Abstract  Objectives First, we present a general analytical approach to estimating the association between medium-term changes in air pollution and health across small areas. As a specific illustration, we then applied the approach to data on London residents from a 4-year period to test whether reductions in traffic-related air pollution were associated with reductions in cardio-respiratory hospital admissions. Methods A binomial distribution was used to model change in admissions over time in each small area, which was measured as the proportion of admissions in 2003–2004 out of admissions over all study years (2001–2004). Annual average concentrations of nitrogen oxides (NOx) were modelled using an emissions-dispersion model. The association between change in NOx and change in hospital admissions was estimated using logistic regression and an instrumental variable approach. Results For some diagnostic groups, suggestive associations between reductions in NOx and reductions in admissions were observed, for example, OR=0.97 (95% CI 0.96 to 0.99) for an IQR decrease in NOx (3 μg/m3) and all respiratory admissions. Accounting for spatial dependence attenuated several of the associations; for respiratory admissions, the OR was 1.00 (95% CI 0.98 to 1.02), leaving only that for bronchiolitis significant (OR=0.91; 95% CI 0.84 to 0.99). In this particular illustration, the instrumental variable approach did not appear to add information. Conclusions In this illustration, there was relatively limited power to detect an association between changes in air pollution and hospital admissions over time. However, the analytical approach could deliver more robust estimates of the health effects of changes in air pollution in settings with greater spatial contrast in changes in air pollution over time.

Abstract  In this article we discuss statistical techniques for modeling data from cohort studies that examine long-term effects of air pollution on children’s health by comparing data from multiple communities with a diverse pollution profile. Under a general multilevel modeling paradigm, we discuss models for different outcome types along with their connections to the generalized mixed effects models methodology. The model specifications include linear and flexible models for continuous lung function data, logistic and/or time-to-event models for symptoms data that account for misspecifications via hidden Markov models and Poisson models for school absence counts. The main aim of the modeling scheme is to be able to estimate effects at various levels (e.g., within subjects across time, within communities across subjects and between communities). We also discuss in detail various recurring issues such as ecologic bias, exposure measurement error, multicollinearity in multipollutant models, interrelationships between major endpoints and choice of appropriate exposure metrics. The key conceptual issues and recent methodologic advances are reviewed, with illustrative results from the Southern California Children’s Health Study, a 10-year study of the effects of air pollution on children’s respiratory health.

Abstract  A new ligand, pyridine-3,5-bis(benzimidazole-2-yl) (pbb), and four complexes containing pbb, namely [pbb(Hpbb)(2)]SO(4)center dot 7H(2)o (1), [Zn(pbb)(2)(H(2)O)(4)](NO(3))(2) center dot 2C(2)H(5)OH center dot 4H(2)O (2), [Cd(pbb)(2)(H(2)O)(4)](NO(3))(2)center dot 2C(2)H(5)OH center dot 4H(2)O (3) and [Zn(2)(pbb)(2)([L-OH)(mu-CAc)](OAc)(2)center dot 7H(2)O (4) (HOAc = acetic acid), have been designed, synthesized and characterized. Complexes 1-4 show 3D supramolecular architectures that are connected through hydrogen bonds and aromatic pi-pi interactions. A self-assembled (H(2)O)(12) cluster with a chair conformation (H(2)O)(6) ring core is observed in 1, which exhibits an unusual association mode of water molecules. Compounds 2 and 3 present 3D supramolecular structures involving I D open channels encapsulating NO(3)(-) ions, and crown-like rings are found in 4. In addition, the preliminary antibacterial activity of pbb and its complexes were investigated by two methods, which indicate a selective inhibition property for the tested strains. Strong emissions from the complexes were also changed by the coordination modes in the sold state. (C) 2008 Elsevier Ltd. All rights reserved.

Abstract  An approach is developed and tested to extend discrete, source-based sensitivity results to provide a complete set of information for source-air quality impacts, including inversion of those results to develop receptor-oriented source-impact sensitivities. First, the decoupled direct sensitivity analysis method in 3D (DDM-3D) is used to calculate a finite number of forward sensitivities from discrete points. These results are then interpolated using tessellation to provide complete fields of forward, emissions-based sensitivities, i.e., how emissions in any one grid cell within the domain impact any other cell. Receptor-oriented sensitivities are then found by inverting the set of forward sensitivities and can be used to identify the area of influence (AOI). This economically provides results similar to what would be found using an adjoint model. The present approach is computationally less intensive than adjoint modeling for a large number of receptors, and provides both source-oriented and receptor-oriented pollutant response fields that can be used for air quality management and health impact analyses. The forward sensitivity interpolation procedure, as well as the receptor-oriented sensitivities, is evaluated using data withholding.

Abstract  This paper presents the contribution to population exposure (PE) of regional background fine primary (PPM"2"."5) and secondary inorganic (SIA) particulate matter and its impact on mortality in Europe during 1997-2003 calculated with a...

Abstract  Analysis of pollution data from a network of monitors in Maricopa County, Arizona, reveals considerable variation in the magnitude of the ozone "weekend effect" depending on how and where it is measured. We used four separate methods to calculate the weekend effect, all of which showed that the phenomenon is stronger in the urban core, where ozone is produced. Spatial linear regressions show that the magnitude of the weekend effect and the goodness of fit of weekly harmonic cycles in ozone is a function of urbanization, described quantitatively using an index of traffic counts, population, and employment within a 4 km buffer zone of monitoring sites. Analysis of diurnal patterns of ozone as well as oxides of nitrogen (NO,) at a representative site in the urban core supports the hypothesis that lower levels of NO, on Sundays reduce the degree to which ozone is titrated, resulting in a higher minimum and hence mean for that day of the week (DOW). Fringe sites, where ozone concentrations are higher in absolute terms than in the urban core, show almost no "weekend effect," regardless of which of the four individual methods we used. Alternative quantification methods show statistically significant DOW differences in ozone levels in urban fringe locations, albeit out of phase with the weekly cycling of ozone in the urban core. Our findings suggest that multiple metrics need to be used to test for the weekend effect and that the causes of DOW differences in ozone concentrations may be location specific. (c) 2006 Elsevier Ltd. All rights reserved.

Abstract  An advanced receptor model was used to elicit source information based on ambient submicron (0.01-0.47 mu m) particle number concentrations, gaseous species, and meteorological variables measured at the New York State Department of Environmental Conservation central monitoring site in Rochester, NY. Four seasonal data sets (winter, spring, summer, and fall) were independently investigated. A total of ten different sources were identified, including two traffic factors, two nucleation factors, industrial emissions, residential/commercial heating, secondary nitrate, secondary sulfate, ozone-rich secondary aerosol, and regionally transported aerosol. The resolved sources were generally characterized by similar number modes for either winter, spring, summer or fall. The size distributions for nucleation were dominated by the smallest particles (<10-30 nm) that gradually grew to larger sizes as could be seen by observing the volume profiles. In addition, the nucleation factors were closely linked to traffic rush hours suggesting that cooling of tail-pipe emissions may have induced nucleation activity in the vicinity of the highways. Although the diurnal pattern of each of the two traffic factors closely followed traffic rush hour for Rochester, their size modes were different suggesting that these factors might represent local and remote emissions. Industrial emissions were dominated by emissions from coal-fired power plants that were located to the northwest of the sampling site. These facilities represent the largest point emission sources Of SO2, and probably ultrafine (<0.1 mu m) or submicron particles, in Rochester. Regionally transported material was characterized by accumulation mode particles. Air parcel back-trajectories showed transport of air masses from the industrial midwest.

Abstract  Suspended particulate matter is significantly related to the degradation of air quality in urban agglomerations, generating adverse health effects. Therefore, the ability to make accurate predictions of particulate ambient concentrations is important in order to improve public awareness and air quality management. This study aims at developing models using multiple regression and neural network (NN) methods that might produce accurate 24-h predictions of daily average (DA) value of PM10 concentration and at comparatively assessing the above mentioned techniques. Pollution and meteorological data were collected in the urban area of Volos, a medium-sized coastal city in central Greece, whose population and industrialization is continuously increasing. Both models utilize five variables as inputs, which incorporate meteorology (difference between daily maximum and minimum hourly value of ground temperature and DA value of wind speed), persistency in PM10 levels and weekly and annual variation of PM10 concentration. The validation of the models revealed that NN model showed slightly better skills in forecasting PM10 concentrations, as the regression and the NN model can forecast 55 and 61% of the variance of the data, respectively. In addition, several statistical indexes were calculated in order to verify the quality and reliability of the developed models. The results showed that their skill scores are satisfying, presenting minor differences. It was also found that both are capable of predicting the exceedances of the limit value of 50 mu g/m(3) at a satisfactory level.

Abstract  Twenty-eight polycyclic aromatic hydrocarbons (PAH) and methylated PAHs (Me-PAH) were measured in daily PM"2"."5 samples collected at an urban site, a suburban site, and a rural site in and near Atlanta during 2004 (5 samples/month/site)....

Abstract  Background: New approaches to link health surveillance data with environmental and population exposure information are needed to examine the health benefits of risk management decisions. Objective: We examined the feasibility of conducting a local assessment of the public health impacts of cumulative air pollution reduction activities from federal, state, local and voluntary actions in the City of New Haven, CT. Methods: Using a hybrid modeling approach that combines regional and local-scale air quality data, we estimated ambient concentrations for multiple air pollutants (e.g., PM2.5, NOx) for base year 2001 and projected emissions for 2010, 2020, and 2030. We assessed the feasibility of detecting health improvements in relation to air pollution reductions for 26 different pollutant/health outcome linkages using both sample size and exploratory epidemiological simulations to further inform decision-making needs. Results: Model projections suggested decreases (~10% to 60%) in pollutant concentrations, mainly due to decreases in pollutants from local sources between 2001 and 2010. Models indicated considerable spatial variability in the concentrations of most pollutants. Sample size analyses supported the feasibility of identifying linkages between reductions in NOx and improvements in all-cause mortality, prevalence of asthma in children and adults, and cardiovascular and respiratory hospitalizations. Conclusion: Substantial reductions in air pollution (e.g., ~60% shown for NOx) are needed to detect health impacts of environmental actions using traditional epidemiologic study designs in small communities like New Haven. In contrast, exploratory epidemiologic simulations suggest that it may be possible to demonstrate the health impacts of PM reductions by predicting intra-urban pollution gradients within New Haven using coupled models.

Abstract  Air quality indices currently in use have been criticized because they do not capture additive effects of multiple pollutants, or reflect the apparent no-threshold concentration-response relationship between air pollution and health. We propose a new air quality health index (AQHI), constructed as the sum of excess mortality risk associated with individual pollutants from a time-series analysis of air pollution and mortality in Canadian cities, adjusted to a 0-10 scale, and calculated hourly on the basis of trailing 3-hr average pollutant concentrations. Extensive sensitivity analyses were conducted using alternative combinations of pollutants from single and multipollutant models. All formulations considered produced frequency distributions of the daily maximum AQHI that were right-skewed, with modal values of 3 or 4, and less than 10% of values at 7 or above on the 10-point scale. In the absence of a gold standard and given the uncertainty in how to best reflect the mix of pollutants, we recommend a formulation based on associations of nitrogen dioxide, ozone, and particulate matter of median aerodynamic diameter less than 2.5 μm with mortality from single-pollutant models. Further sensitivity analyses revealed good agreement of this formulation with others based on alternative sources of coefficients drawn from published studies of mortality and morbidity. These analyses provide evidence that the AQHI represents a valid approach to formulating an index with the objective of allowing people to judge the relative probability of experiencing adverse health effects from day to day. Together with health messages and a graphic display, the AQHI scale appears promising as an air quality risk communication tool. [ABSTRACT FROM AUTHOR] Copyright of Journal of the Air & Waste Management Association (1995) is the property of Air & Waste Management Association and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts)

Abstract  Nitrogen dioxide (NO2) is a ubiquitous atmospheric pollutant due to the widespread prevalence of both natural and anthropogenic sources, and it can be a respiratory irritant when inhaled at elevated concentrations. Evidence for health effects of ambient NO2 derives from three types of studies: observational epidemiology, human clinical exposures, and animal toxicology. Our review focuses on the human clinical studies of adverse health effects of short-term NO2 exposures, given the substantial uncertainties and limitations in interpretation of the other lines of evidence. We examined more than 50 experimental studies of humans inhaling NO2, finding notably that the reporting of statistically significant changes in lung function and bronchial sensitivity did not show a consistent trend with increasing NO2 concentrations. Functional changes were generally mild and transient, the reported effects were not uniformly adverse, and they were not usually accompanied by NO2-dependent increases in symptoms. The available human clinical results do not establish a mechanistic pathway leading to adverse health impacts for short-term NO2 exposures at levels typical of maximum 1-h concentrations in the present-day ambient environment (i.e., below 0.2 ppm). Our review of these data indicates that a health-protective, short-term NO2 guideline level for susceptible (and healthy) populations would reflect a policy choice between 0.2 and 0.6 ppm. EXTENDED ABSTRACT: Nitrogen dioxide (NO2) is a ubiquitous atmospheric pollutant due to the widespread prevalence of both natural and anthropogenic sources, and it can be a respiratory irritant when inhaled at elevated concentrations. Natural NO2 sources include volcanic action, forest fires, lightning, and the stratosphere; man-made NO2 emissions derive from fossil fuel combustion and incineration. The current National Ambient Air Quality Standard (NAAQS) for NO2, initially established in 1971, is 0.053 ppm (annual average). Ambient concentrations monitored in urban areas in the United States are approximately 0.015 ppm, as an annual mean, i.e., below the current NAAQS. Short-term (1-h peak) NO2 concentrations outdoors are not likely to exceed 0.2 ppm, and even 1-h periods exceeding 0.1 ppm are infrequent. Inside homes, 1-h NO2 peaks, typically arising from gas cooking, can range between 0.4 and 1.5 ppm. The health effects evidence of relevance to ambient NO2 derives from three lines of investigation: epidemiology studies, human clinical studies, and animal toxicology studies. The NO2 epidemiology remains inconsistent and uncertain due to the potential for exposure misclassification, residual confounding, and co-pollutant effects, whereas animal toxicology findings using high levels of NO2 exposure require extrapolation to humans exposed at low ambient NO2 levels. Given the limitations and uncertainties in the other lines of health effects evidence, our review thus focused on clinical studies where human volunteers (including asthmatics, children, and elderly) inhaled NO2 at levels from 0.1 to 3.5 ppm during short-term ((1/2)-6-h) exposures, often combined with exercise, and occasionally combined with co-pollutants. We examined the reported biological effects and classified them into (a) lung immune responses and inflammation, (b) lung function changes and airway hyperresponsiveness (AHR), and (c) health effects outside the lungs (extrapulmonary). We examined more than 50 experimental studies of humans inhaling NO2, finding that such clinical data on short-term exposure allowed discrimination of NO2 no-effect levels versus lowest-adverse-effects levels. Our conclusions are summarized by these six points: For lung immune responses and inflammation: (1) healthy subjects exposed to NO2 below 1 ppm do not show pulmonary inflammation; (2) at 2 ppm for 4 h, neutrophils and cytokines in lung-lavage fluid can increase, but these changes do not necessarily correlate with significant or sustained changes in lung function; (3) there is no consistent evidence that NO2 concentrations below 2 ppm increase susceptibility to viral infection; (4) for asthmatics and individuals having chronic obstructive pulmonary disease (COPD), NO2-induced lung inflammation is not expected below 0.6 ppm, although one research group reported enhancement of proinflammatory processes at 0.26 ppm. With regard to NO2-induced AHR: (5) studies of responses to specific or nonspecific airway challenges (e.g., ragweed, methacholine) suggest that asthmatic individuals were not affected by NO2 up to about 0.6 ppm, although some sensitive subsets may respond to levels as low as 0.2 ppm. And finally, for extra-pulmonary effects: (6) such effects (e.g., changes in blood chemistry) generally required NO2 concentrations above 1-2 ppm. Overall, our review of data from experiments with humans indicates that a health-protective, short-term-average NO2 guideline level for susceptible populations (and healthy populations) would reflect a policy choice between 0.2 and 0.6 ppm. The available human clinical results do not establish a mechanistic pathway leading to adverse health impacts for short-term NO2 exposures at levels typical of maximum 1-h concentrations in the present-day ambient environment (i.e., below 0.2 ppm).

Abstract  Fine particulate matter (PM2.5) air pollution is one of the main environmental health problems in developed Countries. According to modeling estimates the PM2.5 concentrations in Poland are among the highest in Europe. In this article we focus on exposure assessment and estimation of adverse health effects due to PM2.5 air pollution. This article consists of two parts. In the first part, we discuss the main methods used to estimate emission-exposure relationships and adverse health effects due to PM2.5 air pollution. In the second part, we present all assessment framework for Poland. We illustrate this framework by estimating the premature deaths and change in life expectancy in Poland caused by anthropogenic, primary PM2.5 emissions from different European countries. and, in proportion, the premature deaths in different European Countries Caused by primary PM2.5 emissions from Poland. The PM2.5 emission were evaluated using the inventory of the European Monitoring and Evaluation Programme (EMEP). The emission-exposure relationships were based on the previously published study and the exposure-response functions for PM2.5 air pollution were estimated in expert elicitation study performed for six European experts on air pollution health effects. Based on the assessment, the anthropogenic primary PM2.5 from the whole of Europe is estimated to cause several thousands of premature deaths in Poland, annually. These premature deaths are both due to PM2.5 emissions front Poland and transportation of PM2.5 from other European Countries, both of these in almost equal parts. The framework presented in this article will be developed in the near future to a full scale integrated assessment, that takes into account both gaseous and PM air pollution.

Abstract  Spokane, WA is prone to frequent particulate pollution episodes due to dust storms, biomass burning, and periods of stagnant meteorological conditions. Spokane is the location of a long-term study examining the association between health effects and chemical or physical constituents of particulate pollution. Positive matrix factorization (PMF) was used to deduce the sources Of PM2.5 (particulate matter less than or equal to2.5 mum in aerodynamic diameter) at a residential site in Spokane from 1995 through 1997. A total of 16 elements in 945 daily PM2.5 samples were measured. The PMF results indicated that seven sources independently contribute to the observed PM2.5 mass: vegetative burning (44%), sulfate aerosol (19%), motor vehicle (11%), nitrate aerosol (9%), airborne soil (9%), chlorine-rich source (6%) and metal processing (3%). Conditional probability functions were computed using surface wind data and the PMF deduced mass contributions from each source and were used to identify local point sources. Concurrently measured carbon monoxide and nitrogen oxides were correlated with the PM2.5 from both motor vehicles and vegetative burning. (C) 2003 Elsevier Science B.V. All rights reserved.

Abstract  Various methods have been developed recently to estimate personal exposures to ambient particulate matter less than 2.5 m in diameter (PM2.5) using fixed outdoor monitors as well as personal exposure monitors. One class of estimators involves extrapolating values using ambient-source components of PM2.5, such as sulfate and iron. A key step in extrapolating these values is to correct for differences in infiltration characteristics of the component used in extrapolation (such as sulfate within PM2.5) and PM2.5. When this is not done, resulting health effect estimates will be biased. Another class of approaches involves factor analysis methods such as positive matrix factorization (PMF). Using either an extrapolation or a factor analysis method in conjunction with regression calibration allows one to estimate the direct effects of ambient PM2.5 on health, eliminating bias caused by using fixed outdoor monitors and estimated personal ambient PM2.5 concentrations. Several forms of the extrapolation method are defined, including some new ones. Health effect estimates that result from the use of these methods are compared with those from an expanded PMF analysis using data collected from a health study of asthmatic children conducted in Denver, Colorado. Examining differences in health effect estimates among the various methods using a measure of lung function (forced expiratory volume in 1 s) as the health indicator demonstrated the importance of the correction factor(s) in the extrapolation methods and that PMF yielded results comparable with the extrapolation methods that incorporated correction factors.

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  An irradiation chamber designed for reproducible generation of inhalation test atmospheres of secondary organic aerosol (SOA) was used to evaluate cardiopulmonary responses in rodents exposed to SOA derived from the oxidation of alpha-pinene. SOA atmospheres were produced with 10:1 ratios of alpha-pinene:nitrogen oxides (NO(x)) and 10:1:1 ratios of alpha-pinene:nitrogen oxides:sulfur dioxide (SO(2)). SOA atmospheres were produced to yield 200 microg m(-3) of particulate matter (PM). Exposures were conducted downstream of honeycomb denuders employed to remove the gas-phase precursors and reaction products. Nose-only exposures were conducted with both rats (pulmonary effects) and mice (pulmonary and cardiovascular effects). Composition of the atmospheres was optimized to ensure that the SOA generated resembled SOA observed in previous irradiation studies, and contained specific SOA compounds of interest (e.g., organosulfates) identified in ambient air. Pulmonary and cardiovascular toxicity were measured in two different rodent species. In situ chemiluminescence and thiobarbituric acid- reactive substances (TBARS) were used to evaluate oxidative reactions in the F344 rats. ApoE(-/-) mice were exposed for 7 days and measurements of TBARS and gene expression of heme oxygenase-1 (HO-1), endothelin-1 (ET-1), matrix metalloproteinase-9 (MMP-9) were made in aorta. Pulmonary inflammatory responses in both species were measured by bronchoalveolar lavage fluid (BALF) cell counts. No pulmonary inflammation was observed in either species. A mild response was observed in mouse aorta for the upregulation of HO-1 and MMP-9, but was not seen for ET-1. Overall, alpha-pinene-derived SOA, including SOA that included organosulfate compounds, revealed limited biological response after short-term inhalation exposures.

Abstract  Environmental epidemiological studies of the health effects of air pollution have been major contributors to the understanding of such effects. The chronic effects of atmospheric pollutants have been studied, but, except for the known respiratory effects of particulate matter (PM), they have not been studied conclusively. There are ongoing studies of the chronic effects of certain pollutant classes, such as ozone, acid rain, airborne toxics, and the chemical form of PM (including diesel exhaust). Acute effects on humans due to outdoor and indoor exposures to several gases/fumes and PM have been demonstrated in epidemiological studies. However, the effects of these environmental factors on susceptible individuals are not known conclusively. These acute effects are especially important because they increase the human burden of minor illnesses, increase disability, and are thought to decrease productivity. They may be related to the increased likelihood of chronic disease as well. Further research is needed in this latter area, to determine the contributions of the time-related activities of individuals in different microenvironments (outdoors, in homes, in transit). Key elements of further studies are the assessment of total exposure to the different pollutants (occurring from indoor and outdoor source) and the interactive effects of pollutants. Major research areas include determination of the contributions of indoor sources and of vehicle emissions to total exposure, how to measure such exposures, and how to measure human susceptibility and responses (including those at the cellular and molecular level). Biomarkers of exposures, doses and responses, including immunochemicals, biochemicals and deoxyribonucleic acid (DNA) adducts, are beginning to promote some basic knowledge of exposure-response, especially the mechanisms. These will be extremely useful additions to standard physiological, immunological, and clinical instruments, and the understanding of biological plausibility. The outcomes of all this work will be the management of risks and the prevention of respiratory diseases related to air pollution.

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  #PURPOSE OF REVIEW: There is evidence for an association between asthma and air pollutants, including ozone, NO2 and particulate matter. Since these pollutants are ubiquitous in the urban atmosphere and typically correlated with each other it has been difficult to ascertain the specific sources of air pollution responsible for the observed effects. Similarly, uncertainty in determining a causal agent, or multiple agents, has complicated efforts to identify the mechanisms involved in pollution-mediated asthma events and whether air pollution may cause asthma as well as exacerbate preexisting cases. RECENT FINDINGS: Numerous studies have examined specific sources of air pollution and their relationship to asthma. This review summarizes recent work conducted, specifically, on traffic pollution and presents results that elucidate several plausible biological mechanisms for the observed effects. Of note are studies linking susceptibility to several genetic polymorphisms. Together, these studies suggest that remaining uncertainties in the asthma-air pollution association may be addressed through enhanced assessment of both exposures and outcomes. SUMMARY: Air-pollution research is evolving rapidly; in the near future, clinicians and public health agencies may be able to use this new information to provide recommendations for asthmatics that go beyond only paying attention to the air-pollution forecast.

Abstract  Air pollution has significant effects on exacerbation of asthma, allergy and other respiratory diseases. Like many other magacities in the world the ambient air quality of Kolkata is also being deteriorated day by day. Automobile exhausts and certain industrial pollutants produce O3 by photochemical reactions. The particulate matter, particularly less than 10 Á in size, can pass through the natural protective mechanism of human respiratory system and plays an important role in genesis and augmentation of allergic disorders. Sources of air pollution in the area and the unique problem arising out of the emission from the vehicles, industries, etc. have been described. Ambient air quality was monitored along with micrometeorological data and the results are discussed. The status of air pollution in the area has been evaluated and a questionnaire survey was conducted to estimate the allergic symptoms and exposure to assess the respiratory disorders. The data are analysed to evaluate the critical situation arising out of the emission of air pollutants and the impact on human health due to respirable diseases (RDs) to middle class sub-population (activity-wise) in the area are assessed. A strategic air quality management plan has been proposed. For the mitigation of air pollution problems in the city, the different measures to be adopted to maintain the balance between sustainable development and environmental management have been discussed.

Abstract  #BACKGROUND: Amsterdam Airport Schiphol is a major source of complaints about aircraft noise, safety risks and concerns about long term adverse health effects, including cancer. We investigated whether residents of the area around Schiphol are at higher risk of developing cancer than the general Dutch population. METHODS: In a population-based study using the regional cancer registry, we estimated the cancer incidence during 1988-2003 in residents of the area surrounding Schiphol. We defined a study area based on aircraft noise contours and 4-digit postal code areas, since historical data on ambient air pollution were not available and recent emission data did not differ from the background urban air quality. RESULTS: In residents of the study area 13 207 cancer cases were diagnosed, which was close to the expected number, using national incidence rates as a reference (standardized incidence ratio [SIR] 1.02). We found a statistically significantly increased incidence of hematological malignancies (SIR 1.12, 95% confidence interval [CI]: 1.05, 1.19), mainly due to high rates for non-Hodgkin lymphoma (SIR 1.22, 95% CI: 1.12, 1.33) and acute lymphoblastic leukemia (SIR 1.34, 95% CI: 0.95, 1.83). The incidence of cancer of the respiratory system was statistically significantly decreased (SIR 0.94, 95% CI: 0.90, 0.99), due to the low rate in males (SIR 0.89). In the core zone of the study area, cancer incidence was slightly higher than in the remaining ring zone (rate ratio of the core zone compared to the ring zone 1.05, 95% CI 1.01, 1.10). This was caused by the higher incidence of cancer of the respiratory system, prostate and the female genital organs in the core zone in comparison to the ring zone. CONCLUSION: The overall cancer incidence in the Schiphol area was similar to the national incidence. The moderately increased risk of hematological malignancies could not be explained by higher levels of ambient air pollution in the Schiphol area. This observation warrants further research, for example in a study with focus on substances in urban ambient air pollution, as similar findings were observed in Greater Amsterdam.

Abstract  In order to investigate the relationship between indoor and outdoor elemental concentrations and to characterize the infiltration behavior of elemental PM2.5constituents, we conducted an analysis of indoor and outdoor PM2.5elemental data collected during a comprehensive particle characterization study of nine nonsmoking homes in Boston, MA. Using data from nighttime periods when little or no particle-generating activity occurred, analyses focused on six elements that were consistently detected in both indoor and outdoor samples and that spanned a range of particle sizes: sulfur, nickel, zinc, iron, potassium, and silicon. Results showed that outdoor levels of all the elements were highly correlated with their corresponding indoor levels. Correlations remained high for different air exchange rate conditions, building characteristics, and seasons, suggesting that variability in ambient elemental infiltration into residences may not be a large source of variability affecting personal-ambient correlations for these elements. Elemental infiltration factors showed strong relationships with air exchange rate and season and were suggestive of an effect of particle size, which was likely obscured by remaining indoor source impacts. Analyses of this small dataset provided an indication that several elements--in particular nickel--could potentially serve as accurate tracers for infiltration of total PM2.5mass- and size-resolved particles into residential buildings. Similar to previously reported findings for sulfur, these elemental tracers showed the poorest performance for smaller and larger particle sizes.

Abstract  Oxides of nitrogen in fresh traffic exhaust are known to scavenge ambient ozone. However, there has only been little study of local variation in ozone resulting from variation in vehicular traffic patterns within communities. Homes of 78 children were selected from a sample of participants in 3 communities in the southern California Children's Health Study. Twenty-four hour ozone measurements were made simultaneously at a home and at a community central site monitor on two occasions between February and November 1994. Homes were geo-coded, and local residential nitrogen oxides (NOx) above regional background due to nearby traffic at each participant's home were estimated using a line source dispersion model. Measured home ozone declined in a predictable manner as modeled residential NOx increased. NOx modeled from local traffic near homes accounted for variation in ozone concentrations of as much as 17 parts per billion. We conclude that residential ozone concentrations may be over- or underestimated by measurements at a community monitor, depending on the variation in local traffic in the community. These findings may have implications for studies of health effects of traffic-related pollutants.

Abstract  Background: Acute myocardial infarction (AMI) is the leading cause of death attributed to cardiovascular diseases. An association between traffic-related air pollution and AMI has been suggested, but the evidence is still limited. Objectives: to evaluate in a multi-centre study association between hospitalisation for first AMI and daily levels of traffic-related air pollution. Methods: We collected data on first AMI hospitalisations in 5 European cities. AMI registers were available in Augsburg and Barcelona; hospital discharge registers (HDRs) were used in Helsinki, Rome and Stockholm. NO2, CO and PM10 (particles <10 mu m) were measured at central monitoring sites. Particle number concentration (PNC), a proxy for ultrafine particles (<0.1 mu m), was measured for a year in each centre, and then modelled retrospectively for the whole study period. We used generalized additive models for statistical analyses. Age and 28-day fatality and season were considered as potential effect modifiers in the 3 HDR centres. Results: Nearly 27 000 cases of first AMI were recorded. There was a suggestion of an association of the same day CO and PNC levels with AMI: RR=1.005 (95% confidence interval: 1.000-1.010) per 0.2 mg/m3 and RR=1.005 (95%CI: 0.996-1.015) per 10000 particles/cm3, respectively. However, associations were only observed in the 3 cities with HDR, where power for city-specific analyses was higher. We observed in these cities the most consistent associations among fatal cases aged <75 years: RR at 1-day lag for CO=1.021 (95%CI: 1.000-1.048) per 0.2 mg/m3, for PNC= 1.058 (95% CI: 1.012-1.107) per 10000 particles/cm3, and for NO2=1.032 (95%CI: 0.998-1.066) per 8 mu g/m3. Effects of air pollution were more pronounced during the warm than the cold season. Conclusions: We found support for the hypothesis that exposure to traffic-related air pollution increases the risk of AMI. Most consistent associations were observed among fatal cases aged <75 years and in the warm season.