged from 5.9 to 16.1 µg m−3 across the basin and over different seasons. Wintertime levels were highest at the source site, while lowest at the desert-like site. Conversely, summertime concentrations peaked at the inland receptor locations. Chemical mass reconstruction revealed that quasi-UFP in the basin consisted of 49­64% organic matter, 3­6.4% elemental carbon, 9­15% secondary ions (SI), 0.7­1.3% trace ions, and 5.7­17% crustal material and trace elements, on a yearly average basis. Organic carbon (OC), a major constituent of PM0.25, exhibited greatest concentrations in fall and winter at all sites, with the exception of the inland areas. Atmospheric stability conditions and particle formation favored by condensation of low-volatility organics contributed to these levels. Inland, OC concentrations peaked in summer due to increased PM0.25 advection from upwind sources coupled with secondary organic aerosol formation. Among SI, nitrate peaked at semi-rural Riverside sites, located downwind of strong ammonia sources. Moreover, ionic balance indicated an overall neutral quasi-UFP aerosol, with somewhat lower degree of neutralization at near-freeway sites in winter. Anthropogenic metals peaked at the urban sites in winter while generally increased at the receptor areas in summer. Lastly, coefficients of divergence analysis showed that while PM0.25 mass is relatively spatially homogeneous in the basin, some of its components, mainly EC, nitrate and several toxic metals, are unevenly distributed. These results suggest that population exposure to quasi-UFP can substantially vary by season and over short spatial scales in the megacity of Los Angeles.

Mitochondrial genetic background modifies the relationship between traffic-related air pollution exposure and systemic biomarkers of inflammation.

BACKGROUND: Mitochondria are the main source of reactive oxygen species (ROS). Human mitochondrial haplogroups are linked to differences in ROS production and oxidative-stress induced inflammation that may influence disease pathogenesis, including coronary artery disease (CAD). We previously showed that traffic-related air pollutants were associated with biomarkers of systemic inflammation in a cohort panel of subjects with CAD in the Los Angeles air basin. OBJECTIVE: We tested whether air pollutant exposure-associated inflammation was stronger in mitochondrial haplogroup H than U (high versus low ROS production) in this panel (38 subjects and 417 observations). METHODS: Inflammation biomarkers were measured weekly in each subject (≤ 12 weeks), including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), C-reactive protein, interleukin-6 soluble receptor and tumor necrosis factor-soluble receptor II. We determined haplogroup by restriction fragment length polymorphism analysis. Air pollutants included nitrogen oxides (NOx), carbon monoxide (CO), organic carbon, elemental and black carbon (EC, BC); and particulate matter mass, three size fractions (<0.25 µm, 0.25-2.5 µm, and 2.5-10 µm in aerodynamic diameter). Particulate matter extracts were analyzed for organic compounds, including polycyclic aromatic hydrocarbons (PAH), and in vitro oxidative potential of aqueous extracts. Associations between exposures and biomarkers, stratified by haplogroup, were analyzed by mixed-effects models. RESULTS: IL-6 and TNF-α were associated with traffic-related air pollutants (BC, CO, NOx and PAH), and with mass and oxidative potential of quasi-ultrafine particles <0.25 µm. These associations were stronger for haplogroup H than haplogroup U. CONCLUSIONS: Results suggest that mitochondrial haplogroup U is a novel protective factor for air pollution-related systemic inflammation in this small group of subjects.