Size-fractionated Particulate Matter Research Articles

Chemical characterization of selected metals by X-ray fluorescence method in particulate matter collected in the area of Krakow, Poland

This study presents the results of year long (2007–2008) particulate matter collecting campaigns. The three particle size fractions of particulate matter were collected in Krakow, Poland. Fine fraction consists of particles of a diameter below 2.5 µm, medium is between 2.5 and 8 µm and coarse fraction contains particles above 8 µm. Elemental concentrations were evaluated for each sample. Following elements were measured by EDXRF method: K, Ca, Ti, Cr, Mn, Fe, Cu, Zn, Br, and Pb. During each sampling campaign meteorological parameters such as temperature, wind speed, wind direction, humidity were taken from the same place. The highest values of mass particulate matter showed results from January 2008 and April 2008. These were about 14 µg/m 3 for fine fraction, 8 µg/m 3 for medium and 16 µg/m 3 for coarse fraction. The lowest values were observed in May 2007, they were 4, 6, 6 µg/m 3, respectively. During the winter season the wind speed was low and particulate matter remained in the air in high concentrations. In May 2007 the speed of wind was higher, reaching 2–3 m/s. PM was blown away from the city from the direction of N–W. Measured concentrations of elements were low, they were below permissible values specified by EU. The coarse fraction concentrations of Ca, Mn, and Fe were higher and characterized by the same trend. These samples were collected when the wind speed was low and its direction was from south-east. As concentrations of Cr, Cu, and Zn were low, these elements did not come from the south-east direction of Krakow. Concentration of Br correlates to the concentration of Pb. It suggests that they came from the same source (vehicles fuels burning).

The Adjuvant Effect of Ambient Particulate Matter Is Closely Reflected by the Particulate Oxidant Potential

The Adjuvant Effect of Ambient Particulate Matter Is Closely Reflected by the Particulate Oxidant Potential

Airborne Particulate Matter and Human Health: Toxicological Assessment and Importance of Size and Composition of Particles for Oxidative Damage and Carcinogenic Mechanisms

Air pollution has been considered a hazard to human health. In the past decades, many studies highlighted the role of ambient airborne particulate matter (PM) as an important environmental pollutant for many different cardiopulmonary diseases and lung cancer. Numerous epidemiological studies in the past 30 years found a strong exposure-response relationship between PM for short-term effects (premature mortality, hospital admissions) and long-term or cumulative health effects (morbidity, lung cancer, cardiovascular and cardiopulmonary diseases, etc). Current research on airborne particle-induced health effects investigates the critical characteristics of particulate matter that determine their biological effects. Several independent groups of investigators have shown that the size of the airborne particles and their surface area determine the potential to elicit inflammatory injury, oxidative damage, and other biological effects. These effects are stronger for fine and ultrafine particles because they can penetrate deeper into the airways of the respiratory tract and can reach the alveoli in which 50% are retained in the lung parenchyma. Composition of the PM varies greatly and depends on many factors. The major components of PM are transition metals, ions (sulfate, nitrate), organic compound, quinoid stable radicals of carbonaceous material, minerals, reactive gases, and materials of biologic origin. Results from toxicological research have shown that PM have several mechanisms of adverse cellular effects, such as cytotoxicity through oxidative stress mechanisms, oxygen-free radical-generating activity, DNA oxidative damage, mutagenicity, and stimulation of proinflammatory factors. In this review, the results of the most recent epidemiological and toxicological studies are summarized. In general, the evaluation of most of these studies shows that the smaller the size of PM the higher the toxicity through mechanisms of oxidative stress and inflammation. Some studies showed that the extractable organic compounds (a variety of chemicals with mutagenic and cytotoxic properties) contribute to various mechanisms of cytotoxicity; in addition, the water-soluble faction (mainly transition metals with redox potential) play an important role in the initiation of oxidative DNA damage and membrane lipid peroxidation. Associations between chemical compositions and particle toxicity tend to be stronger for the fine and ultrafine PM size fractions. Vehicular exhaust particles are found to be most responsible for small-sized airborne PM air pollution in urban areas. With these aspects in mind, future research should aim at establishing a cleared picture of the cytotoxic and carcinogenic mechanisms of PM in the lungs, as well as mechanisms of formation during internal engine combustion processes and other sources of airborne fine particles of air pollution.

Hydrodynamic Separation of Particulate Matter Transported by Source Area Runoff

Hydrodynamic separation is a preliminary unit operation frequently utilized in wastewater and more recently in storm water for separation of coarse particulate matter (PM) and gross solids. In order to examine the behavior and separation mechanisms of a screened hydrodynamic separator (HS) not influenced by scour, this study examined the event-based performance of an empty-bed (clean sump and volute) HS for PM fractions transported in eight runoff events from a 1,088 m2 paved source area urban watershed. Influent particle-size distributions (PSDs) { d50 m from 270 to 2,202 μm } and HS particle separation efficiency (PSE) (from 38 to 70% of mass) exhibited variations influenced by hydrology and previous loadings. When examined as PM size fractions, results demonstrate separation of the sediment fraction (>75 μm) ranging from 76 to 94% while for settleable and suspended (1–25 μm) fractions, the PSE was variable and significantly lower; from 3 to 57% and 2 to 43%, respectively. Results demonstrate a correlat...

Elemental analysis of size-fractionated particulate matter sampled in Göteborg, Sweden

The aim of the study was to investigate the mass distribution of trace elements in aerosol samples collected in the urban area of Göteborg, Sweden, with special focus on the impact of different air masses and anthropogenic activities. Three measurement campaigns were conducted during December 2006 and January 2007. A PIXE cascade impactor was used to collect particulate matter in 9 size fractions ranging from 16 to 0.06 µm aerodynamic diameter. Polished quartz carriers were chosen as collection substrates for the subsequent direct analysis by TXRF. To investigate the sources of the analyzed air masses, backward trajectories were calculated. Our results showed that diurnal sampling was sufficient to investigate the mass distribution for Br, Ca, Cl, Cu, Fe, K, Sr and Zn, whereas a 5-day sampling period resulted in additional information on mass distribution for Cr and S. Unimodal mass distributions were found in the study area for the elements Ca, Cl, Fe and Zn, whereas the distributions for Br, Cu, Cr, K, Ni and S were bimodal, indicating high temperature processes as source of the submicron particle components. The measurement period including the New Year firework activities showed both an extensive increase in concentrations as well as a shift to the submicron range for K and Sr, elements that are typically found in fireworks. Further research is required to validate the quantification of trace elements directly collected on sample carriers.

Comparisons of commuter's exposure to particulate matters while using different transportation modes

This study compared commuters' exposures to particulate matter (PM) while using motorcycles, cars, buses, and the mass rapid transit (MRT) on the same routes in Taipei, Taiwan. Motorcycle commuters who had the shortest travel time (28.4 ± 4.2 min) were exposed to the highest concentrations of PM 10 (112.8 ± 38.3 μg/m 3), PM 2.5 (67.5 ± 31.3 μg/m 3), and PM 1.0 (48.4 ± 24.7 μg/m 3) among four commuting modes. By contrast, car commuters were exposed to the lowest PM concentrations and had the second shortest travel time among them. Motorcycle commuters' high trip-averaged PM concentrations and bus commuters' long commuting time (43.1 ± 5.1 min) resulted in their high whole-trip PM exposures. Size fractions of PM were relatively consistent across PM exposures of the four commuting modes with fine particles (PM 2.5) contributing to 53–60% of PM 10 and submicron particle (PM 1) contributing to 39–43% of PM 10. Motorcycles idled at traffic lights and bus doors opened at stops increased commuters' PM exposures. Fixed-site monitoring data explained well the variation of whole-trip PM 10 exposure of car ( r 2 = 0.63) and MRT ( r 2 = 0.52) commuters, and of whole-trip PM 2.5 exposure of car ( r 2 = 0.76), MRT ( r 2 = 0.73) and motorcycle ( r 2 = 0.64) commuters in regression analyses. The coefficients (slopes) of regression between fixed-site monitoring data and PM 2.5 exposures were less than 1 for car and MRT commuters but greater than 1 for motorcycle commuters. In conclusion, proximity to traffic emissions contributes to a person's high PM exposure during his or her daily commute. This proximity occurs when people use motorcycles on roads and when bus/MRT commuters walk or wait along commuting routes. Fixed-site air monitoring data can under-estimate motorcycle commuters' PM 2.5 exposures but over-estimate car and MRT commuters' PM 2.5 exposures.

Contribution of nitrated polycyclic aromatic hydrocarbons to the mutagenicity of ultrafine particles in the roadside atmosphere

This is the first report of the quantification of nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) in ultrafine particles in the roadside atmosphere and their contribution to the direct-acting mutagenicity of ultrafine particles. The detailed size distributions of six nitro-PAHs (2-nitrofluoranthene, 1-nitropyrene, 6-nitrobenzo[a]pyrene, 1,3-dinitropyrene, 1,6-dinitropyrene, and 1,8-dinitropyrene) were measured by highly sensitive gas chromatography–negative ion chemical ionization tandem mass spectrometry. Direct-acting mutagenicity of size-fractionated particulate matter (PM) was determined by the Ames test using Salmonella typhimurium strains TA98 and YG1024. The amounts of nitro-PAHs per unit mass of ultrafine particles (<0.12 μm) were significantly higher than those of accumulation mode particles (0.12–2.1 μm) and of coarse particles (>2.1 μm). Therefore, more than 20% of each nitro-PAH, with the exception of 2-nitrofluoranthene, was observed in the ultrafine particle fraction, although the contribution of ultrafine particles to the total PM mass in the roadside atmosphere was only 2.3%. Also, in both tester strains TA98 and YG1024, the mutagenicity per unit mass of ultrafine particles was significantly higher than those of accumulation mode particles or coarse particles. The contributions of 2-nitrofluoranthene, 1-nitropyrene, 1,3-dinitropyrene, 1,6-dinitropyrene, and 1,8-dinitropyrene to the direct-acting mutagenicity of ultrafine particles were 0.56, 1.5, 0.57, 2.2, and 9.2%, respectively, in the TA98 strain, and 0.54, 1.1, 0.71, 5.0, and 17%, respectively, in the YG1024 strain, while the contribution of 6-nitrobenzo[a]pyrene was less than 0.01% in both strains. 1,8-Dinitropyrene was the largest contributor to the mutagenicity not only of ultrafine particles but also of accumulation mode particles in both strains. Only five nitro-PAHs accounted for as much as 14 and 24% of the direct-acting mutagenicity of ultrafine particles in the roadside atmosphere in the TA98 strain and the YG1024 strain, respectively. This result indicated that nitro-PAHs, especially 1,8-dinitropyrene, were important contributors to the high direct-acting mutagenicity of ultrafine particles in the roadside atmosphere.

Personal coarse particulate matter exposures in an adult cohort

Volunteers associated with the North Carolina Adult Asthma and Environment Study (NCAAES) participated in an investigation of personal daily exposures to coarse and fine particulate matter size fractions (PM 10–2.5, PM 2.5). Data from these personal measurements were then compared to community-based measures that might typically represent surrogate measurements of exposure often used in epidemiological assessments. To determine personal exposures to various particulate matter (PM) size fractions, a recently evaluated personal PM monitor capable of direct PM 10–2.5 size fraction collection was used. Participants living in the central region of North Carolina and enrolled in the NCAAES were asked to wear the monitor attached to a supporting backpack for 24-h collection periods. These volunteers were monitored for 2 to 4 days with subsequent gravimetric analysis of their PM samples. Personal PM 10–2.5 mass concentrations were observed to be highly variable and ranged from 7.6 to 40.2 μg/m 3 over an 8-month period. The median for this measurement from all participants (50th percentile) was 13.7 μg/m 3. A coefficient of determination ( r 2) of 0.02 was established for community-based PM 10–2.5 mass concentrations versus personal exposures. Similar coefficients established for PM 2.5 mass revealed only a modest improvement in agreement ( r 2 = 0.12). Data from the exposure findings are reported here.

Circulating Biomarkers of Inflammation, Antioxidant Activity, and Platelet Activation Are Associated with Primary Combustion Aerosols in Subjects with Coronary Artery Disease

BackgroundBiomarkers of systemic inflammation have been associated with risk of cardiovascular morbidity and mortality.ObjectivesWe aimed to clarify associations of particulate matter (PM) air pollution with systemic inflammation using models based on size-fractionated PM mass and markers of primary and secondary aerosols.MethodsWe followed a panel of 29 nonsmoking elderly subjects with a history of coronary artery disease (CAD) living in retirement communities in the Los Angeles, California, air basin. Blood plasma biomarkers were measured weekly over 12 weeks and included C-reactive protein (CRP), fibrinogen, tumor necrosis factor-α (TNF-α) and its soluble receptor-II (sTNF-RII), interleukin-6 (IL-6) and its soluble receptor (IL-6sR), fibrin D-dimer, soluble platelet selectin (sP-selectin), soluble vascular cell adhesion molecule-1 (sVCAM-1), intracellular adhesion molecule-1 (sICAM-1), and myeloperoxidase (MPO). To assess changes in antioxidant capacity, we assayed erythrocyte lysates for glutathione peroxidase-1 (GPx-1) and copper-zinc superoxide dismutase (Cu,Zn-SOD) activities. We measured indoor and outdoor home daily size-fractionated PM mass, and hourly pollutant gases, total particle number (PN), fine PM elemental carbon (EC) and organic carbon (OC), estimated secondary organic aerosol (SOA) and primary OC (OCpri) from total OC, and black carbon (BC). We analyzed data with mixed models controlling for temperature and excluding weeks with infections.ResultsWe found significant positive associations for CRP, IL-6, sTNF-RII, and sP-selectin with outdoor and/or indoor concentrations of quasi-ultrafine PM ≤ 0.25 μm in diameter, EC, OCpri, BC, PN, carbon monoxide, and nitrogen dioxide from the current-day and multiday averages. We found consistent positive but largely nonsignificant coefficients for TNF-α, sVCAM-1, and sICAM-1, but not fibrinogen, IL-6sR, or D-dimer. We found inverse associations for erythrocyte Cu,Zn-SOD with these pollutants and other PM size fractions (0.25–2.5 and 2.5–10 μm). Inverse associations of GPx-1 and MPO with pollutants were largely nonsignificant. Indoor associations were often stronger for estimated indoor EC, OCpri, and PN of outdoor origin than for uncharacterized indoor measurements. There was no evidence for positive associations with SOA.ConclusionsResults suggest that traffic emission sources of OCpri and quasi-ultrafine particles lead to increased systemic inflammation and platelet activation and decreased antioxidant enzyme activity in elderly people with CAD.

Intra-community spatial variation of size-fractionated PM mass, OC, EC, and trace elements in the Long Beach, CA area

Local traffic patterns and proximity to pollution sources are important in assessing particulate matter (PM) exposure in urban communities. This study investigated the intra-community spatial variation of PM in an urban area impacted by numerous local and regional sources. Weekly size-segregated (<0.25, 0.25–2.5, and >2.5 μm) PM samples were collected in the winter of 2005. During each 1-week sampling cycle, data were collected concurrently at four sites within four miles of one another in the Long Beach, CA area. Coefficients of divergence analyses for size-fractionated PM mass, organic and elemental carbon, sulfur, and 18 other metals and trace elements suggest a wide range of spatial divergence. High spatial variability was observed in the <0.25 μm and 0.25–2.5 μm PM fractions for many elements associated with motor vehicle emissions. Relatively lower spatial divergence was observed in the coarse fraction, although road dust components were spatially diverse but highly correlated with each other. Mass and OC concentrations were homogeneously distributed over the sampling sites. Possible oil combustion sources were identified using previously documented markers such as vanadium and nickel and by distinguishing between primary sulfur and secondary sulfate contributions. This study shows that, although PM mass in different size fractions is spatially homogeneous within a community, the spatial distribution of some elemental components can be heterogeneous. This is evidence for the argument that epidemiological studies using only PM mass concentrations from central sites may not accurately assess exposure to toxicologically relevant PM components.

Source Apportionment of Particulate Matter in the U.S. and Associations with Lung Inflammatory Markers

Size-fractionated particulate matter (PM) samples were collected from six U.S. cities and chemically analyzed as part of the Multiple Air Pollutant Study. Particles were administered to cultured lung cells and the production of three different proinflammatory markers was measured to explore the association between the health effect markers and PM. Ultrafine, fine, and coarse PM samples were collected between December 2003 and May 2004 over a 4-wk period in each city. Filters were pooled for each city and the PM samples were extracted then analyzed for trace metals, ions, and elemental carbon. Particle extracts were applied to cultured human primary airway epithelial cells, and the secreted levels of interleukin-8 (IL-8), heme oxygenase-1, and cyclooxygenase-2 were measured 1 and 24 h following exposure. Fine PM sources were quantified by the chemical mass balance (CMB) model. The relationship between toxicological measures, PM sources, and individual species were evaluated using linear regression. Ultrafine and fine PM mass were associated with increases in IL-8 (r2 = .80 for ultrafine and r2 = .52 for fine). Sources of fine PM and their relative contributions varied across the sampling sites and a strong linear association was observed between IL-8 and secondary sulfate from coal combustion (r2 = .79). Ultrafine vanadium, lead, copper, and sulfate were also associated with increases in IL-8. Increases in inflammatory markers were not observed for coarse PM mass and source markers. These findings suggest that certain PM size fractions and sources are associated with markers of lung injury or inflammation.

Ambient Air Particulate Matter Exposure and Tissue Factor Expression in Atherosclerosis

Recent studies have suggested a link between inhaled particulate matter (PM) exposure and atherogenesis. We investigated tissue factor (TF) expression with ambient fine particulate matter (diameter < 2.5 μ m, PM2.5) exposure and in response to in vitro exposure to fine and ultrafine PM in cultured human bronchial epithelial cells, vascular smooth muscle cells (hSMCs), and monocytes. ApoE−/− mice, fed with normal chow (NC) or high-fat chow (HFC), were exposed to concentrated PM2.5 or filtered air (FA) for 6 mo (6 h/day, 5 day/wk, n = 28). Following in vivo ultrasound bio-microscopy (UBM) assessment of plaque area, macrophage infiltration (CD68) and TF expression in the aorta were quantified. Cultured cells were incubated with size-fractionated PM from cascade impactors, or with standard reference PM material (SRM, number 1649a) and assayed for TF protein, mRNA, and activity. UBM-derived plaque areas were 7 ± 1% larger in the PM2.5-HFC than the FA-HFC group (p = .04), but not significantly different between the PM2.5-NC and FA-NC groups (p = .07). Immunohistochemistry revealed increased TF (15 ± 3% vs. 8 ± 2%, p < .01) and macrophage infiltration (19 ± 2% vs. 14 ± 3%, p < .01) in the plaques of PM2.5-HFC compared with FA-HFC groups. Impactor-collected PM2.5 and ultrafine particles consistently increased TF protein in bronchial epithelial cells, monocytes, and hSMCs. TF mRNA expression increased rapidly (within 1 h) in response to SRM PM. We conclude that in vivo and in vitro exposure to ambient air PM2.5 induces TF expression.

Relationship between redox activity and chemical speciation of size-fractionated particulate matter

BackgroundAlthough the mechanisms of airborne particulate matter (PM) related health effects remain incompletely understood, one emerging hypothesis is that these adverse effects derive from oxidative stress, initiated by the formation of reactive oxygen species (ROS) within affected cells. Typically, ROS are formed in cells through the reduction of oxygen by biological reducing agents, with the catalytic assistance of electron transfer enzymes and redox active chemical species such as redox active organic chemicals and metals. The purpose of this study was to relate the electron transfer ability, or redox activity, of the PM samples to their content in polycyclic aromatic hydrocarbons and various inorganic species. The redox activity of the samples has been shown to correlate with the induction of the stress protein, hemeoxygenase-1.ResultsSize-fractionated (i.e. < 0.15; < 2.5 and 2.5 – 10 μm in diameter) ambient PM samples were collected from four different locations in the period from June 2003 to July 2005, and were chemically analyzed for elemental and organic carbon, ions, elements and trace metals and polycyclic aromatic hydrocarbons. The redox activity of the samples was evaluated by means of the dithiothreitol activity assay and was related to their chemical speciation by means of correlation analysis. Our analysis indicated a higher redox activity on a per PM mass basis for ultrafine (< 0.15 μm) particles compared to those of larger sizes. The PM redox activity was highly correlated with the organic carbon (OC) content of PM as well as the mass fractions of species such as polycyclic aromatic hydrocarbons (PAH), and selected metals.ConclusionThe results of this work demonstrate the utility of the dithiothreitol assay for quantitatively assessing the redox potential of airborne particulate matter from a wide range of sources. Studies to characterize the redox activity of PM from various sources throughout the Los Angeles basin are currently underway.

Spatial variability of particulates in homes: Implications for infant exposure

Personal monitoring of particulate matter (PM) exposure in infants is difficult. Indirect, microenvironment modelling methods are more practical. Infants spend most of their time indoors at home and the aim of this study was to investigate spatial variations in PM concentrations within homes. Three size fractions of PM - particles with an aerodynamic diameter of less than 10 microm (PM(10)), less than 2.5 microm (PM(2.5)) and total suspended particulates (TSP) - were monitored in the homes of 77 infants (0-2 years) using a multi-stage virtual impactor. In all homes PM was monitored simultaneously in the main living room at heights of 1.4 m and 0.2 m from the floor. In 26 of these homes monitoring was also conducted simultaneously in the infant's bedroom. Further, PM(10) was measured simultaneously in the living room, bedroom and child's cot in 14 homes using a real-time photometer. All homes in the study were non-smoking households. On average, there were no significant differences between concentrations of any of the different PM size fractions measured at the two heights (living room) and between living room and bedroom concentrations. However, there were only moderate correlations in concentrations between the different microenvironments and in some homes there was considerable variation between sampling sites. From the real-time measurements there seemed to be good agreement between concentrations measured in different rooms and in the cot and short-term peak concentrations at one sampling site were often mirrored at other sites. These results suggest that, although large variations in PM concentrations between rooms within homes can occur, a single monitoring station can provide a reasonable estimate of indoor concentrations.

A Comparison of Studies on the Effects of Controlled Exposure to Fine, Coarse and Ultrafine Ambient Particulate Matter from a Single Location

Particle size has been implicated by epidemiological and toxicological studies as an important determinant of the toxicity of ambient particulate matter (PM). In an effort to characterize the cardiovascular, hematological and pulmonary effects of different PM size fractions in humans, we have conducted controlled human exposures of normal volunteers to ultrafine-, fine- and coarse- fraction PM concentrated from ambient air in Chapel Hill, North Carolina. Healthy non-smoking male and female subjects between the ages of 18 and 35 participated in these studies. Exposures were undertaken with the use of particle concentrators fitted with size-selective outlets. These devices are capable of generating concentration factors between 10- and 20-fold over ambient levels. Cardiovascular endpoints measured include heart rate variability and T-wave alternans, as well as pulmonary function parameters. Subjects underwent bronchoscopy and bronchoalveolar lavage 18 hrs following exposure to PM or to clean air. Lavage fluids and blood samples were assayed for a battery of markers of hematological, cytotoxic and inflammatory injury. The design of these studies permits direct comparison of the effects of concentrated ambient PM as a function of particle size. The data to be presented reveal modest size fraction-dependent effects of concentrated PM exposure on cardiovascular, pulmonary and hematological parameters in normal adult human subjects. These findings have relevant implications for the design of future chamber studies and the role of particle size fraction in the adverse health effects of PM exposure in humans.

Particulate matter properties and health effects: consistency of epidemiological and toxicological studies

Identifying the ambient particulate matter (PM) fractions or constituents, critically involved in eliciting adverse health effects, is crucial to the implementation of more cost-efficient abatement strategies to improve air quality. This review focuses on the importance of different particle properties for PM-induced effects, and whether there is consistency in the results from epidemiological and experimental studies. An evident problem for such comparisons is that epidemiological and experimental data on the effects of specific components of ambient PM are limited. Despite this, some conclusions can be drawn. With respect to the importance of the PM size-fractions, experimental and epidemiological studies are somewhat conflicting, but there seems to be a certain consistency in that the coarse fraction (PM10-2.5) has an effect that should not be neglected. Better exposure characterization may improve the consistency between the results from experimental and epidemiological studies, in particular for ultrafine particles. Experimental data indicate that surface area is an important metric, but composition may play an even greater role in eliciting effects. The consistency between epidemiological and experimental findings for specific PM-components appears most convincing for metals, which seem to be important for the development of both pulmonary and cardiovascular disease. Metals may also be involved in PM-induced allergic sensitization, but the epidemiological evidence for this is scarce. Soluble organic compounds appear to be implicated in PM-induced allergy and cancer, but the data from epidemiological studies are insufficient for any conclusions. The present review suggests that there may be a need for improvements in research designs. In particular, there is a need for better exposure assessments in epidemiological investigations, whereas experimental data would benefit from an improved comparability of studies. Combined experimental and epidemiological investigations may also help answer some of the unresolved issues.

Temporal variability of stable carbon and nitrogen isotopic composition of size-fractionated particulate organic matter in the hypertrophic Sumida River Estuary of Tokyo Bay, Japan

To clarify the major factors that control stable carbon and nitrogen isotopic compositions (δ 13C and δ 15N) of suspended particulate organic matter in a hypertrophic estuary, seasonal variation in concentrations and stable isotopic compositions of particulate organic carbon and nitrogen (POC, PN), chlorophyll a content (Chl) and dry weight of suspended solid (SS) was studied in the Sumida River estuary of Tokyo Bay. Particulate material was fractioned into four size-fractions (3–20, 20–53, 53–250, 250–1000 μm). At the lower-estuarine (LE) site, the finer size fraction (<20 μm) was predominant (>80% Chl) during the autumnal bloom (Aug–Sep 2003). The middle size fractions (20–53 and 53–250 μm) however increased during the spring bloom (50–80% Chl; Feb–Apr 2004), reflecting difference in taxonomic composition of phytoplankton. At the upper-estuarine and the riverine sites, the <20 μm fraction was most abundant throughout the survey period. δ 13C POC and δ 15N PN varied between −32 and −16‰ and between −8 and +12‰, respectively. Relationships of δ 13C POC with POC/Chl and POC/PN ratios could be explained by assuming two end members: allochthonous (terrestrial) POC with a δ 13C close to −26.5‰, and autochthonous (planktonic) POC whose δ 13C was variable and apparently correlated with δ 13C of ambient DIC (−10 to 0‰) and phytoplankton abundance (Chl). δ 15N PN was apparently controlled by water temperature and NH 4 + concentration. The variability of δ 13C and δ 15N was different between size fractions: the apparent dependence of δ 13C on Chl as well as that of δ 15N on water temperature was significantly stronger for the middle size fractions (mainly diatoms) than the finer fraction (mainly microflagellates), suggesting different physiological response between taxa. The second objective of this study was to evaluate contribution of terrestrial organic carbon (TPOC) to the POC size fractions by using δ 13C of isolated chlorophyll a at LE site as surrogate for the autochthonous δ 13C end member. During the autumnal bloom, TPOC was 23–36% on average for the middle size fractions (20–53 and 53–250 μm), and ≥59% for the finest (3–20 μm) and coarsest (250–1000 μm) fractions. During the spring bloom, the average contribution of TPOC was generally low (≤21%) except for the finest fraction (36%). Negative correlation between salinity and calculated TPOC suggested that transport of terrestrial organic carbon to this estuary was controlled principally by the river discharge.

Mutagenic Activity of Atmospheric Ultrafine Particles at a Roadside Site and a Suburban Site

The mutagenic activity of size-fractionated atmospheric particulate matter (PM) was investigated at both a roadside site and a suburban site in Saitama, Japan. Sampling was carried out using a low-pressure cascade impactor between January and February 2005. The mutagenic activity of the size-fractionated PM was determined by the Ames test using Salmonella typhimurium strain TA98 without metabolic activation (S9). Most of the mutagenic activity was found in the fine particle fraction (< 2.1 µm) at both sites. There was almost no difference in the contribution of fine particles to the mutagenic activity of total PM between the two sites. On the other hand, there was a clear difference in the contribution of ultrafine particles (< 0.12 µm) to the mutagenic activity between the two sites. At the suburban site, ultrafine particles accounted for 5.7% of the mutagenic activity of total PM. In contrast, at the roadside site, ultrafine particles contributed as much as 12% to the mutagenic activity of total PM, although their contribution to the total PM mass was only 2.3%. Moreover, the mutagenic activity per unit air volume in the ultrafine particle fraction at the roadside site (1.2 revertants/m 3 ) was 3.1-fold higher than that at the suburban site (0.38 revertants/m 3 ), although the activity in the fine particle fraction at the roadside site was only 1.4-fold higher than that at the suburban site. These results indicated that, with regard to mutagenicity, the health risk due to ultrafine particles is relatively high at roadside areas.

Oxidative stress-induced DNA damage by particulate air pollution

Exposure to ambient air particulate matter (PM) is associated with pulmonary and cardiovascular diseases and cancer. The mechanisms of PM-induced health effects are believed to involve inflammation and oxidative stress. The oxidative stress mediated by PM may arise from direct generation of reactive oxygen species from the surface of particles, soluble compounds such as transition metals or organic compounds, altered function of mitochondria or NADPH-oxidase, and activation of inflammatory cells capable of generating ROS and reactive nitrogen species. Resulting oxidative DNA damage may be implicated in cancer risk and may serve as marker for oxidative stress relevant for other ailments caused by particulate air pollution. There is overwhelming evidence from animal experimental models, cell culture experiments, and cell free systems that exposure to diesel exhaust and diesel exhaust particles causes oxidative DNA damage. Similarly, various preparations of ambient air PM induce oxidative DNA damage in in vitro systems, whereas in vivo studies are scarce. Studies with various model/surrogate particle preparations, such as carbon black, suggest that the surface area is the most important determinant of effect for ultrafine particles (diameter less than 100 nm), whereas chemical composition may be more important for larger particles. The knowledge concerning mechanisms of action of PM has prompted the use of markers of oxidative stress and DNA damage for human biomonitoring in relation to ambient air. By means of personal monitoring and biomarkers a few studies have attempted to characterize individual exposure, explore mechanisms and identify significant sources to size fractions of ambient air PM with respect to relevant biological effects. In these studies guanine oxidation in DNA has been correlated with exposure to PM 2.5 and ultrafine particles outdoor and indoor. Oxidative stress-induced DNA damage appears to an important mechanism of action of urban particulate air pollution. Related biomarkers and personal monitoring may be useful tools for risk characterization.

Potential Role of Ultrafine Particles in Associations between Airborne Particle Mass and Cardiovascular Health

Numerous epidemiologic time-series studies have shown generally consistent associations of cardiovascular hospital admissions and mortality with outdoor air pollution, particularly mass concentrations of particulate matter (PM) ≤2.5 or ≤10 μm in diameter (PM2.5, PM10). Panel studies with repeated measures have supported the time-series results showing associations between PM and risk of cardiac ischemia and arrhythmias, increased blood pressure, decreased heart rate variability, and increased circulating markers of inflammation and thrombosis. The causal components driving the PM associations remain to be identified. Epidemiologic data using pollutant gases and particle characteristics such as particle number concentration and elemental carbon have provided indirect evidence that products of fossil fuel combustion are important. Ultrafine particles < 0.1 μm (UFPs) dominate particle number concentrations and surface area and are therefore capable of carrying large concentrations of adsorbed or condensed toxic air pollutants. It is likely that redox-active components in UFPs from fossil fuel combustion reach cardiovascular target sites. High UFP exposures may lead to systemic inflammation through oxidative stress responses to reactive oxygen species and thereby promote the progression of atherosclerosis and precipitate acute cardiovascular responses ranging from increased blood pressure to myocardial infarction. The next steps in epidemiologic research are to identify more clearly the putative PM casual components and size fractions linked to their sources. To advance this, we discuss in a companion article (Sioutas C, Delfino RJ, Singh M. 2005. Environ Health Perspect 113:947–955) the need for and methods of UFP exposure assessment.