Abstract  It has been well documented that pollution and dust from east Asia can be transported across the North Pacific basin, reaching North America and beyond. In this study, we assess the transpacific transport of ``pollution aerosol' (defined as a mixture of aerosols from urban/industrial pollution and biomass burning) by taking advantage of the much improved measurement accuracy and enhanced new capabilities of satellite sensors in recent years. A 4-year (2002 to 2005) climatology of optical depth for pollution aerosol was generated from Moderate Resolution Imaging Spectroradiometer (MODIS) observations of fine- and coarse-mode aerosol optical depths. The pollution aerosol mass loading and fluxes were then calculated using measurements of the dependence of aerosol mass extinction efficiency on relative humidity and of aerosol vertical distributions from field campaigns and available satellite observations in the region. We estimated that about 18 Tg/a pollution aerosol is exported from east Asia to the northwestern Pacific Ocean, of which about 25% reaches the west coast of North America. The imported flux of 4.4 Tg/a to North America is equivalent to about 15% of local emissions from the United States and Canada. The pollution fluxes are largest in spring and smallest in summer. For the period we have examined the strongest export and import of pollution particulates occurred in 2003, largely because of record intense Eurasia boreal forest fires in spring and summer. The overall uncertainty of pollution fluxes is estimated at a factor of 2. Simulations by the Goddard Chemistry Aerosol Radiation and Transport (GOCART) and Global Modeling Initiative (GMI) models agree quite well with the satellite-based estimates of annual and latitude-integrated fluxes, with larger model-satellite differences in latitudinal and seasonal variations of fluxes.

Abstract  Several epidemiological studies have linked particulate matter exposure to numerous adverse health effects on the respiratory, cardiovascular, and reproductive systems (Braga et al., 1999; Zanobetti et al., 2000; Anderson et al., 2001; Farhat et al., 2005). More recently, ambient levels of black carbon were associated to impaired cognitive function in children (Suglia et al., 2008), suggesting that the central nervous system (CNS) may be a target of air pollutants. The present study was conducted to (a) determine whether chronic residual oil fly ash (ROFA) exposure promotes behavioral changes and lipid peroxidation in rat brain areas, and (b) determine whether N-acetylcysteine (NAC), a general antioxidant, prevents these effects. Forty-five-day-old male Wistar rats were exposed or not to ROFA by intranasal instillation and were treated or not with NAC (150 mg/kg) ip for 30 days. One day later, rats were submitted to the open field test to evaluate the motor/exploratory activities and emotionality followed by decapitation. Striatum and cerebellum were dissected to determine lipid peroxidation by the accumulation of thiobarbituric acid-reactive substances (TBARS). ROFA instillation induced an increase in lipid peroxidation level in striatum (p = .033) and cerebellum (p = .030), as compared with the control group. NAC treatment blocked these changes. ROFA promoted a decrease in the frequency of peripheral walking (p = .006) and a decrease in exploration (p = .001), which were not blocked by N-acetylcysteine. The present study provides evidence that toxic particles, administered by the respiratory route, induce oxidative stress in structures of the central nervous system, as well as behavioral alterations. The administration of NAC reduces lipid peroxidation at the striatum and cerebellum levels, but does not influence behavioral disturbances.

Abstract  Nanoparticles can be administered via nasal, oral, intraocular, intratracheal (pulmonary toxicity), tail vein and other routes. Here, we focus on the time-dependent translocation and potential damage of TiO(2) nanoparticles on central nervous system (CNS) through intranasal instillation. Size and structural properties are important to assess biological effects of TiO(2) nanoparticles. In present study, female mice were intranasally instilled with two types of well-characterized TiO(2) nanoparticles (i.e. 80 nm, rutile and 155 nm, anatase; purity>99%) every other day. Pure water instilled mice were served as controls. The brain tissues were collected and evaluated for accumulation and distribution of TiO(2), histopathology, oxidative stress, and inflammatory markers at post-instillation time points of 2, 10, 20 and 30 days. The titanium contents in the sub-brain regions including olfactory bulb, cerebral cortex, hippocampus, and cerebellum were determined by inductively coupled plasma mass spectrometry (ICP-MS). Results indicated that the instilled TiO(2) directly entered the brain through olfactory bulb in the whole exposure period, especially deposited in the hippocampus region. After exposure for 30 days, the pathological changes were observed in the hippocampus and olfactory bulb using Nissl staining and transmission electron microscope. The oxidative damage expressed as lipid peroxidation increased significantly, in particular in the exposed group of anatase TiO(2) particles at 30 days postexposure. Exposure to anatase TiO(2) particles also produced higher inflammation responses, in association with the significantly increased tumor necrosis factor alpha (TNF-alpha) and interleukin (IL-1 beta) levels. We conclude that subtle differences in responses to anatase TiO(2) particles versus the rutile ones could be related to crystal structure. Thus, based on these results, rutile ultrafine-TiO(2) particles are expected to have a little lower risk potential for producing adverse effects on central nervous system. Although understanding the mechanisms requires further investigation, the present results suggest that we should pay attention to potential risk of occupational exposure for large-scaled production of TiO(2) nanoparticles.

Abstract  Animal studies have shown exposure to diesel exhaust particles (DEPs) to induce production of reactive oxygen species (ROSs) and increase levels of 8-hydroxydeoxyquanosine (8-OHdG). Controversial results have been obtained regarding the effects of workplace exposure on urinary 8-OHdG level. This study assessed concentrations of environmental PM(2.5) in DEP (DEP(2.5)), personal DEP(2.5) and urinary 8-OHdG of diesel engine exhaust emission inspector (inspector) at a diesel vehicle emission inspection station (inspection station). The analysis specifically focuses on the factors that influence inspector urinary 8-OHdG. Repeated-measures study design was used to sample for five consecutive days. A total of 25 environmental PM(2.5) measurements were analyzed at 5 different locations by using a dichotomous sampler, and a total of 55 personal PM(2.5) measurements were analyzed from inspectors by using PM(2.5) personal sampler. During the sampling period, a total of 110 pre- and post-work urine samples from inspectors, and 32 samples from the control group were collected. Following age and sex matching between the inspectors and the control group, levels of urinary 8-OHdG were analyzed. Environmental and personal concentrations of DEP(2.5) were 107.25+/-39.76 (mean+/-SD) and 155.96+/-75.70 microg/m(3), respectively. Also, the concentration of urinary 8-OHdG differed significantly between inspector and control non-smokers, averaging 14.05+/-12.71 and 6.58+/-4.39 microg/g creatinine, respectively. Additionally, urinary 8-OHdG concentrations were associated with diesel exposure after controlling for smoking and cooking at home. Compared with the control group, the inspector displayed significantly increased levels of urinary 8-OHdG. Diesel exhaust is the single pollutant involved in the exposure of DEP(2.5) at the inspection station, as confirmed by the final results.

Abstract  This paper describes a number of global regulations dealing with very fine ambient particulate matter, PM2.5 and PM10 and the measurements aspects of PM2.5 emission measurement methods for stationary sources, particularly of dilution techniques that promote simulation of atmospheric transformation of stack gases allowing for the use of the resulting near-ambient emission data in source apportionment and health risk studies, along with the current progress on international standardization of source PM2.5 measurement methods.

Abstract  ABSTRACT: BACKGROUND: The island factor of the cities of Las Palmas de Gran Canaria and Santa Cruz de Tenerife, along with their proximity to Africa and their meteorology, create a particular setting that influences the air quality of these cities and provides researchers an opportunity to analyze the acute effects of air-pollutants on daily mortality. METHODS: From 2000 to 2004, the relationship between daily changes in PM10, PM2.5, SO2, NO2, CO, and ozone levels and daily total mortality and mortality due to respiratory and heart diseases were assessed using Generalized Additive Poisson models controlled for potential confounders. The lag effect (up to five days) as well as the concurrent and previous day averages and distributed lag models were all estimated. Single and two pollutant models were also constructed. RESULTS: Daily levels of PM10, PM2.5, NO2, and SO2 were found to be associated with an increase in respiratory mortality in Santa Cruz de Tenerife and with increased heart disease mortality in Las Palmas de Gran Canaria, thus indicating an association between daily ozone levels and mortality from heart diseases. The effects spread over five successive days. SO2 was the only air pollutant significantly related with total mortality (lag 0). CONCLUSIONS: There is a short-term association between current exposure levels to air pollution and mortality (total as well as that due specifically to heart and respiratory diseases) in both cities. Risk coefficients were higher for respiratory and cardiovascular mortality, showing a delayed effect over several days.

Abstract  This Staff Paper, prepared by staff in the U.S. Environmental Protection Agency's (EPA) Office of Air Quality Planning and Standards (OAQPS), evaluates the policy implications of the key studies and scientific information contained in the document, Air Quality Criteria for Particulate Matter (EPA, 2004; henceforth referred to as the Criteria Document (CD) and cited as CD), prepared by EPA's National Center for Environmental Assessment (NCEA). This Staff Paper also presents and interprets results from staff analyses (e.g., air quality analyses, human health risk assessments, and visibility analyses) that staff believes should be considered in EPA's current review of the national ambient air quality standards (NAAQS) for particulate matter (PM). Finally, this Staff Paper presents staff conclusions and recommendations as to potential revisions of the primary (health-based) and secondary (welfare-based) PM NAAQS, based on consideration of the available scientific information and analyses and related limitations and uncertainties.

Abstract  Multipollutant models are frequently used to differentiate roles of multiple pollutants in epidemiologic studies of ambient air pollution. In the presence of differing levels of measurement error across pollutants under consideration, however, they can be biased and as misleading as single-pollutant models. Their appropriate interpretation depends on the relationships among the pollutant measurements and the outcomes in question. In situations where two or more pollutant variables may be acting as surrogates for the etiologic agent(s), multipollutant models can help identify the best surrogate, but the risk estimates may be influenced by inclusion of a second variable that is not itself an independent risk factor for the outcome in question. In this paper, these issues will be illustrated in the context of an ongoing study of emergency visits in Atlanta. Emergency department visits from 41 of 42 hospitals serving the twenty-county Atlanta metropolitan area for the period 1993-2004 (n=10,206,389 visits) were studied in relation to ambient pollutant levels, including speciated particle measurements from an intensive monitoring campaign at a downtown station starting in 1998. Relative to our earlier publications, reporting results through 2000, the period for which the speciated data are now available is now tripled (six years in length). Poisson generalized linear models were used to examine outcome counts in relation to three-day moving average concentrations of pollutants of a priori interest (ozone, nitrogen dioxide, carbon monoxide, sulfur dioxide, oxygenated hydrocarbons, PM10, coarse PM, PM2.5, and the following components of PM2.5: elemental carbon, organic carbon, sulfate, water-soluble transition metals.) In the present analysis, we report results for two outcome groups: a respiratory outcomes group and a cardiovascular outcomes group. For cardiovascular visits, associations were observed with CO, 3 NO2, and PM2.5 elemental carbon and organic carbon. In multipollutant models, CO was the strongest predictor. For respiratory visits, associations were observed with ozone, PM10, CO and NO2 in single-pollutant models. In multipollutant models, PM10 and ozone persisted as predictors, with ozone the stronger predictor. Caveats and considerations in interpreting the multipollutant model results are discussed.

Abstract  The æroad-to-ambientÆ evolution of particle number distributions near the 405 and 710 freeways in Los Angeles, California, in both summer and winter, were analyzed and then simulated by a multi-component sectional aerosol dynamic model. Condensation/evaporation and dilution were demonstrated to be the major mechanisms in altering aerosol size distribution, while coagulation and deposition play minor roles. Seasonal effects were significant with winters generally less dynamic than summers. A large number of particles grew into the >10 nm range around 30û90 m downwind of the freeways. Beyond 90 m some shrink to <10 nm range and some continued growing to >100 nm as a result of competition between partial pressure and vapor pressure. Particle compositions probably change dramatically as components adapt to decreasing gas-phase concentration due to dilution, so number distribution evolution is also an evolution of composition. As a result, people who live within about 90 m of roadways are exposed to particle sizes and compositions that others are not.

Abstract  This article describes the governing equations, computational algorithms, and other components entering into the Community Multiscale Air Quality (CMAQ) modeling system. This system has been designed to approach air quality as a whole by including state-of-the-science capabilities for modeling multiple air quality issues, including tropospheric ozone, fine particles, acid deposition, and visibility degradation. CMAQ was also designed to have multiscale capabilities so that separate models were not needed for urban and regional scale air quality modeling. By making CMAQ a modeling system that addresses multiple pollutants and different spatial scales, it has a "one-atmosphere" perspective that combines the efforts of the scientific community. To implement multiscale capabilities in CMAQ, several issues (such as scalable atmospheric dynamics and generalized coordinates), which depend on the desired model resolution, are addressed. A set of governing equations for compressible nonhydrostatic atmospheres is available to better resolve atmospheric dynamics at smaller scales. Because CMAQ is designed to handle scale-dependent meteorological formulations and a large amount of flexibility, its governing equations are expressed in a generalized coordinate system. This approach ensures consistency between CMAQ and the meteorological modeling system. The generalized coordinate system determines the necessary grid and coordinate transformations, and it can accommodate various vertical coordinates and map projections. The CMAQ modeling system simulates various chemical and physical processes that are thought to be important for understanding atmospheric trace gas transformations and distributions. The modeling system contains three types of modeling components (Models-3): a meteorological modeling system for the description of atmospheric states and motions, emission models for man-made and natural emissions that are injected into the atmosphere, and a chemistry-transport modeling system for simulation of the chemical transformation and fate. The chemical transport model includes the following process modules: horizontal advection, vertical advection, mass conservation adjustments for advection processes, horizontal diffusion, vertical diffusion, gas-phase chemical reactions and solvers, photolytic rate computation, aqueous-phase reactions and cloud mixing, aerosol dynamics, size distributions and chemistry, plume chemistry effects, and gas and aerosol deposition velocity estimation. This paper describes the Models-3 CMAQ system, its governing equations, important science algorithms, and a few application examples.

Abstract  Land use regression (LUR) is a promising technique for predicting ambient air pollutant concentrations at high spatial resolution. We expand on previous work by modeling oxides of nitrogen and fine particulate matter in Vancouver, Canada, using two measures of traffic. Systematic review of historical data identified optimal sampling periods for NO and NO2. Integrated 14-day mean concentrations were measured with passive samplers at 116 sites in the spring and fall of 2003. Study estimates for annual mean NO and NO2 ranged from 5.4-98.7 and 4.8-28.0 ppb, respectively. Regulatory measurements ranged from 4.8-29.7 and 9.0-24.1 ppb and exhibited less spatial variability. Measurements of particle mass concentration (PM2.5) and light absorbance (ABS) were made at a subset of 25 sites during another campaign. Fifty-five variables describing each sampling site were generated in a Geographic Information System (GIS) and linear regression models for NO, NO2, PM2.5, and ABS were built with the most predictive covariates. Adjusted R 2 values ranged from 0.39 to 0.62 and were similar across traffic metrics. Resulting maps show the distribution of NO to be more heterogeneous than that of NO2, supporting the usefulness of this approach for assessing spatial patterns of traffic-related pollution.

Abstract  Few studies have addressed associations between traffic-related air pollution and respiratory disease in young children. The present authors assessed the development of asthmatic/allergic symptoms and respiratory infections during the first 4 yrs of life in a birth cohort study (n = approximately 4,000). Outdoor concentrations of traffic-related air pollutants (nitrogen dioxide PM(2.5), particles with a 50% cut-off aerodynamic diameter of 2.5 mum and soot) were assigned to birthplace home addresses with a land-use regression model. They were linked by logistic regression to questionnaire data on doctor-diagnosed asthma, bronchitis, influenza and eczema and to self-reported wheeze, dry night-time cough, ear/nose/throat infections and skin rash. Total and specific immunoglobulin (Ig)E to common allergens were measured in a subgroup (n = 713). Adjusted odds ratios (95% confidence intervals) per interquartile pollution range were elevated for wheeze (1.2 (1.0-1.4) for soot), doctor-diagnosed asthma (1.3 (1.0-1.7)), ear/nose/throat infections (1.2 (1.0-1.3)) and flu/serious colds (1.2 (1.0-1.4)). No consistent associations were observed for other end-points. Positive associations between air pollution and specific sensitisation to common food allergens (1.6 (1.2-2.2) for soot), but not total IgE, were found in the subgroup with IgE measurements. Traffic-related pollution was associated with respiratory infections and some measures of asthma and allergy during the first 4 yrs of life.

Abstract  The American Cancer Society (ACS) Study and its reanalysis are built upon in order to examine the impact of scale on the observed relationship between sulfates and mortality. The limitations of the original ACS Study (Pope et al., 1995) and the reanalysis of this study (Krewski et al., 2000) are discussed; while the latter dealt with some issues in using ecological data, it did not address scale. Next, the article outlines the county-scale study, the methods used to aggregate data, and the two-stage analysis used to derive relative risk (RR). Finally, the results of working at the county scale are compared with those obtained by the reanalysis team using larger metropolitan areas. Less than half of the cohort used in the metropolitan study were used at the county scale because of the limited availability of sulfate monitors and because five-digit ZIP codes more accurately assigned individuals to geographical areas. Therefore, the county data should be considered as new and not as a reorganization of the original data set. The reanalysis and the county studies should be considered as two separate studies that took different scales as their basic organizing principle. The RR of all-cause mortality from sulfate exposure at the county scale was 1.50 (1.30, 1.73) compared with 1.25 (1.13, 1.37) at the metropolitan scale; for cardiopulmonary mortality, the RR was 1.75 (1.48, 2.08) at the county scale compared with 1.29 (1.15, 1.46) at the metropolitan scale. Because lung cancer mortality was low in some counties, the two-stage random effects model became unstable. At the county scale, the RR from sulfates was more robust to the inclusion of ecologic covariates. Other place-specific ecologic covariates were either insignificant or barely significant (with a lower 95% confidence limit near 0.99 or 1.00) when included in the two-stage regression model for all-cause mortality with sulfates. Moreover, no ecologic covariate changed the RR of all-cause mortality from sulfates by 25% or more. Both population change and unemployment rate affected the RR for cardiopulmonary mortality from sulfate exposure by 25% or more in the county-scale analysis. However, when these two variables were entered into a multiple covariate analysis, the RR from sulfates decreased but remained strongly significant. Sulfur dioxide was not an important covariate at the county scale. Thus, at the county scale, long-term exposure to sulfates appears to be more strongly associated with increased risk of all-cause and cardiopulmonary mortality than previously indicated by the ACS study and its reanalysis.

Abstract  Background Airborne particulate matter (PM) is an important factor associated with the enhanced prevalence of respiratory allergy. The PM adjuvant activity on allergic sensitization is a possible mechanism of action involved, and the induction of airway inflammation is suggested to be of importance in PM-induced adjuvant activity. Objective Because differently sized PM have different toxic potentials, we studied the role of particle size in the induction of airway inflammation and allergic sensitization. This was done using fine (0.250 and 0.260 μm) and ultrafine (0.029 and 0.014 μm) titanium dioxide (TiO2) and carbon black particles (CBP) with known differences in airway toxicity. Methods Mice were intranasally exposed to ovalbumin (OVA) alone or in combination with one of the different particles. The induction of airway inflammation and the immune adjuvant activity were studied in the lungs and lung-draining peribronchial lymph nodes (PBLN) at day 8. OVA-specific antibodies were measured at day 21, and the development of allergic airway inflammation was studied after OVA challenges (day 28). Results When administered at the same total particle mass (200 μg), exposure to ultrafine TiO2 and CBP-induced airway inflammation, and had immune adjuvant activity. The latter was shown by increasing both the PBLN cell numbers and the production of OVA-specific T-helper type 2 (Th2) cytokines (IL-4, IL-5, IL-10 and IL-13). Whereas OVA-specific IgE and IgG1 levels in serum were only increased in animals exposed to the ultrafine TiO2, allergic airway inflammation could be detected in both ultrafine TiO2-and CBP-treated groups after challenges with OVA. Conclusion Our data show that only the ultrafine particles, with a small diameter and a large total surface area/mass, cause airway inflammation and have immune adjuvant activity in the current model supporting the hypothesis that particle toxicity is site-dependent and related to adjuvant activity.

Abstract  We use the fractional aerosol optical depth (AOD) values derived from Multiangle Imaging Spectroradiometer (MISR) aerosol component measurements, along with aerosol transport model constraints, to estimate ground-level concentrations of fine particulate matter (PM2.5) mass and its major constituents in the continental United States. Regression models using fractional AODs predict PM2.5 mass and sulfate (SO4) concentrations in both the eastern and western United States, and nitrate (NO3) concentrations in the western United States reasonably well, compared with the available ground-level U.S. Environment Protection Agency (EPA) measurements. These models show substantially improved predictive power when compared with similar models using total-column AOD as a single predictor, especially in the western United States. The relative contributions of the MISR aerosol components in these regression models are used to estimate size distributions of EPA PM2.5 species. This method captures the overall shapes of the size distributions of PM2.5 mass and SO4 particles in the east and west, and NO3 particles in the west. However, the estimated PM2.5 and SO4 mode diameters are smaller than those previously reported by monitoring studies conducted at ground level. This is likely due to the satellite sampling bias caused by the inability to retrieve aerosols through cloud cover, and the impact of particle hygroscopicity on measured particle size distributions at ground level.

Abstract  Objective: The authors conducted an investigation of the association between air pollution and arrhythmia. Methods: A prospective panel study (October 2000-April 2001) was conducted in Erfurt, Germany. Fifty-seven men with coronary heart disease were subjected to six 24-hour electrocardiogram recordings. Runs of supraventricular and ventricular tachycardia were associated with continuous ultrafine particle counts (UFP), accumulation mode particle counts (ACP), PM2,5, and gaseous pollutants. Poisson and linear regression models were applied adjusting for trend, weekday, and meteorologic data. Results: Elevated concentrations of UFP, ACP, PM2,5, and nitrogen dioxide increased the risk for supraventricular runs and the number of ventricular runs at almost all lags. Statistically significant associations were found predominantly in the previous 24 to 71 hours and with the 5-day moving average. Conclusion: Elevated concentrations of fine and ultrafine particle increased the risk of arrhythmia in men with coronary heart disease.

Abstract  The National Children's Study is considering a wide spectrum of airborne pollutants that are hypothesized to potentially influence pregnancy outcomes, neurodevelopment, asthma, atopy, immune development, obesity, and pubertal development. In this article we summarize six applicable exposure assessment lessons learned from the Centers for Children's Environmental Health and Disease Prevention Research that may enhance the National Children's Study: a) Selecting individual study subjects with a wide range of pollution exposure profiles maximizes spatial-scale exposure contrasts for key pollutants of study interest. b) In studies with large sample sizes, long duration, and diverse outcomes and exposures, exposure assessment efforts should rely on modeling to provide estimates for the entire cohort, supported by subject-derived questionnaire data. c) Assessment of some exposures of interest requires individual measurements of exposures using snapshots of personal and microenvironmental exposures over short periods and/or in selected microenvironments. d) Understanding issues of spatial-temporal correlations of air pollutants, the surrogacy of specific pollutants for components of the complex mixture, and the exposure misclassification inherent in exposure estimates is critical in analysis and interpretation. e) "Usual" temporal, spatial, and physical patterns of activity can be used as modifiers of the exposure/outcome relationships. f) Biomarkers of exposure are useful for evaluation of specific exposures that have multiple routes of exposure. If these lessons are applied, the National Children's Study offers a unique opportunity to assess the adverse effects of air pollution on interrelated health outcomes during the critical early life period.

Abstract  Background: Extreme temperatures have been associated with increased mortality worldwide. The extent to which air pollutants may confound or modify this association remains unclear.

Methods: We examined the association between mean apparent temperature and total mortality in 9 cities across the United States during the warm season (May to September) from 1999 to 2002. We applied case-crossover and time-series analyses, adjusting for day of the week and season in time-series analysis. City-specific estimates were then combined using a meta-analysis. A total of 213,438 deaths for all causes occurred in these cities during the study period.

Results: We found that mortality increased with apparent temperature. A 5.5 degrees C (10 degrees F)increase in apparent temperature was associated with an increase in mortality of 1.8% (95% confidence interval = 1.09% to 2.5%) when using case-crossover analysis and with an increase of 2.7% (2.0% to 3.5%) using the time-series analysis.

Conclusions: This study provides evidence of increased mortality due to elevated apparent temperature exposure, with no confounding or effect modification due to air pollution.

Abstract  Mucociliary transport is responsible for the cleansing of inhaled particles from the conducting airways of the lung. The characteristics of human tracheobronchial mucociliary transport have been investigated using radiotagged aerosols. These methods are critically reviewed together with alternative techniques. The role of predictive mathematical models of tracheobronchial clearance is discussed. Major findings regarding mucociliary clearance in health and the effects of drugs, inhaled pollutants, and disease are summarized. Throughout, areas requiring problem-solving are delineated.

Abstract  Recent papers have reported that Asian dust events have been associated with increased risks of all-cause mortality and rates of respiratory illness. The current study was designed to estimate the relative risk of mortality associated with Asian dust events. We used the daily counts of non-accidental deaths, air pollution and meteorological data in Seoul, Korea from 2000 to 2004. We divided all days during the study period into two groups according to the presence or absence of Asian dust events. For each group, we conducted time-series analysis to estimate the relative risk of total non-accidental death when the concentration of each air pollutant increased by the inter-quartile range (IQR). The average concentrations of every air pollutant on the days without a dust event were lower than those on the days with such an event. We found that the effect sizes of air pollution on daily death rates in the model without Asian dust events were larger than those in the model with Asian dust events, and were statistically significant for all air pollutants (PM10, CO, NO2, and SO2) except for O-3. Our results Suggest that we are likely to underestimate the risk of urban air particles if we analyze the effect size of air pollution on daily mortality during Asian dust events. We hypothesize that the real health effect is much larger than previous results suggested.

Abstract  Increased production of industrial devices constructed with nanostructured materials raises the possibility of environmental and occupational human exposure with consequent adverse health effects. Ultrafine (nano) particles are suspected of having increased toxicity due to their size characteristics that serve as carrier transports. For this reason, it is critical to refine and improve existing deposition models in the nano-size range. A mathematical model of nanoparticle transport by airflow convection, axial diffusion, and convective mixing (dispersion) was developed in realistic stochastically generated asymmetric human lung geometries. The cross-sectional averaged convective-diffusion equation was solved analytically to find closed-form solutions for particle concentration and losses per lung airway. Airway losses were combined to find lobar, regional, and total lung deposition. Axial transport by diffusion and dispersion was found to have an effect on particle deposition. The primary impact was in the pulmonary region of the lung for particles larger than 10 nm in diameter. Particles below 10 nm in diameter were effectively removed from the inhaled air in the tracheobronchial region with little or no penetration into the pulmonary region. Significant variation in deposition was observed when different asymmetric lung geometries were used. Lobar deposition was found to be highest in the left lower lobe. Good agreement was found between predicted depositions of ultrafine (nano) particles with measurements in the literature. The approach used in the proposed model is recommended for more realistic assessment of regional deposition of diffusion-dominated particles in the lung, as it provides a means to more accurately relate exposure and dose to lung injury and other biological responses.

Abstract  BACKGROUND: Fine particulate matter has been linked to allergies by experimental and epidemiological data having used aggregated data or concentrations provided by fixed-site monitoring stations, which may have led to misclassification of individual exposure to air pollution. METHODS: A semi-individual design was employed to relate individual data on asthma and allergy of 5338 school children (10.4 +/- 0.7 years) attending 108 randomly chosen schools in 6 French cities to the concentrations of PM2.5 (fine particles with aerodynamic diameter 2.5 microm) assessed in proximity of their homes. Children underwent a medical visit including skin prick test (SPT) to common allergens, exercise-induced bronchial (EIB) reactivity and skin examination for flexural dermatitis. Their parents filled in a standardised health questionnaire. RESULTS: After adjustment for confounders and NO2 as a potential modifier, the odds of suffering from EIB and flexural dermatitis at the period of the survey, past year atopic asthma and SPT positivity to indoor allergens were significantly increased in residential settings with PM2.5 concentrations exceeding 10 microg/m3 (WHO air quality limit values). The relationships were strengthened in long-term residents (current address for at least 8 years). CONCLUSIONS: Findings support the hypothesis that changes in allergy prevalence observed in recent decades might be partly related to interactions between traffic-related air pollution and allergens. Further longitudinal investigations are needed to corroborate such results.