Abstract  This study describes the short-term relationships between the daily levels of PM10, PM2.5, NO2 and the number of doctors' house calls for asthma, upper respiratory diseases (URD) and lower respiratory diseases (LRD) in Greater Paris for the years 2000-3. Doctors' house calls are a relevant health indicator for the study of short-term health effects of air pollution. Indeed, it is potentially more sensitive than indicators such as general hospital admissions due to the severity of diseases motivating the call. In this study, time-series analysis was used. The daily numbers of doctor's house calls were adjusted for time trends, seasonal factors, day of the week, influenza, weather and pollen. Up to 15 days of lag between exposure and health effects was considered using distributed lag models. A total of about 1,760,000 doctors' house calls for all causes occurred during the study period, among which 8027 were for asthma, 52,928 for LRD and 74,845 for URD. No significant increase in risk was found between air pollution and doctors' house calls for asthma. No significant association was found between NO2 and doctors' house calls. An increase of 10 microg/m3 in the mean levels of PM10 and PM2.5 encountered during the 3 previous days was associated with an increase of 3% (0.8% and 5.3%) and 5.9% (2.9% and 9.0%) in the number of doctor's house calls for URD and LRD, respectively. Considering up to 15 days between exposure and health outcomes, effects persist until 4 days after exposure and then decrease progressively. No morbidity displacement was observed. This study shows a significant heath effect of ambient particles (PM2.5 and PM10). When compared to the RRs obtained for mortality or hospital admissions in the same area, the values of the RRs obtained in this study confirm the higher sensibility of doctor's house calls for respiratory diseases as a health indicator.

Abstract  BACKGROUND: Health concerns about the exposure to genotoxic and carcinogenic agents in the air are particularly significant for outdoor workers in less developed countries. AIMS: To investigate the association between personal exposure to a group of air pollutants and severity of DNA damage in outdoor workers from two Mexican cities. METHODS: DNA damage (Comet assay) and personal exposure to volatile organic compounds, PM(2.5), and ozone were investigated in 55 outdoor and indoor workers from MÚxico City and Puebla. RESULTS: In MÚxico City, outdoor workers had greater DNA damage, reflected by a longer tail length, than indoor workers (median 46.8 v 30.1 mum), and a greater percentage of highly damaged cells (cells with tail length > or =41 microm); in Puebla, outdoor and indoor workers had similar DNA damage. There were more alkali labile sites in outdoor than indoor workers. The DNA damage magnitude was positively correlated with PM(2.5) and ozone exposure. Outdoor and indoor workers with > or =60% of highly damaged cells (highly damaged workers) had significantly higher exposures to PM(2.5), ozone, and some volatile organic compounds. The main factors associated with the highly damaged workers were ozone, PM(2.5), and 1-ethyl-2-methyl benzene exposure. CONCLUSIONS: With this approach, the effects of some air pollutants could be correlated with biological endpoints from the Comet assay. It is suggested that the use of personal exposure assessment and biological endpoints evaluation could be an important tool to generate a more precise assessment of the associated potential health risks.

Abstract  BACKGROUND: Particulate air pollution has been associated with several adverse cardiovascular health outcomes, and people with diabetes may be especially vulnerable. One potential pathway is inflammation and endothelial dysfunction-processes in which cell adhesion molecules and inflammatory markers play important roles. AIM: To examine whether plasma levels of soluble intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1) and von Willebrand factor (vWF) were associated with particle exposure in 92 Boston area residents with type 2 diabetes. METHODS: Daily average ambient levels of air pollution (fine particles (PM2.5), black carbon (BC) and sulphates) were measured approximately 500 m from the patient examination site and evaluated for associations with ICAM-1, VCAM-1 and vWF. Linear regressions were fit to plasma levels of ICAM-1, VCAM-1 and vWF, with the particulate pollutant index, apparent temperature, season, age, race, sex, glycosylated haemoglobin, cholesterol, smoking history and body mass index as predictors. RESULTS: Air pollutant exposure measures showed consistently positive point estimates of association with the inflammatory markers. Among participants not taking statins and those with a history of smoking, associations between PM(2.5), BC and VCAM-1 were particularly strong. CONCLUSIONS: These results corroborate evidence suggesting that inflammatory mechanisms may explain the increased risk of air pollution-associated cardiovascular events among those with diabetes.

Abstract  BACKGROUND: Epidemiological studies on health effects of air pollution have consistently shown adverse cardiovascular effects. Toxicological studies have provided evidence for thrombogenic effects of particles.A prospective panel study in a susceptible population was conducted in Erfurt, Germany, to study the effects of daily changes in ambient particles on various blood cells and soluble CD40ligand (sCD40L, also known as CD154), a marker for platelet activation that can cause increased coagulation and inflammation.Blood cells and plasma sCD40L levels were repeatedly measured in 57 male patients with coronary heart disease (CHD) during winter 2000/2001. Fixed effects linear regression models were applied, adjusting for trend, weekday and meteorological parameters.Hourly data on ultrafine particles (UFP, number concentration of particles from 0.01 to 0.1 microm), mass concentration of particles less than 10 and 2.5 microm in diameter (PM10, PM2.5), accumulation mode particle counts (AP, 0.1-1.0 microm), elemental and organic carbon, gaseous pollutants and meteorological data were collected at central monitoring sites. RESULTS: An immediate increase in plasma sCD40L was found in association with UFP and AP (% change from geometric mean: 7.1; CI: [0.1, 14.5] and 6.9; CI: [0.5, 13.8], respectively). Platelet counts decreased in association with UFP showing an immediate, a three days delayed (lag 3) and a 5-day average response (% change from the mean: -1.8; CI: [-3.4,-0.2]; -2.4; CI: [-4.5,-0.3] and -2.2; CI: [-4.0,-0.3] respectively). CONCLUSION: The increased plasma sCD40L levels support the hypothesis that higher levels of ambient air pollution lead to an inflammatory response in patients with CHD thus providing a possible explanation for the observed association between air pollution and cardiovascular morbidity and mortality in susceptible parts of the population.

Abstract  AIMS: To assess any relationship between the levels of ambient air pollutants and hospital admissions for chronic obstructive pulmonary disease (COPD) in Hong Kong. METHODS: A retrospective ecological study was undertaken. Data of daily emergency hospital admissions to 15 major hospitals in Hong Kong for COPD and indices of air pollutants (sulphur dioxide (SO(2)), nitrogen dioxide (NO(2)), ozone (O(3)), particulates with an aerodynamic diameter of <10 microm (PM(10)) and 2.5 microm (PM(2.5))) and meteorological variables from January 2000 to December 2004 were obtained from several government departments. Analysis was performed using generalised additive models with Poisson distribution, adjusted for the effects of time trend, season, other cyclical factors, temperature and humidity. Autocorrelation and overdispersion were corrected. RESULTS: Significant associations were found between hospital admissions for COPD with all five air pollutants. Relative risks for admission for every 10 microg/m(3) increase in SO(2), NO(2), O(3), PM(10) and PM(2.5) were 1.007, 1.026, 1.034, 1.024 and 1.031, respectively, at a lag day ranging from lag 0 to cumulative lag 0-5. In a multipollutant model, O(3), SO(2) and PM(2.5) were significantly associated with increased admissions for COPD. SO(2), NO(2) and O(3) had a greater effect on COPD admissions in the cold season (December to March) than during the warm season. CONCLUSION: Ambient concentrations of air pollutants have an adverse effect on hospital admissions for COPD in Hong Kong, especially during the winter season. This might be due to indoor exposure to outdoor pollution through open windows as central heating is not required in the mild winter. Measures to improve air quality are urgently needed.

Abstract  [1] Field studies have been performed in Lindon, Utah (February 2003) and Rubidoux, California (July 2003) to determine if the Rupprecht and Patashnick (R&P) Filter Dynamic Measurement System (FDMS) determines total fine particulate mass, including the semivolatile ammonium nitrate and organic material. Collocated measurements were made with the FDMS, a conventional tapered element oscillating microbalance (TEOM) monitor with a heated filter, an R&P differential TEOM monitor, the Brigham Young University (BYU) Real-Time Total Ambient Mass Sampler (RAMS), the BYU particle concentrator-organic sampling system (PC-BOSS), a PM2.5 Federal Reference Method (FRM), a PM2.5 speciation sampler, an R&P continuous nitrate monitor, and two Sunset continuous carbon monitors (one to measure quartz filter-retained particulate carbon and one to measure particulate semivolatile carbonaceous material lost from the particles on a filter during sampling). The RAMS and PC-BOSS samplers have been shown to determine fine particulate material, including both the semivolatile and the nonvolatile components. Linear regression analysis at the Lindon site between the FDMS (X) and the PC-BOSS (Y), and the FDMS (X) and the RAMS (Y), resulted in zero-intercept slopes of 1.01 ± 0.06 (r2 = 0.63) and 1.00 ± 0.01 (r2 = 0.69), respectively. At the Rubidoux sampling site, linear regression analysis between the PC-BOSS (X) and the FDMS (Y) gave a zero-intercept slope of 0.96 ± 0.02 (r2 = 0.90). Linear regression analysis between the FDMS (X) and the RAMS (Y) resulted in a zero-intercept slope of 0.99 ± 0.01 (r2 = 0.80). Measurements made at the two sites indicate that the FDMS and the R&P differential TEOM monitors do measure total fine particulate mass, including the semivolatile ammonium nitrate and organic material. Both the heated TEOM monitor and PM2.5 FRM did not measure the semivolatile material. The difference between the FDMS and a heated TEOM monitor was explained by the semivolatile ammonium nitrate and organic material measured by the various chemical composition monitors.

Abstract  Two studies at three sites in the UK provided confirmation that systematic positive bias in NO2 diffusion tube measurement occurred because of changes to "within-tube" chemistry, rather than eddy diffusion at the mouth of the tube. In the first study in Cambridge, UK, sampler overestimation for 1 and 2 week exposures was compared to corresponding time-averaged monitor measurements (NO-NO2-NOx, O3) and weather variables. Noninearity between sampler and monitor NO2 measurements was interpreted in terms of spatial and temporal variations in relative and absolute availability of NO, NO2 and O3 at the site. A maximum overestimation occurred for an exposure mean NO2/NOx approximately 0.5. The separate contributions of reduced NO2 photolysis and eddy diffusion were compared in Study II using samplers of two materials, acrylic and quartz, and of different lengths (40, 55, 71 and 120 mm) at three sites: Norwich background, Cambridge intermediate, London kerbside. For compared sites, NO2 measured by acrylic samplers was significantly higher than for equivalent quartz samplers. For quartz samplers [NO2]mean was only just above the monitor at Norwich and London; sampler/monitor NO2 = 1.04 (P = 0.59) and 1.01(P = 0.76), respectively. For acrylic samplers the order of [NO2]mean was 40 mm > 120 mm > 71 mm > or = 55 mm. Excepting 40 mm samplers, this accords with a chemical bias where co-diffusing NO and 03 molecules in longer tubes have more time to react to form excess NO2. Bias in 40 mm samplers is discussed. Eddy diffusion is negligible for standard samplers because [NO2]mean was equivalent for 55 mm and 71 mm acrylic samplers and close to monitor NO2 for 71 mm quartz tubes. Both studies showed that sampler accuracy was dependent on location. Significantly, overestimation was greatest (approximately 3-4 ppb) where the NO2 annual mean was approximately 20 ppb, close to the UK and EU air quality standard of 21 ppb.

Abstract  BACKGROUND: The Democratic National Convention (DNC) in Boston, Massachusetts in 2004 provided an opportunity to evaluate the impacts of a localized and short-term but potentially significant change in traffic patterns on air quality, and to determine the optimal monitoring approach to address events of this nature. It was anticipated that the road closures associated with the DNC would both influence the overall air pollution level and the distribution of concentrations across the city, through shifts in traffic patterns. METHODS: To capture these effects, we placed passive nitrogen dioxide badges at 40 sites around metropolitan Boston before, during, and after the DNC, with the goal of capturing the array of hypothesized impacts. In addition, we continuously measured elemental carbon at three sites, and gathered continuous air pollution data from US EPA fixed-site monitors and traffic count data from the Massachusetts Highway Department. RESULTS: There were significant reductions in traffic volume on the highway with closures north of Boston, with relatively little change along other highways, indicating a more isolated traffic reduction rather than an across-the-board decrease. For our nitrogen dioxide samples, while there was a relatively small change in mean concentrations, there was significant heterogeneity across sites, which corresponded with our a priori classifications of road segments. The median ratio of nitrogen dioxide concentrations during the DNC relative to non-DNC sampling periods was 0.58 at sites with hypothesized traffic reductions, versus 0.88 for sites with no changes hypothesized and 1.15 for sites with hypothesized traffic increases. Continuous monitors measured slightly lower concentrations of elemental carbon and nitrogen dioxide during road closure periods at monitors proximate to closed highway segments, but not for PM2.5 or further from major highways. CONCLUSION: We conclude that there was a small but measurable influence of DNC-related road closures on air quality patterns in the Boston area, and that a low-cost monitoring study combining passive badges for spatial heterogeneity and continuous monitors for temporal heterogeneity can provide useful insight for community air quality assessments.

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  Rising atmospheric carbon dioxide has the potential to alter leaf litter chemistry, potentially affecting decomposition and rates of carbon and nitrogen cycling in forest ecosystems. This study was conducted to determine whether growth under elevated atmospheric CO2 altered the quality and microbial decomposition of leaf litter of a widely distributed northern hardwood species at sites of low and high soil nitrogen availability. In addition, we assessed whether the carbonûnutrient balance (CNB) and growth differentiation balance (GDB) hypotheses could be extended to predict changes in litter quality in response to resource availability. Sugar maple (Acer saccharum) was grown in the field in open-top chambers at 36 and 55 Pa partial pressure CO2, and initial soil mineralization rates of 45 and 348 Ág N g1 d1. Naturally senesced leaf litter was assessed for chemical composition and incubated in the laboratory for 111 d. Microbial respiration and the production of dissolved organic carbon (DOC) were quantified as estimates of decomposition. Elevated CO2 and low soil nitrogen resulted in higher litter concentrations of nonstructural carbohydrates and condensed tannins, higher C/N ratios and lower N concentrations. Soil N availability appears to have had a greater effect on litter quality than did atmospheric CO2, although the treatments were additive, with highest concentrations of nonstructural carbohydrates and condensed tannins occurring under elevated CO2ûlow soil N. Rates of microbial respiration and the production of DOC were insensitive to differences in litter quality. In general, concentrations of litter constituents, except for starch, were highly correlated to those in live foliage, and the CNB/GDB hypotheses proved useful in predicting changes in litter quality. We conclude the chemical composition of sugar maple litter will change in the future in response to rising atmospheric CO2, and that soil N availability will exert a major control. It appears that microbial metabolism will not be directly affected by changes in litter quality, although conclusions regarding decomposition as a whole must consider the entire soil food web.

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  Background: The induction of cytokines by airway cells in vitro has been widely used to assess the effects of ambient and occupational particles. This study measured cytotoxicity and the release of the proinflammatory cytokines IL-6 and IL-8 by human bronchial epithelial cells treated with manufactured nano- and micron-sized particles of Al2O3, CeO2, Fe2O3, NiO, SiO2, and TiO2, with soil-derived particles from fugitive dust sources, and with the positive controls LPS, TNF-alpha, and VOSO4. Results: The nano-sized particles were not consistently more potent than an equal mass of micron-sized particles of the same nominal composition for the induction of IL-6 and IL-8 secretion in the in vitro models used in this study. The manufactured pure oxides were much less potent than natural PM2.5 particles derived from soil dust, and the cells were highly responsive to the positive controls. The nano-sized particles in the media caused artifacts in the measurement of IL-6 by ELISA due to adsorption of the cytokine on the high-surface-area particles. The potency for inducing IL-6 secretion by BEAS-2B cells did not correlate with the generation of reactive oxygen species in cell-free media. Conclusions: Direct comparisons of manufactured metal oxide nanoparticles and previously studied types of particles and surrogate proinflammatory agonists showed that the metal oxide particles have low potency to induce IL-6 secretion in BEAS-2B cells. Particle artifacts from non-biological effects need to be considered in experiments of this type, and the limitations inherent in cell culture studies must be considered when interpreting in vitro results. This study suggests that manufactured metal oxide nanoparticles are not highly toxic to lung cells compared to environmental particles.

Abstract  #Concurrent measurements of ultra-fine (r<5 nm) particle (UFP) formation, OH and SO2 concentrations in the coastal environment are examined to further elucidate the processes leading to tidal-related homogeneous heteromolecular nucleation. During almost daily nucleation events, UFP concentration approached approximate to 300,000 cm(-3) under conditions of solar radiation and low tide. Simultaneous measurements of OH illustrate that, as well as occurring during low tide, these events occur during conditions of peak OH concentration, suggesting that at least one of the nucleating species is photochemically produced. Derived H2SO4 production also exhibited remarkable coherence, although phase-lagged, with UFP formation, thus suggesting its involvement, although binary nucleation of H2SO4 and H2O can be ruled out asa plausible mechanism. Ternary nucleation involving NH3 seems most likely as a trigger mechanism, however, at least a fourth condensable species, X, is required for growth to detectable sizes. Since UFP are only observed during low tide events, it is thought that species X, or it's parent, is emitted from the shore biota - without which, no nucleation is detected. Species X remains to be identified. Model simulations indicate that, in order to reproduce the observations, a nucleation rate of 10(7) cm(-3) s(-1), and a condensable vapour concentration of 5 x 10(7) cm(-3), are required.

Abstract  The aim of the investigation was to assess the relations between pairs of personal, indoor, and outdoor levels of fine particles and their components with respect to effects for older subjects with cardiovascular disease. In the framework of a study funded by the European Union (Exposure and Risk Assessment for Fine and Ultrafine Particles in Ambient Air; referred to as ULTRA)*, panel studies were conducted in Amsterdam (The Netherlands) and Helsinki (Finland). Concentrations of outdoor particulate matter 2.5 pm or smaller in aerodynamic diameter (PM2.5) were measured at a fixed site in each location. With HEI funding, each subject's personal and indoor PM2.5 exposure was measured every other week for 6 months during the 24-hour period preceding intensive health measurements. Particle reflectance was measured as a marker for diesel exhaust. Elemental content of more than 50% of the personal and indoor samples and all corresponding outdoor samples was measured using x-ray fluorescence (XRF). Ion content (sulfate, nitrate) was measured using chromatography. For Amsterdam, 337 personal and 409 indoor measurements were collected from 37 subjects; for Helsinki, 336 personal and 503 indoor measurements were collected from 47 subjects. Median personal, indoor, and outdoor PM2.5 concentrations were 13.6, 13.6, and 16.5 microg/m3 in Amsterdam and 9.2, 9.2, and 11.1 microg/m3 in Helsinki. In both cities, personal and indoor PM2.5 concentrations were lower than and highly correlated with outdoor concentrations (median correlation coefficient [R] 0.7-0.8). For most elements, personal and indoor concentrations were also highly correlated with outdoor concentrations. The highest correlations (median R > 0.9) were found for sulfur (S), sulfate, and particle reflectance (reported as the absorption coefficient). Reflectance was a useful proxy for elemental carbon (EC), but site-specific calibration with EC data is necessary. The findings of this study support using fixed-site measurements as a measure of exposure to PM in time-series studies linking the day-to-day variations in PM to the day-to-day variations in health endpoints, especially for components of PM that are generally associated with fine particles and have few indoor sources.

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  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  There is mounting evidence that maternal exposure to ambient air pollution during pregnancy is associated with adverse birth outcomes. We examined birth weight and small for gestational age (SGA <10th percentile for age and gender) among 26,617 singleton full-term births in Brisbane, Australia (July 2000-June 2003), in relation to ambient pollution during pregnancy. We also examined head circumference (HC) and crown-heel length (CHL) among a sub-sample (n=21,432) of the term neonates. Maternal exposure to PM(10), visibility reducing particles (bsp), O(3) and NO(2) was assessed by calculating average exposure estimates over months and trimesters of pregnancy based on a citywide average of the pollutants. Linear and logistic regression models were employed to examine the effect of these pollutants on the birth outcomes after adjusting for potential confounders and season of birth. The regression coefficients were based on an inter-quartile range (IQR) increase in exposure as well as quartiles of exposure with the lowest used as a reference category. Trimester- and monthly specific exposures to all pollutants were not significantly associated with a reduction in either birth weight or HC, or an increased risk of SGA. An IQR increase in NO(2) during the third trimester was associated with a reduction in CHL (beta=-0.15cm, 95% CI -0.25 to -0.05cm) and this was concentrated around exposure during month nine. No other pollutants were associated with a reduction in CHL. In conclusion, there was no strong evidence suggesting that ambient air pollution during pregnancy is associated with sub-optimal fetal growth in Brisbane.

Abstract  OBJECTIVES: Nitrogen dioxide (NO2) has been inconsistently associated with gradual decreases in lung function. Here, we studied the effects of NO2 exposure in asthmatics by examining the association between changes in lung function and concentrations of NO2 which were personally measured. METHODS: Peak expiratory flow (PEF) and daily personal exposures to NO2 were recorded on 28 patients with asthma (confirmed by methacholine provocation test) over 4 weeks. We used generalized estimating equations to assess the relationship between personal NO2 exposure and PEF, adjusting for potential confounders such as age, gender, outdoor particulate matter, temperature, humidity, and exposure to environmental tobacco smoke. RESULTS: The personal NO2 exposures were higher than the corresponding ambient levels. The mean personal: ambient ratio for NO2 was 1.48. The personal NO2 exposures were not associated with the morning PEF, evening PEF, or the diurnal PEF variability. However, environmental tobacco smoke was negatively associated with both the morning and evening PEF. CONCLUSIONS: Among the asthmatic adults who participated in this study, we found no apparent impact of personal NO2 exposures on the peak expiratory flow.

Abstract  BACKGROUND: Short-term increases in particulate air pollution are linked with increased daily mortality and morbidity. Socioeconomic status (SES) is a determinant of overall health. We investigated whether social class is an effect modifier of the PM10 (particulate matter with diameter <10 micron)-daily mortality association, and possible mechanisms for this effect modification. METHODS: Area-based traffic emissions, income, and SES were available for each resident in Rome. All natural deaths (83,253 subjects) occurring in Rome among city residents (aged 35+ years) during the period 1998-2001 were identified. For each deceased individual, all the previous hospitalizations within 2 years before death were available via a record linkage procedure. PM10 daily data were available from two urban monitoring sites. A case-crossover analysis was utilized in which control days were selected according to the time stratified approach (same day of the week during the same month). Conditional logistic regression was used. RESULTS: Due to the social class distribution in the city, exposure to traffic emissions was higher among those with higher area-based income and SES. Meanwhile, people of lower social class had suffered to a larger extent from chronic diseases before death than more affluent residents, especially diabetes mellitus, hypertension, heart failure, and chronic obstructive pulmonary diseases. Overall, PM10 (lag 0-1) was strongly associated with mortality (1.1% increase, 95%CI = 0.7-1.6%, per 10 microg/m3). The effect was more pronounced among persons with lower income and SES (1.9% and 1.4% per 10 microg/m3, respectively) compared to those in the upper income and SES levels (0.0% and 0.1%, respectively). CONCLUSIONS: The results confirm previous suggestions of a stronger effect of particulate air pollution among people in low social class. Given the uneven geographical distributions of social deprivation and traffic emissions in Rome, the most likely explanation is a differential burden of chronic health conditions conferring a greater susceptibility to less advantaged people.

Abstract  BACKGROUND: Consistent evidence has indicated that air pollution increases the risk of cardiovascular diseases. The underlying mechanisms linking air pollutants to increased cardiovascular risk are unclear. OBJECTIVES: We investigated the association between the pollution levels and changes in such global coagulation tests as the prothrombin time (PT) and the activated partial thromboplastin time (APTT) in 1218 normal subjects from the Lombardia Region, Italy. Plasma fibrinogen and naturally occurring anticoagulant proteins were also evaluated. METHODS: Hourly concentrations of particulate (PM10) and gaseous pollutants (CO, NO2, SO2, and O3) were obtained from 53 monitoring sites covering the study area. Generalized additive models were applied to compute standardized regression coefficients controlled for age, gender, body mass index, smoking, alcohol, hormone use, temperature, day of the year, and long-term trends. RESULTS: The PT became shorter with higher ambient air concentrations at the time of the study of PM10 (coefficient = -0.06; P < 0.05), CO (coefficient = -0.11; P < 0.001) and NO2 (coefficient =-0.06; P < 0.05). In the 30 days before blood sampling, the PT was also negatively associated with the average PM10 (coefficient = -0.08; P < 0.05) and NO2 (coefficient = -0.08; P < 0.05). No association was found between the APTT and air pollutant levels. In addition, no consistent relations with air pollution were found for fibrinogen, antithrombin, protein C and protein S. CONCLUSIONS: This investigation shows that air pollution is associated with changes in the global coagulation function, suggesting a tendency towards hypercoagulability after short-term exposure to air pollution. Whether these changes contribute to trigger cardiovascular events remains to be established.

Abstract  OBJECTIVES: To estimate long-term exposure to traffic-related air pollutants on an individual basis and to assess adverse health effects using a combination of air pollution measurement data, data from geographical information systems (GIS) and questionnaire data. METHODS: 40 measurement sites in the city of Munich, Germany were selected at which to collect particulate matter with a 50% cut-off aerodynamic diameter of 2.5 microm (PM2.5) and to measure PM2.5 absorbance and nitrogen dioxide (NO2). A pool of GIS variables (information about street length, household and population density and land use) was collected for the Munich metropolitan area and was used in multiple linear regression models to predict traffic-related air pollutants. These models were also applied to the birth addresses of two birth cohorts (German Infant Nutritional Intervention Study (GINI) and Influence of Life-style factors on the development of the Immune System and Allergies in East and West Germany (LISA)) in the Munich metropolitan area. Associations between air pollution concentrations at birth address and 1-year and 2-year incidences of respiratory symptoms were analysed. RESULTS: The following means for the estimated exposures to PM2.5, PM2.5 absorbance and NO2 were obtained: 12.8 microg/m3, 1.7x10(-5) m(-1) and 35.3 mug/m3, respectively. Adjusted odds ratios (ORs) for wheezing, cough without infection, dry cough at night, bronchial asthma, bronchitis and respiratory infections indicated positive associations with traffic-related air pollutants. After controlling for individual confounders, significant associations were found between the pollutant PM2.5 and sneezing, runny/stuffed nose during the first year of life (OR 1.16, 95% confidence interval 1.01 to 1.34) Similar effects were observed for the second year of life. These findings are similar to those from our previous analysis that were restricted to a subcohort in Munich city. The extended study also showed significant effects for sneezing, running/stuffed nose. Additionally, significant associations were found between NO2 and dry cough at night (or bronchitis) during the first year of life. The variable "living close to major roads" (<50 m), which was not analysed for the previous inner city cohort with birth addresses in the city of Munich, turned out to increase the risk of wheezing and asthmatic/spastic/obstructive bronchitis. CONCLUSIONS: Effects on asthma and hay fever are subject to confirmation at older ages, when these outcomes can be more validly assessed.

Abstract  BACKGROUND: Otitis media is one of the most common infections in young children. Although exposure to environmental tobacco smoke is a known risk factor associated with otitis media, little information is available regarding the potential association with air pollution. OBJECTIVE: We set out to study the relationship between exposure to traffic-related air pollution and otitis media in two birth cohorts. METHODS: Individual estimates of outdoor concentrations of traffic-related air pollutants-nitrogen dioxide, fine particles [particulate matter with aerodynamic diameters

Abstract  Aims: To investigate the chronic effects of air pollution caused mainly by automobiles in healthy adult females. Methods: Respiratory symptoms were investigated in 5682 adult females who had lived in the Tokyo metropolitan area for three years or more in 1987; 733 of them were subjected to pulmonary function tests over eight years from 1987 to 1994. The subjects were divided into three groups by the level of air pollution they were exposed to during the study period. The concentrations of nitrogen dioxide and suspended particulate matter were the highest in group 1, and the lowest in group 3. Results: The prevalence rates of respiratory symptoms in group 1 were higher than those in groups 2 and 3, except for wheezing. Multiple logistic regression analysis showed significant differences in persistent phlegm and breathlessness. The subjects selected for the analysis of pulmonary function were 94, 210, and 102 females in groups 1, 2, and 3, respectively. The annual mean change of FEV1 in group 1 was the largest (-0.020 l/y), followed by that in group 2 (-0.015 l/y), and that in group 3 (-0.009 l/y). Testing for trends showed a significant larger decrease of FEV1 with the increase in the level of air pollution. Conclusions: The subjects living in areas with high levels of air pollution showed higher prevalence rates of respiratory symptoms and a larger decrease of FEV1 compared with those living in areas with low levels of air pollution. Since the traffic density is larger in areas with high air pollution, the differences among the groups may reflect the effect of air pollution attributable to particulate matter found in automobile exhaust.

Abstract  Background: Short term increases in exposure to particulate matter (PM) air pollution are associated with increased cardiovascular morbidity and mortality. The mechanism behind this effect is unclear, although changes in autonomic control have been observed. It was hypothesised that increases in fine PM measured at the subjects' home in the preceding hour would be associated with decreased high frequency heart rate variability (HF-HRV) in individuals with pre-existing cardiac disease. Methods: Two hundred and eighty five daily 20 minute measures of HRV (including a paced breathing protocol) were made in the homes of 34 elderly individuals with (n=21) and without (n=13) cardiovascular disease (CVD) over a 10 day period in Seattle between February 2000 and March 2002. Fine PM was continuously measured by nephelometry at the individuals' homes. Results: The median age of the study population was 77 years (range 57-87) and 44% were male. Models that adjusted for health status, relative humidity, temperature, mean heart rate, and medication use did not find a significant association between a 10 ?g/m3increase in 1 hour mean outdoor PM2.5 before the HRV measurement and a change in HF-HRV power in individuals with CVD (3% increase in median HF-HRV (95% CI -19 to 32)) or without CVD (5% decrease in median HF-HRV (95% Cl -34 to 36)). Similarly, no association was evident using 4 hour and 24 hour mean outdoor PM2.5 exposures before the HRV measurement. Conclusion: No association was found between increased residence levels of fine PM and frequency domain measures of HRV in elderly individuals.

Abstract  Background: Many chronic diseases are the product of an underlying pathologic condition and superimposed acute exacerbations. This model may apply to several conditions such as asthma, other obstructive lung diseases, or atherosclerosis. For exposures affecting both the development of chronic disease and its exacerbation, the usual methods to derive attributable risks (AR) are inappropriate. Methods: We expand traditional risk assessment methods to estimate the AR for exacerbations under a "chronic disease model." We use asthma in children as the chronic disease and air pollution as the exposure of interest. We estimate bronchitis symptom exacerbations attributable to air pollution, using data from the Children's Health Study to estimate asthma prevalence and symptom occurrence, and we examine the distribution of exposure and its acute and chronic effects. Results: In the combined AR model, 39.8% of exacerbations were attributable to air pollution, compared with 33.5% in the traditional model, which ignores a chronic effect of pollution on asthma development. Thus, there is a 1.19-fold higher estimated burden with the combined model. The difference is due to exacerbations caused by other factors (ie, not by air pollution) but nonetheless occurring among those assumed to have asthma that developed due to traffic-related pollution. The proposed model is applicable to other risk factors that play a role both in both the development of a chronic disease and its exacerbation. Conclusions: Traditional approaches to the calculation of attributable risk may underestimate the health impact of long-term environmental or other exposures that produce both chronic and acute disease.