Abstract  The Near-Road Exposures and Effects of Urban Air Pollutants Study (NEXUS) was designed to examine the relationship between near-roadway exposures to air pollutants and respiratory outcomes in a cohort of asthmatic children who live close to major roadways in Detroit, Michigan USA. From September 2010 to December 2012 a total of 139 children with asthma, ages 6-14, were enrolled in the study on the basis of the proximity of their home to major roadways that carried different amounts of diesel traffic. The goal of the study was to investigate the effects of traffic-associated exposures on adverse respiratory outcomes, biomolecular markers of inflammatory and oxidative stress, and how these exposures affect the frequency and severity of respiratory viral infections in a cohort of children with asthma. An integrated measurement and modeling approach was used to quantitatively estimate the contribution of traffic sources to near-roadway air pollution and evaluate predictive models for assessing the impact of near-roadway pollution on children's exposures. Two intensive field campaigns were conducted in Fall 2010 and Spring 2011 to measure a suite of air pollutants including PM2.5 mass and composition, oxides of nitrogen (NO and NO2), carbon monoxide, and black carbon indoors and outdoors of 25 participants' homes, at two area schools, and along a spatial transect adjacent to I-96, a major highway in Detroit. These data were used to evaluate and refine models to estimate air quality and exposures for each child on a daily basis for the health analyses. The study design and methods are described, and selected measurement results from the Fall 2010 field intensive are presented to illustrate the design and successful implementation of the study. These data provide evidence of roadway impacts and exposure variability between study participants that will be further explored for associations with the health measures.

Abstract  The diffusing capacity, DL, is a critical physiological parameter of the lung used to assess gas exchange clinically. Most models developed to analyze experimental data from a single breath maneuver have assumed a well-mixed or uniform alveolar region, including the clinically accepted Jones-Meade method. In addition, all previous models have assumed a constant DL, which is independent of alveolar volume, VA. In contrast, experimental data provide evidence for a non-uniform alveolar region coupled with sequential filling of the lung. In addition, although the DL for carbon monoxide is a weak function of VA, the DL of nitric oxide depends strongly on VA. We have developed a new mathematical model of the single breath maneuver that considers both a variable degree of sequential filling and a variable DL. Our model predicts that the Jones-Meade method overestimates DL when the exhaled gas sample is collected late in the exhalation, but underestimates DL if the exhaled gas sample is collected early in the exhalation phase due to the effect of sequential filling. Utilizing a prolonged constant exhalation method, or a three-equation method, will also produce erroneous predictions of DL. We conclude that current methods may introduce significant error in the estimation of DL by ignoring the sequential filling of the lung, and the dependence of DL on VA.

Abstract  In this work we discuss the uncertainty in estimating the human health risk due to exposure to air pollution, including personal and population average exposure error, epidemiological designs and methods of analysis. Different epidemiological models may lead to very different conclusions for the same set of data. Thus, evaluation of the assumptions made and sensitivity analysis are necessary.Short-term health impact indicators may be calculated using concentration-response (C-R) functions. We discuss different methods to combine C-R function estimates from a given locale and time period with the larger body of evidence from other locales and periods and with the literature. A shrunken method is recommended to combine C-R function estimates from multiple-locales. This shrunken estimate includes information from the overall and the local estimates, and thus it characterizes the estimated excess of risk due to heterogeneity between the different locations.

Abstract  This paper tests factors thought to be important in explaining the choices people make in where they spend time. Three aggregate locations are analyzed: outdoors, indoors, and in-vehicles for two different sample groups: a year-long (longitudinal) sample of one individual and a cross-sectional sample of 169 individuals from the US Environmental Protection Agency's Consolidated Human Activity Database (CHAD). The cross-sectional sample consists of persons similar to the longitudinal subject in terms of age, work status, education, and residential type. The sample groups are remarkably similar in the time spent per day in the tested locations, although there are differences in participation rates: the percentage of days frequenting a particular location. Time spent outdoors exhibits the most relative variability of any location tested, with in-vehicle time being the next. The factors found to be most important in explaining daily time usage in both sample groups are: season of the year, season/temperature combinations, precipitation levels, and day-type (work/nonwork is the most distinct, but weekday/weekend is also significant). Season, season/temperature, and day-type are also important for explaining time spent indoors. None of the variables tested are consistent in explaining in-vehicle time in either the cross-sectional or longitudinal samples. Given these findings, we recommend that exposure modelers subdivide their population activity data into at least season/temperature, precipitation, and day-type "cohorts" as these factors are important discriminating variables affecting where people spend their time.

Abstract  Land use regression (LUR) models are often used in epidemiologic studies to predict the air pollution exposure of health study participants. Such models are often based on a small to moderate number of air pollution measurement sites across the study area, and on a set of variables characterizing factors such as traffic patterns and surrounding land uses that are used as potential predictors. We used resampling techniques on a set of 148 measurement sites of NO2 in the urban area of Girona (Spain) to investigate the effect of the number of measurement sites on the LUR model performance, in particular on predictive ability and on the variables being chosen in the final model. In addition, we investigated the effect of the number of potential predictors and the variable selection algorithm used, and the consequences of the use of LUR predictions in regression models for a health outcome. Our results showed that, especially in small samples, both the adjusted within-sample R-2 and the leave-one-out cross-validation R-2 tended to give highly inflated values when compared to their prediction ability in a validation dataset. When the number of potential predictors was high, LUR models developed with a small number of measurement sites tended to give higher within-sample and cross-validated R-2 than those developed with more sites. Validation dataset R-2 showed a poor performance of models developed with a small number of sites that improved as the number of sites increased. Models developed with a small number of sites tended to select a different set of variables every time, were very sensitive to the number of potential predictors offered and resulted in stronger attenuation of coefficients when air pollution predictions were used in a health model. Our results suggest that LUR models aimed at characterizing local air pollution levels in complex urban settings should be based on a large number of measurement sites (>80 in our setting) and that the set of potential predictors should be restricted.

Abstract  To date, the assessment of public health consequences of air pollution has largely focused on a single-pollutant approach aimed at estimating the increased risk of adverse health outcomes associated with the exposure to a single air pollutant, adjusted for the exposure to other air pollutants. However, air masses always contain many pollutants in differing amounts, depending on the types of emission sources and atmospheric conditions. Because humans are simultaneously exposed to a complex mixture of air pollutants, many organizations have encouraged moving towards “a multipollutant approach to air quality.” Although there is general agreement that multipollutant approaches are desirable, the challenges of implementing them are vast.

Abstract  A Special Report of the Institute's Panel on the Health Effects of Traffic-Related Air Pollution This report is the most comprehensive and systematic review to date of the scientific literature on emissions, exposure, and health effects from traffic-related air pollution. It includes conclusions about the populations exposed around major roads, the associations between exposure to air pollution from traffic and human health, and important remaining data gaps. Compared with the initial pre-print version released in May 2009, this final version has undergone data verification and editorial changes; however, the overall conclusions did not change.

Abstract  BACKGROUND: Maternal exposure to air pollution has been related to fetal growth in a number of recent scientific studies. The objective of this study was to assess the association between exposure to air pollution during pregnancy and anthropometric measures at birth in a cohort in Valencia, Spain. METHODS: Seven hundred and eighty-five pregnant women and their singleton newborns participated in the study. Exposure to ambient nitrogen dioxide (NO2) was estimated by means of land use regression. NO2 spatial estimations were adjusted to correspond to relevant pregnancy periods (whole pregnancy and trimesters) for each woman. Outcome variables were birth weight, length, and head circumference (HC), along with being small for gestational age (SGA). The association between exposure to residential outdoor NO2 and outcomes was assessed controlling for potential confounders and examining the shape of the relationship using generalized additive models (GAM). RESULTS: For continuous anthropometric measures, GAM indicated a change in slope at NO2 concentrations of around 40 mcg/m3. NO2 exposure >40 mcg/m3 during the first trimester was associated with a change in birth length of -0.27 cm (95% CI: -0.51 to -0.03) and with a change in birth weight of -40.3 grams (-96.3 to 15.6); the same exposure throughout the whole pregnancy was associated with a change in birth HC of -0.17 cm (-0.34 to -0.003). The shape of the relation was seen to be roughly linear for the risk of being SGA. A 10 mcg/m3 increase in NO2 during the second trimester was associated with being SGA-weight, OR: 1.37 (1.01-1.85). For SGA-length the estimate for the same comparison was OR: 1.42 (0.89-2.25). CONCLUSIONS: Prenatal exposure to traffic-related air pollution may reduce fetal growth. Findings from this study provide further evidence of the need for developing strategies to reduce air pollution in order to prevent risks to fetal health and development.

Abstract  We review gases that can affect oxidative stress and that themselves may be radicals. We discuss O-2 toxicity, invoking superoxide, hydrogen peroxide, and the hydroxyl radical. We also discuss superoxide dismutase (SOD) and both ground-state, triplet oxygen (O-3(2)), and the more energetic, reactive singlet oxygen (O-1(2)). Nitric oxide ((NO)-N-.) is a free radical with cell signaling functions. Besides its role as a vasorelaxant, (NO)-N-. and related species have other functions. Other endogenously produced gases include carbon monoxide (CO), carbon dioxide (CO2), and hydrogen sulfide (H2S). Like (NO)-N-., these species impact free radical biochemistry. The coordinated regulation of these species suggests that they all are used in cell signaling. Nitric oxide, nitrogen dioxide, and the carbonate radical (CO3.-) react selectively at moderate rates with nonradicals, but react fast with a second radical. These reactions establish "cross talk" between reactive oxygen (ROS) and reactive nitrogen species (RNS). Some of these species can react to produce nitrated proteins and nitrolipids. It has been suggested that ozone is formed in vivo. However, the biomarkers that were used to probe for ozone reactions may be formed by non-ozone-dependent reactions. We discuss this fascinating problem in the section on ozone. Very low levels of ROS or RNS may be mitogenic, but very high levels cause an oxidative stress that can result in growth arrest ( transient or permanent), apoptosis, or necrosis. Between these extremes, many of the gasses discussed in this review will induce transient adaptive responses in gene expression that enable cells and tissues to survive. Such adaptive mechanisms are thought to be of evolutionary importance.

Abstract  BACKGROUND: Relatively few studies have been conducted of the association between air pollution and emergency department (ED) visits, and most of these have been based on a small number of visits, for a limited number of health conditions and pollutants, and only daily measures of exposure and response. METHODS: A time-series analysis was conducted on nearly 400,000 ED visits to 14 hospitals in seven Canadian cities during the 1990 s and early 2000s. Associations were examined between carbon monoxide (CO), nitrogen dioxide (NO2), ozone (O3), sulfur dioxide (SO2), and particulate matter (PM 10 and PM2.5), and visits for angina/myocardial infarction, heart failure, dysrhythmia/conduction disturbance, asthma, chronic obstructive pulmonary disease (COPD), and respiratory infections. Daily and 3-hourly visit counts were modeled as quasi-Poisson and analyses controlled for effects of temporal cycles, weather, day of week and holidays. RESULTS: 24-hour average concentrations of CO and NO2 lag 0 days exhibited the most consistent associations with cardiac conditions (2.1% (95% CI, 0.0-4.2%) and 2.6% (95% CI, 0.2-5.0%) increase in visits for myocardial infarction/angina per 0.7 ppm CO and 18.4 ppb NO2 respectively; 3.8% (95% CI, 0.7-6.9%) and 4.7% (95% CI, 1.2-8.4%) increase in visits for heart failure). Ozone (lag 2 days) was most consistently associated with respiratory visits (3.2% (95% CI, 0.3-6.2%), and 3.7% (95% CI, -0.5-7.9%) increases in asthma and COPD visits respectively per 18.4 ppb). Associations tended to be of greater magnitude during the warm season (April - September). In particular, the associations of PM 10 and PM2.5 with asthma visits were respectively nearly three- and over fourfold larger vs. all year analyses (14.4% increase in visits, 95% CI, 0.2-30.7, per 20.6 microg/m3 PM 10 and 7.6% increase in visits, 95% CI, 5.1-10.1, per 8.2 microg/m3 PM2.5). No consistent associations were observed between three hour average pollutant concentrations and same-day three hour averages of ED visits. CONCLUSION: In this large multicenter analysis, daily average concentrations of CO and NO2 exhibited the most consistent associations with ED visits for cardiac conditions, while ozone exhibited the most consistent associations with visits for respiratory conditions. PM 10 and PM2.5 were strongly associated with asthma visits during the warm season.

Abstract  Plans to build a third runway at London Heathrow (LHR) airport have been held back because of concerns that the development would lead to annual mean concentrations of nitrogen dioxide (NO2) in excess of the EU Directive limit value, which must be met by 2010. The dominant effect of other sources of NOx close to the airport, primarily from road traffic, makes it difficult to detect and quantify the contribution made by the airport to local NOx and NO2 concentrations. This work presents approaches that aim to detect and quantify the airport contribution to NOx concentrations for a network of seven measurement sites close to the airport. Two principal approaches are used. First, a graphical technique using bivariate polar plots that develops the idea of a pollution rose is used to help discriminate between different source types. The sampling uncertainties associated with the technique have been calculated through a randomised re-sampling approach. Second, the unique pattern of aircraft activity at LHR enables data filtering techniques to be used to statistically verify the presence of aircraft sources. It is shown that aircraft NO, sources can be detected to at least 2.6 km from the airport, even though the airport contribution at that distance is very small. Using these approaches, estimates have been made of the airport contribution to long-term mean concentrations of NOx and NO2. At the airfield boundary we estimate that approximately 27% of the annual mean NOx and NO2 is due to airport operations. At background locations 2-3 km downwind of the airport we estimate that the upper limit of the airport contribution to be less than 15% (< 10 mu g m(-3)). This work also provides approaches that would help validate and refine dispersion modelling studies used for airport assessments. (c) 2006 Elsevier Ltd. All rights reserved.

Abstract  The history of geochronology in Australia is intimately related to the history of geochronology in Western Australia. The pioneering research of Edward Simpson in the first decade of the 20th century was followed by the establishment of a mass spectrometer laboratory at the University of Western Australia in the early 1950s by Peter Jeffery where the U-Pb, Rb-Sr and the K-Ar geochronological techniques were developed, and a number of young graduates trained. One of these was Bill Compston, who was destined to play a major role in the evolution of geochronology in this country, including the development of SHRIMP. The collaboration between Curtn University, the Geological Survey of Western Australia and the University of Western Australia has been a longstanding and successful feature of geochronology in Western Australia, culminating in the formation of a State-funded Centre of Excellence in Mass Spectrometry. CSIRO is now a partner in the re-funded Centre. The Centre operates two SHRIMPS and a Cameca 1280. Research of international interest has been carried out on Hadean zircons from the Jack Hills region of Western Australia, which has far-reaching implications to the early evolution of this planet.

Abstract  BACKGROUND: The association of long-term air pollution and lung function has not been studied across adult European multi-national populations before. The aim of this study was to determine the association between long-term urban background air pollution and lung function levels, as well as change in lung function among European adults. METHODS:Forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and the ratio thereof (FEV1/FVC) were assessed at baseline and after 9 years of follow-up in adults from 21 European centres (followed-up sample 5610). Fine particles (PM(2.5)) were measured in 2000/2001 using central monitors. RESULTS: Despite sufficient statistical power no significant associations were found between city-specific annual mean PM(2.5) and average lung function levels. The findings also do not support an effect on change in lung function, albeit statistical power was insufficient to significantly detect such an association. CONCLUSIONS: The inability to refuse the null hypothesis may reflect (i) no effect of urban air pollution on lung function or (ii) inherent biases due to the study design. Examples of the latter are lack of individual-level air quality assignment, not quantified within-city contrasts in traffic-related pollution, or the heterogeneity of the studied populations and their urban environments. Future studies on long-term effects of air pollution on lung function could increase statistical power and reduce potential misclassification and confounding by characterizing exposure on the level of individuals, capturing contrasts due to local sources, in particular traffic.

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

Abstract  Associations of particulate matter (PM) and ozone with morbidity and mortality have been reported in many recent observational epidemiology studies. These studies often considered other gaseous co-pollutants also as potential confounders, including nitrogen dioxide (NO2), sulfur dioxide (SO2), and carbon monoxide (CO). However, because each of these air pollutants can have different seasonal patterns and chemical interactions, the estimation and interpretation of each pollutant's individual risk estimates may not be straightforward. Multi-collinearity among the air pollution and weather variables also leaves the possibility of confounding and over- or under-fitting of meteorological variables, thereby potentially influencing the health effect estimates for the various pollutants in differing ways. To investigate these issues, we examined the temporal relationships among air pollution and weather variables in the context of air pollution health effects models. We compiled daily data for PM less than 2.5 mum (PM2.5), ozone, NO2, SO2, CO, temperature, dew point, relative humidity, wind speed, and barometric pressure for New York City for the years 1999-2002. We conducted several sets of analyses to characterize air pollution and weather data interactions, to assess different aspects of these data issues: (1) spatial/temporal variation of PM2.5 and gaseous pollutants measured at multiple monitors; (2) temporal relationships among air pollution and weather variables; and (3) extent and nature of multi-collinearity of air pollution and weather variables in the context of health effects models. The air pollution variables showed a varying extent of intercorrelations with each other and with weather variables, and these correlations also varied across seasons. For example, NO2 exhibited the strongest negative correlation with wind speed among the pollutants considered, while ozone's correlation with PM2.5 changed signs across the seasons (positive in summer and negative in winter). The extent of multi-collinearity problems also varied across pollutants and choice of health effects models commonly used in the literature. These results indicate that the health effects regression need to be run by season for some pollutants to provide the most meaningful results. We also find that model choice and interpretation needs to take into consideration the varying pollutant concurvities with the model co-variables in each pollutant's health effects model specification. Finally, we provide an example for analysis of associations between these air pollutants and asthma emergency department visits in New York City, which evaluate the relationship between the various pollutants' risk estimates and their respective concurvities, and discuss the limitations that these results imply about the interpretability of multi-pollutant health effects models.

Abstract  Rationale: The role of air pollution exposure in the development of asthma, allergies, and related symptoms remains unclear, due in part to the limited number of prospective cohort studies with sufficiently long follow-ups addressing this problem. Objectives: We studied the association between traffic-related air pollution and the development of asthma, allergy, and related symptoms in a prospective birth cohort study with a unique 8-year follow-up. Methods: Annual questionnaire reports of asthma, hay fever, and related symptoms during the first 8 years of life were analyzed for 3,863 children. At age 8, measurements of allergic sensitization and bronchial hyperresponsiveness were performed for subpopulations (n = 1,700 and 936, respectively). Individual exposures to nitrogen dioxide (NO(2)), particulate matter (PM(2.5)), and soot at the birth address were estimated by land-use regression models. Associations between exposure to traffic-related air pollution and repeated measures of health outcomes were assessed by repeated-measures logistic regression analysis. Effects are presented for an interquartile range increase in exposure after adjusting for covariates. Measurements and Main Results: Annual prevalence was 3 to 6% for asthma and 12 to 23% for asthma symptoms. Annual incidence of asthma was 6% at age 1, and 1 to 2% at later ages. PM(2.5) levels were associated with a significant increase in incidence of asthma (odds ratio [OR], 1.28; 95% confidence interval [CI], 1.10-1.49), prevalence of asthma (OR, 1.26; 95% CI, 1.04-1.51), and prevalence of asthma symptoms (OR, 1.15; 95% CI, 1.02-1.28). Findings were similar for NO(2) and soot. Associations were stronger for children who had not moved since birth. Positive associations with hay fever were found in nonmovers only. No associations were found with atopic eczema, allergic sensitization, and bronchial hyperresponsiveness. Conclusions: Exposure to traffic-related air pollution may cause asthma in children.

Abstract  Air quality data on trace metals, other constituents of PM2.5, and criteria air pollutants were used to examine relationships with long-term mortality in a cohort of male U.S. military veterans, along with data on vehicular traffic density (annual vehicle-miles traveled per unit of land area). The analysis used county-level environmental data for the period 1997-2002 and cohort mortality for 1997-2001. The proportional hazards model included individual data on age, race, smoking, body mass index, height, blood pressure, and selected interactions; contextual variables also controlled for climate, education, and income. In single-pollutant models, traffic density appears to be the most important predictor of survival, but potential contributions are also seen for NO2, NO3-, elemental carbon, nickel, and vanadium. The effects of the other main constituents of PM2.5, of crustal particles, and of peak levels of CO, O3, or SO2 appear to be less important. Traffic density is also consistently the most important environmental predictor in multiple-pollutant models, with combined relative risks up to about 1.2. However, from these findings it is not possible to discern which aspects of traffic (pollution, noise, stress) may be the most relevant to public health or whether an area-based predictor such as traffic density may have an inherent advantage over localized measures of ambient air quality. It is also possible that traffic density could be a marker for unmeasured pollutants or for geographic gradients per se. Pending resolution of these issues, including replication in other cohorts, it will be difficult to formulate additional cost-effective pollution control strategies that are likely to benefit public health.

Abstract  OBJECTIVE: We sought to determine whether nitrogen dioxide (NO2) can enhance airway inflammation after allergen challenge in asthmatic subjects. METHODS: Fifteen house-dust-mite (HDM)-sensitive asthmatic subjects were exposed for 3 hours to filtered air or 0.4 ppm NO2, followed by inhalational challenge with HDM allergen. Markers of inflammation were measured in sputum at 6 hours and 26 hours after allergen challenge. RESULTS: After exposure to NO2, eosinophil concentration decreased significantly in the 6-hour postallergen sputum. No significant NO2-related difference was observed for other variables. CONCLUSIONS: Our results suggest that, in most asthmatic individuals, multi-hour exposure to a high ambient concentration of NO2 does not enhance the inflammatory response to subsequent inhaled allergen as assessed by cell distribution in induced sputum. Because the decrease in airway eosinophils has been reported in previous animal studies, future research should be directed toward the mechanism of this effect.

Abstract  BACKGROUND: This paper examines the short-term health effects of air pollution on daily hospital admissions in Australian cities (those considered comprise more than 50% of the Australian population) for the period 1996-99. METHODS: The study used a similar protocol to overseas studies and derived single city and pooled estimates using different statistical approaches to assess the accuracy of the results. RESULTS: There was little difference between the results derived from the different statistical approaches for cardiovascular admissions, while in those for respiratory admissions there were differences. For three of the four cities (for the other the results were positive but not significant), fine particles (measured by nephelometry - bsp) and nitrogen dioxide (NO2) have a significant impact on cardiovascular admissions (for total cardiac admissions, RR = 1.0856 for a one-unit increase in bsp (10(-4) x m(-1)), RR = 1.0023 for a 1 ppb increase in NO2). For three of the four cities (for the other, the results were negative and significant), fine particles, NO2 and ozone have a significant impact on respiratory admissions (for total elderly respiratory admissions, RR = 1.0552 per 1 unit (10(-4) x m(-1)) increase in bsp, RR = 1.0027 per 1ppb increase in NO2, RR = 10014 per 1 ppb increase in ozone for elderly asthma and COPD admissions). In all analyses the particle and NO2 impacts appear to be related. CONCLUSIONS: Similar to overseas studies, air pollution has an impact on hospital admissions in Australian cities, but there can be significant differences between cities.

Abstract  BACKGROUND: Air pollution from road traffic is a serious health hazard, and people with preexisting respiratory disease may be at increased risk. We investigated the effects of short-term exposure to diesel traffic in people with asthma in an urban, roadside environment. METHODS: We recruited 60 adults with either mild or moderate asthma to participate in a randomized, crossover study. Each participant walked for 2 hours along a London street (Oxford Street) and, on a separate occasion, through a nearby park (Hyde Park). We performed detailed real-time exposure, physiological, and immunologic measurements. RESULTS: Participants had significantly higher exposures to fine particles (<2.5 microm in aerodynamic diameter), ultrafine particles, elemental carbon, and nitrogen dioxide on Oxford Street than in Hyde Park. Walking for 2 hours on Oxford Street induced asymptomatic but consistent reductions in the forced expiratory volume in 1 second (FEV1) (up to 6.1%) and forced vital capacity (FVC) (up to 5.4%) that were significantly larger than the reductions in FEV1 and FVC after exposure in Hyde Park (P=0.04 and P=0.01, respectively, for the overall effect of exposure, and P<0.005 at some time points). The effects were greater in subjects with moderate asthma than in those with mild asthma. These changes were accompanied by increases in biomarkers of neutrophilic inflammation (sputum myeloperoxidase, 4.24 ng per milliliter after exposure in Hyde Park vs. 24.5 ng per milliliter after exposure on Oxford Street; P=0.05) and airway acidification (maximum decrease in pH, 0.04% after exposure in Hyde Park and 1.9% after exposure on Oxford Street; P=0.003). The changes were associated most consistently with exposures to ultrafine particles and elemental carbon. CONCLUSIONS: Our observations serve as a demonstration and explanation of the epidemiologic evidence that associates the degree of traffic exposure with lung function in asthma.

Abstract  The authors investigated the association of early-life exposure to indoor air pollution with neuropsychological development in preschoolers and assessed whether this association differs by glutathione-S-transferase gene (GSTP1) polymorphisms. A prospective, population-based birth cohort was set up in Menorca, Spain, in 1997–1999 (n = 482). Children were assessed for cognitive functioning (McCarthy Scales of Children's Abilities) and attention-hyperactivity behaviors (Diagnostic and Statistical Manual of Mental Disorders, 4th Edition) at age 4 years. During the first 3 months of life, information about gas appliances at home and indoor nitrogen dioxide concentration was collected at each participant's home (n = 398, 83%). Genotyping was conducted for the GSTP1 coding variant Ile105Val. Use of gas appliances was inversely associated with cognitive outcomes (β coefficient for general cognition = –5.10, 95% confidence interval (CI): –9.92, –0.28; odds ratio for inattention symptoms = 3.59, 95% CI: 1.14, 11.33), independent of social class and other confounders. Nitrogen dioxide concentrations were associated with cognitive function (a decrease of 0.27 point per 1 ppb, 95% CI: –0.48, –0.07) and inattention symptoms (odds ratio = 1.06, 95% CI: 1.01, 1.12). The deleterious effect of indoor pollution from gas appliances on neuropsychological outcomes was stronger in children with the GSTP1 Val-105 allele. Early-life exposure to air pollution from indoor gas appliances may be negatively associated with neuropsychological development through the first 4 years of life, particularly among genetically susceptible children.

Abstract  In this paper, a shifted power-law model, based on the wind profile model, had been supposed to simulate concentration gradient of nitrogen dioxide (NO2) with distance from a highway. Field experiments were performed for NO2 gradients from a highway in Shanghai by using passive samplers. The shifted power-law model was fitted well with experimental results of field experiments both in this study and in the literature. The results not only verified the validity of shifted power-law relationship between NO2 concentration and the distance from a highway, but also partially demonstrated that there were some significant similarities between wind profile and air pollutants concentration profile near highway. With known concentration of chosen reference point and appropriate value of the parameter k, the model could be practically applied for predicting the NO2 distributions near a highway. The methods of determining the parameter k were also discussed for further detailed studies. (c) 2006 Elsevier Ltd. All rights reserved.

Abstract  BACKGROUND: Road traffic is a source of both air pollution and noise; two environmental hazards both found to increase the risk of ischemic heart disease. Given the high correlation between these pollutants, it is important to investigate combined effects, in relation to myocardial infarction (MI).

METHODS: Among 50,744 middle-aged Danes enrolled into the Diet, Cancer and Health cohort from 1993 to 97, we identified 2403 cases of incident MI during a median follow-up of 14.5 years. Present and historical residential addresses from 1987 to 2011 were found in national registries, and traffic noise (Lden) and air pollution (NO2) were modelled for all addresses. Analyses were performed using Cox proportional hazard models.

RESULTS: Road traffic noise and NO2 were both individually associated with a higher risk of MI, with hazard ratios of 1.14 (1.07-1.21) and 1.08 (1.03-1.12) per inter-quartile range higher 10-year mean of road traffic noise and NO2, respectively. Mutual exposure adjustment reduced the association with 10-year NO2 exposure (1.02 (0.96-1.08)), whereas the association with road traffic noise remained: 1.12 (1.03-1.21). For fatal incident MI, the pattern was similar, but the associations for both pollutants were stronger. In analyses of tertiles across both pollutants, the strongest effects were seen for combined medium/high exposure, especially for fatal MI's.

CONCLUSION: Both road traffic noise and NO2 were associated with a higher risk of MI in single-pollutant models. In two-pollutant models, mainly noise was associated with MI. Combined exposure to both pollutants was associated with the highest risk.