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Introduction: Systemic inflammation may be one of the mechanisms mediating the association between ambient air pollution and cardiovascular morbidity and mortality. Interleukin-6 (IL-6) and fibrinogen are biomarkers of systemic inflammation that are independent risk factors for cardio-vascular disease., Objective: We investigated the association between ambient air pollution and systemic inflammation using baseline measurements of IL-6 and fibrinogen from controlled human exposure studies., Methods: In this retrospective analysis we used repeated-measures data in 45 nonsmoking subjects. Hourly and daily moving averages were calculated for ozone, nitrogen dioxide, sulfur dioxide, and particulate matter

The Critical Review of Hoff and Christopher, along with the discussants, provides an important perspective on the interface between satellite measurement science and air quality observations. A top-down picture of the usefulness of satellite observations in terms of air quality regulatory and technical support requirements can be summarized. The air quality requirements are (1) determination of compliance with the ambient air quality standards, (2) inference of human and ecosystem exposure, (3) identification of intra- and intercontinental events relevant to EE, (4) establishment of trends in ambient concentrations relevant to accountability, (5) regulatory and forecast model applications, and (6) extension of fundamental knowledge relevant to air quality. Each of these topics is important to air quality management, and each has detailed technical issues associated with spatial and temporal resolution, accuracy, and precision, etc. In any case, one can summarize the broad capabilities of measurement systems to address these requirements as listed in Table 1. From this rather superficial summary table, investigators should be encouraged to forward increased interaction between the various measurement communities and to facilitate the utility of a comprehensive portfolio of measurements and adjunct analyses for improved air quality applications. The Critical Review has done much to educate air quality scientists on the possibilities for using satellite remote sensing for various purposes. However, space scientists also need a better education on air quality science. Recently published reviews on PM air quality measurements are available that complement the Hoff-Christopher paper on this topic. The need for greater collaboration of air quality and space scientists is evident in an article published in the July issue of the journal. Al-Hamdan et al. provide an interesting and useful analysis of relationships between surface air quality and space-based satellite AOD to estimate human exposure. They obtain mostly urban PM data from EPA's Air Quality System (AQS), but they neglect the potentially more useful PM2.5 and chemical speciation data from the nonurban Interagency Monitoring of Protected Visual Environments (IMPROVE) and the Southeastern Aerosol Research and Characterization (SEARCH) networks. They correlate PM2.5 mass with optical depth, although visibility assessments show that light extinction is better represented by a weighted sum of PM2.5 sulfate, nitrate, organic carbon, elemental carbon, and soil dust. Their comparison of hourly measurements with filter measurements does not specify the source of the hourly values as TEOM or BAM. Spatial outliers for ground-level measurements are removed to improve the correlation of PM2.5 with AOD, although these "outliers" are probably real values that relate to human exposure or a nearby source effect. The point here is not to overly criticize a good publication that will be highly cited. The intent is to demonstrate the value of air quality and space scientists working together more closely on this topic. This is something the review authors alluded to in their review, but if, as they concluded, the "promised land" has not been reached, then perhaps it is an appropriate time for the atmospheric community to ask, "Can near-term satellite observations play a role in characterizing broad-based (outdoor) exposure to pollutants and consequently influence public health improvement?" and, if so, then, "What comprehensive, integrated system is needed if satellite observations are to be used together with ground-based observations and modeling to continue improving air quality management options?"

Fine particulate matter air pollution plus ozone impairs vascular function and raises diastolic blood pressure. We aimed to determine the mechanism and air pollutant responsible. The effects of pollution on heart rate variability, blood pressure, biomarkers, and brachial flow-mediated dilatation were determined in 2 randomized, double-blind, crossover studies. In Ann Arbor, 50 subjects were exposed to fine particles (150 microg/m(3)) plus ozone (120 parts per billion) for 2 hours on 3 occasions with pretreatments of an endothelin antagonist (Bosentan, 250 mg), antioxidant (Vitamin C, 2 g), or placebo. In Toronto, 31 subjects were exposed to 4 different conditions (particles plus ozone, particles, ozone, and filtered air). In Toronto, diastolic blood pressure significantly increased (2.9 and 3.6 mm Hg) only during particle-containing exposures in association with particulate matter concentration and reductions in heart rate variability. Flow-mediated dilatation significantly decreased (2.0% and 2.9%) only 24 hours after particle-containing exposures in association with particulate matter concentration and increases in blood tumor necrosis factor alpha. In Ann Arbor, diastolic blood pressure significantly similarly increased during all of the exposures (2.5 to 4.0 mm Hg), a response not mitigated by pretreatments. Flow-mediated dilatation remained unaltered. Particulate matter, not ozone, was responsible for increasing diastolic blood pressure during air pollution inhalation, most plausibly by instigating acute autonomic imbalance. Only particles from urban Toronto additionally impaired endothelial function, likely via slower proinflammatory pathways. Our findings demonstrate credible mechanisms whereby fine particulate matter could trigger acute cardiovascular events and that aspects of exposure location may be an important determinant of the health consequences.

Background: Chronic exposure to traffic-related air pollution (TRAP) may contribute to premature mortality, but few studies to date have addressed this topic., Objectives: In this study we assessed the association between TRAP and mortality in Toronto, Ontario, Canada., Methods: We collected nitrogen dioxide samples over two seasons using duplicate two-sided Ogawa passive diffusion samplers at 143 locations across Toronto. We calibrated land use regressions to predict NO2 exposure on a fine scale within Toronto. We used interpolations to predict levels of particulate matter with aerodynamic diameter < or = 2.5 microm (PM(2.5)) and ozone levels. We assigned predicted pollution exposures to 2,360 subjects from a respiratory clinic, and abstracted health data on these subjects from medical billings, lung function tests, and diagnoses by pulmonologists. We tracked mortality between 1992 and 2002. We used standard and multilevel Cox proportional hazard models to test associations between air pollution and mortality., Results: After controlling for age, sex, lung function, obesity, smoking, and neighborhood deprivation, we observed a 17% increase in all-cause mortality and a 40% increase in circulatory mortality from an exposure contrast across the interquartile range of 4 ppb NO2. We observed no significant associations with other pollutants., Conclusions: Exposure to TRAP was significantly associated with increased all-cause and circulatory mortality in this cohort. A high prevalence of cardiopulmonary disease in the cohort probably limits inference of the findings to populations with a substantial proportion of susceptible individuals.

The spatiotemporal variability of ground-level ozone (GLO) in the rural Annapolis Valley, Nova Scotia was investigated between August 29, 2006, and September 28, 2007, using Ogawa nitrite-impregnated passive diffusion samplers (PS). A total of 353 PS measurements were made at 17 ambient and 1 indoor locations over 18 sampling periods ranging from 2 to 4 weeks. The calculated PS detection limit was 0.8 +/- 0.02 parts per billion by volume (ppbv), for a 14-day sampling period. Duplicate samplers were routinely deployed at three sites and these showed excellent agreement (R2 values of 0.88 [n = 11], 0.95 [n = 17], and 0.96 [n = 17]), giving an overall PS imprecision value of 5.4%. Comparisons between PS and automated continuous ozone analyzers at three sites also demonstrated excellent agreement with R2 values of 0.82, 0.95, and 0.95, and gradients not significantly different from unity. The minimum, maximum, and mean (+/- 1 sigma) ambient annual GLO concentrations observed were 7.7, 72.1, and 34.3 +/- 10.1 ppbv, respectively. The three highest sampling sites had significantly greater (P = 0.032) GLO concentrations than three Valley floor sites, and there was a strong correlation between concentration and elevation (R2 = 0.82). Multivariate models were used to parameterize the observed GLO concentrations in terms of prevailing meteorology at an elevated site found at Kejimkujik National Park and also at a site on the Valley floor. Validation of the multivariate models using 30 months of historical meteorological data at these sites yielded R2 values of 0.70 (elevated site) and 0.61 (Valley floor). The mean indoor ozone concentration was 5.4 +/- 3.3 ppbv and related to ambient GLO concentration by the equation: indoor = 0.34 x ambient - 5.07. This study has demonstrated the suitability of PS for long-term studies of GLO over a wide geographic area and the effect of topographical and meteorological influences on GLO in this region.

This comprehensive review of the recent literature was undertaken to determine the current state of knowledge of the risk factors involved in the development of asthma in order to focus investigations in a proposed new longitudinal birth cohort study. The origins of asthma appear to lie in the prenatal and early postnatal period, and renewed investigations in this period with long-term close follow-up and objective phenotypic characterization will help to unravel the role of the multiple putative environmental factors in the development of asthma. It is only after understanding these effects that one can hope to design rational prevention studies for asthma.

We evaluated the impact on personal exposure to air pollutants of following advice which typically accompanies air quality advisories and indices. Scripts prescribed the time, location, duration and nature of activities intended to simulate daily activity patterns for adults and children. Scripts were paired such that one individual would proceed with usual activities (base scenario), whereas the other (intervention scenario) would alter activities as if following advice. Other than commuting, where the intervention group walked or used public transportation rather than riding in personal vehicles, this group generally spent less time outdoors. Ultra-fine particles (UFPs), particulate matter of median aerodynamic diameter less than 2.5 mum (PM(2.5)) and total volatile organic compounds (VOCs) were measured using samplers carried by individuals during the course of daily activities. During daytime activities (e.g., work, daycare) constituting the largest share of sampling time (approximately 6 h per day), the intervention group experienced a 14% reduction in exposure to UFPs (P=0.01), a 21% reduction in exposure to PM(2.5) (P=0.08), and an 86% increase in exposure to VOCs (P=0.02). Other findings included an 89% increase in exposure to UFPs (P=0.02) and a threefold increase in exposure to VOCs (P=0.08) in the intervention group during evening cooking. Following smog advisory advice results in reduced exposures to some pollutants, while at the same time increasing exposure to others. Advice needs to be refined giving consideration to overall personal exposure.

We discuss Bukowski's hypothesis that unmeasured, individual risk factors, notably stress caused by being in traffic or at work, may confound the association found in many time-series studies between air pollution and cardiovascular outcomes. In replying to these concerns, we describe the methods used to carry out time-series studies and discuss whether it is reasonable to believe that stress can confound the association. Our analysis suggests that these factors are unlikely to cause bias in time-series studies, although it may be important in panel and other longitudinal studies. Specifically, we argue that: (1) persons most likely to be susceptible to the effects of air pollution, notably the very young and the elderly, and those suffering from certain chronic diseases (e.g., congestive heart failure), are unlikely to be highly exposed to traffic and therefore to traffic-related stress and (2) over lengthy periods of time and sub-populations, levels of individual stress are unlikely to act coherently to create an association with ambient air pollution.

This guidance document is a reference for air quality policymakers and managers providing state-of-the-art, evidence-based information on key determinants of air quality management decisions. The document reflects the findings of five annual meetings of the NERAM (Network for Environmental Risk Assessment and Management) International Colloquium Series on Air Quality Management (2001-2006), as well as the results of supporting international research. The topics covered in the guidance document reflect critical science and policy aspects of air quality risk management including i) health effects, ii) air quality emissions, measurement and modeling, iii) air quality management interventions, and iv) clean air policy challenges and opportunities.

There are acknowledged difficulties in epidemiological studies to accurately assign exposure to air pollution for large populations, and large, long-term cohort studies have typically relied upon data from central monitoring stations. This approach has generally been adequate when populations span large areas or diverse cities. However, when the effects of intra-urban differences in exposure are being studied, the use of these existing central sites are likely to be inadequate for representing spatial variability that exists within an urban area. As part of the Border Air Quality Strategy (BAQS), an international agreement between the governments of Canada and the United States, a number of air health effects studies are being undertaken by Health Canada and the US EPA. Health Canada's research largely focuses on the chronic exposure of elementary school children to air pollution. The exposure characterization for this population to a variety of air pollutants has been assessed using land-use regression (LUR) models. This approach has been applied in several cities to nitrogen dioxide (NO2), as an assumed traffic exposure marker. However, the models have largely been developed from limited periods of saturation monitoring data and often only represent one or two seasons. Two key questions from these previous efforts, which are examined in this paper, are: If NO2 is a traffic marker, what other pollutants, potentially traffic related, might it actually represent? How well is the within city spatial variability of NO2, and other traffic-related pollutants, characterized by a single saturation monitoring campaign. Input data for the models developed in this paper were obtained across a network of 54 monitoring sites situated across Windsor, Ontario. The pollutants studied were NO2, sulfur dioxide (SO2) and volatile organic compounds, which were measured in all four seasons by deploying passive samplers for 2-week periods. Correlations among these pollutants were calculated to assess what other pollutants NO2 might represent, and correlations across seasons for a given pollutant were determined to assess how much the within-city spatial pattern varies with time. LUR models were then developed for NO2, SO2, benzene, and toluene. A multiple regression model including proximity to the Ambassador Bridge (the main Canada-US border crossing point), and proximity to highways and major roads, predicted NO2 concentrations with an R2=0.77. The SO2 model predictors included distance to the Ambassador Bridge, dwelling density within 1500m, and Detroit-based SO2 emitters within 3000m resulting in a model with an R2=0.69. Benzene and toluene LUR models included traffic predictors as well as point source emitters resulting in R2=0.73 and 0.46, respectively. Between season pollutant correlations were all significant although actual concentrations for each site varied by season. This suggests that if one season were to be selected to represent the annual concentrations for a specific site this may lead to a potential under or overestimation in exposure, which could be significant for health research. All pollutants had strong inter-pollutant correlations suggesting that NO2 could represent SO2, benzene, and toluene.

In this paper, the pooled NO2 association with nonaccidental mortality is examined across 10 cities in Canada in single- and two-pollutant time-series models. The results reaffirm that NO2 has the strongest association with mortality, particularly in the warm season. Although attributing such effects to NO2 cannot be ruled out, it is plausible that NO2 is acting as an indicator for some other exposure affecting the population. This could include PM2.5, as has been suggested from some personal exposure data, but it could also be indicating a more specific type of PM2.5, such as traffic-related particles, given that in cities the main source of NO2 is motor vehicle exhaust. NO2 could also be acting as a surrogate for other pollutant(s) originating from motor vehicles or high-temperature combustion, such as volatile organic compounds (VOCs) or polycyclic aromatic hydrocarbons. Another possibility is other oxidized nitrogen species ("NO(z)") or photochemically produced pollutants that can co-vary with NO2, especially during urban stagnation events. Data to test these different possibilities across several Canadian cities are examined. The focus is on correlations in time or space between NO2 and other pollutants that are more strongly linked to vehicle emissions. The results support the hypothesis that NO2 is a better indicator than PM2.5 of a range of other toxic pollutants. This includes VOCs, aldehydes, NO(z) and particle-bound organics in motor vehicle exhaust. Thus, overall, the strong effect of NO2 in Canadian cities could be a result of it being the best indicator, among the pollutants monitored, of fresh combustion (likely motor vehicles) as well as photochemically processed urban air.

The objectives of this study were: (1) to quantify the errors associated with saturation air quality monitoring in estimating the long-term (i.e., annual and 5 yr) mean at a given site from four 2-week measurements, once per season; and (2) to develop a sampling strategy to guide the deployment of mobile air quality facilities for characterizing intraurban gradients of air pollutants, that is, to determine how often a given location should be visited to obtain relatively accurate estimates of the mean air pollutant concentrations. Computer simulations were conducted by randomly sampling ambient monitoring data collected in six Canadian cities at a variety of settings (e.g., population-based sites, near-roadway sites). The 5-yr (1998-2002) dataset consisted of hourly measurements of nitric oxide (NO), nitrogen dioxide (NO2), oxides of nitrogen (NOx), sulfur dioxide (SO2), coarse particulate matter (PM10), fine particulate matter (PM2.5), and CO. The strategy of randomly selecting one 2-week measurement per season to determine the annual or long-term average concentration yields estimates within 30% of the true value 95% of the time for NO2, PM10 and NOx. Larger errors, up to 50%, are expected for NO, SO2, PM2.5, and CO. Combining concentrations from 85 random 1-hr visits per season provides annual and 5-yr average estimates within 30% of the true value with good confidence. Overall, the magnitude of error in the estimates was strongly correlated with the variability of the pollutant. A better estimation can be expected for pollutants known to be less temporally variable and/or over geographic areas where concentrations are less variable. By using multiple sites located in different settings, the relationships determined for estimation error versus number of measurement periods used to determine long-term average are expected to realistically portray the true distribution. Thus, the results should be a good indication of the potential errors one could expect in a variety of different cities, particularly in more northern latitudes.

The objective of this paper is to model determinants of intraurban variation in ambient concentrations of nitrogen dioxide (NO2) in Toronto, Canada, with a land use regression (LUR) model. Although researchers have conducted similar studies in Europe, this work represents the first attempt in a North American setting to characterize variation in traffic pollution through the LUR method. NO2 samples were collected over 2 wk using duplicate two-sided Ogawa passive diffusion samplers at 95 locations across Toronto. Independent variables employed in subsequent regression models as predictors of NO2 were derived by the Arc 8 geographic information system (GIS). Some 85 indicators of land use, traffic, population density, and physical geography were tested. The final regression model yielded a coefficient of determination (R2) of .69. For the traffic variables, density of 24-h traffic counts and road measures display positive associations. For the land use variables, industrial land use and counts of dwellings within 2000 m of the monitoring location were positively associated with NO2. Locations up to 1500 m downwind of major expressways had elevated NO2 levels. The results suggest that a good predictive surface can be derived for North American cities with the LUR method. The predictive maps from the LUR appear to capture small-area variation in NO2 concentrations. These small-area variations in traffic pollution are probably important to the exposure experience of the population and may detect health effects that would have gone unnoticed with other exposure estimates.

The human health effects of fine particulate matter (PM2.5) have provided impetus for the establishment of new air quality standards or guidelines in many countries. This has led to the need for information on the main sources responsible for PM2.5. In urban locations being impacted by regional-scale transport, source-receptor relationships for PM2.5 are complex and require the application of multiple receptor-based analysis methods to gain a better understanding. This approach is being followed to study the sources of PM2.5 impacting southern Ontario, Canada, and its major city of Toronto. Existing monitoring data in the region around Toronto and within Toronto itself are utilized to estimate that 30-45% of the PM2.5 is from local sources, which implies that 55-70% is transported into the area. In addition, there are locations in the city that can be shown to experience a greater impact from local sources such as motor vehicle traffic. Detailed PM2.5 chemical characterization data were collected in Toronto in order to apply two different multivariate receptor models to determine the main sources of the PM2.5. Both approaches produced similar results, indicating that motor-vehicle-related emissions, most likely of local origin, are directly responsible for about 20% of the PM2.5. Gasoline engine vehicles were found to be a greater overall contributor (13%) compared to diesel vehicles (8%). Secondary PM2.5 from coal-fired power plants continues to be a significant contributor (20-25%) and also played a role in enhancing production of secondary organic carbon mass (15%) on fine particles. Secondary fine particle nitrate was the single most important source (35%), with a large fraction of this likely related to motor vehicle emissions. Independent use of different receptor models helps provide more confidence in the source apportionment, as does comparison of results among complementary receptor-based data analysis approaches.

Measured ozone (O(3)) and carbon dioxide (CO(2)) concentrations and fluxes over five different canopies (mixed coniferous-deciduous forest, deciduous forest, corn, soybean and pasture) in the eastern USA were analyzed to investigate the stomatal uptake of O(3). It was found that the ambient O(3) concentration levels had little effect on stomatal conductance. However, the accumulated stomatal uptake of O(3), upon reaching a threshold value on any given day, appears to reduce the rate of further O(3) uptake substantially. This may explain why the maximum O(3) deposition velocity often appeared in the early morning hours over some forest canopies. Substantially reduced CO(2) fluxes over wet canopies compared to dry canopies suggest that stomata were likely partially or totally blocked by water droplets or films when canopies were wet. By using a big-leaf dry deposition model, measured O(3) fluxes were separated into stomatal and non-stomatal portions. It was estimated that stomatal uptake contributed 55-75% of the total daytime O(3) fluxes and 40-60% of the total daytime plus nighttime fluxes, depending on canopy type. This suggests that about half of the total O(3) flux occurred through the non-stomatal pathway. At three locations (deciduous forest, corn and soybean sites), O(3) concentrations of 30-60 ppb and of 60-85 ppb contributed equally to the accumulated stomatal fluxes, while at the other two locations (mixed coniferous-deciduous forest and pasture sites), concentrations of 30-60 ppb contributed twice as much as those from 60 to 85 ppb.

A longitudinal study investigating personal exposures to PM(2.5), nitrogen dioxide (NO(2)), and carbon monoxide (CO) for cardiac compromised individuals was conducted in Toronto, Canada. The aim of the study was (1) to examine the distribution of exposures to PM(2.5), NO(2), and CO; and (2) to investigate the relationship between personal exposures and fixed-site ambient measurements of PM(2.5), NO(2), and CO. In total, 28 subjects with coronary artery disease wore the Rupprecht & Patashnick ChemPass Personal Sampling System one day a week for a maximum of 10 weeks. The mean (SD) personal exposures were 22 microg m(-3) (42), 14 p.p.b. (6), and 1.4 p.p.m (0.5) for PM(2.5), NO(2), and CO, respectively. PM(2.5) and CO personal exposures were greater than central fixed-site ambient measurements, while the reverse pattern was observed for NO(2). Ambient PM(2.5) and NO(2) were correlated with personal exposures to PM(2.5) and NO(2) with median Spearman's correlation coefficients of 0.69 and 0.57, respectively. The correlations between personal exposures and ambient measurements made closest to the subjects' homes or the average of all stations within the study were not stronger than the correlation between personal exposures and central fixed-site measurements. Personal exposures to PM(2.5) were correlated with personal exposures to NO(2) (median Spearman's correlation coefficient of 0.43). This study suggests that central fixed-site measurements of PM(2.5) and NO(2) may be treated as surrogates for personal exposures to PM(2.5) and NO(2) in epidemiological studies, and that NO(2) is a potential confounder of PM(2.5).

Background: Recent studies suggest that persons with diabetes and with cardiovascular disease may be at higher risk for the short-term effects of air pollution. We carried out this mortality time series study in Montreal, Quebec, Canada to confirm these observations and to determine whether diabetics who had other health conditions were also at higher risk of dying when air pollution increases., Methods and Results: In one analysis, we related daily deaths from diabetes (using the underlying cause) to daily concentrations of particles and gaseous pollutants. In another analysis, we created subgroups by identifying subjects diagnosed 1 year before death with diabetes and other major health conditions from billing and prescription data from the universal Quebec Health Insurance Plan. The analysis made use of parametric log-linear Poisson models that were adjusted for long-term temporal trends and daily weather conditions. We found positive associations between most air pollutants and daily mortality from diabetes as well as among subjects diagnosed with diabetes 1 year before death. In the latter group of subjects, greater effects were found generally in the warm season and especially among subjects who had diabetes and who also had any cardiovascular disease, chronic coronary disease, and atherosclerosis. We did not find evidence of associations among persons who only had diabetes (i.e., did not also have cancer, cardiovascular disease, or lower respiratory disease)., Conclusions: These data indicate that individuals with diabetes who also have cardiovascular disease may be susceptible to the short-term effects of air pollution.

Exposure to air pollution has been shown to cause arterial vasoconstriction and alter autonomic balance. Because these biologic responses may influence systemic hemodynamics, we investigated the effect of air pollution on blood pressure (BP). Responses during 2-hr exposures to concentrated ambient fine particles (particulate matter < 2.5 microm in aerodynamic diameter; PM2.5) plus ozone (CAP+O3) were compared with those of particle-free air (PFA) in 23 normotensive, nonsmoking healthy adults. Mean concentrations of PM2.5 were 147 +/- 27 versus 2 +/- 2 microg/m3, respectively, and those of O3 were 121 +/- 3 versus 8 +/- 5 ppb, respectively (p < 0.0001 for both). A significant increase in diastolic BP (DBP) was observed at 2 hr of CAP+O3 [median change, 6 mm Hg (9.3%); binomial 95% confidence interval (CI), 0 to 11; p = 0.013, Wilcoxon signed rank test] above the 0-hr value. This increase was significantly different (p = 0.017, unadjusted for basal BP) from the small 2-hr change during PFA (median change, 1 mm Hg; 95% CI, -2 to 4; p = 0.24). This prompted further investigation of the CAP+O3 response, which showed a strong association between the 2-hr change in DBP (and mean arterial pressure) and the concentration of the organic carbon fraction of PM2.5 (r = 0.53, p < 0.01; r = 0.56, p < 0.01, respectively) but not with total PM2.5 mass (r < or = 0.25, p > or = 0.27). These findings suggest that exposure to environmentally relevant concentrations of PM2.5 and O3 rapidly increases DBP. The magnitude of BP change is associated with the PM2.5 carbon content. Exposure to vehicular traffic may provide a common link between our observations and previous studies in which traffic exposure was identified as a potential risk factor for cardiovascular disease.

Individuals are exposed to particulate matter from both indoor and outdoor sources. The aim of this study was to compare the relative contributions of three sources of personal exposure to fine particles (PM2.5) by using chemical tracers. The study design incorporated repeated 24-hr personal exposure measurements of air pollution from 28 cardiac-compromised residents of Toronto, Ontario, Canada. Each study participant wore the Rupprecht & Patashnick ChemPass Personal Sampling System 1 day a week for a maximum of 10 weeks. During their individual exposure measurement days the subjects reported to have spent an average of 89% of their time indoors. Particle phase elemental carbon, sulfate, and calcium personal exposure data were used in a mixed-effects model as tracers for outdoor PM2.5 from traffic-related combustion, regional, and local crustal materials, respectively. These three sources were found to contribute 13% +/- 10%, 17% +/- 16%, and 7% +/- 6% of PM2.5 exposures. The remaining fraction of the personal PM2.5 is hypothesized to be predominantly related to indoor sources. For comparison, central site outdoor PM2.5 measurements for the same dates as personal measurements were used to construct a receptor model using the same three tracers. In this case, traffic-related combustion, regional, and local crustal materials were found to contribute 19% +/- 17%, 52% +/- 22%, and 10% +/- 7%, respectively. Our results indicate that the three outdoor PM2.5 sources considered are statistically significant contributors to personal exposure to PM2.5. Our results also suggest that among the Toronto subjects, who spent a considerable amount of time indoors, exposure to outdoor PM2.5 includes a greater relative contribution from combustion sources compared with outdoor PM2.5 measurements where regional sources are the dominant contributor.

The purpose of this study was to derive a land-use regression model to estimate on a geographical basis ambient concentrations of nitrogen dioxide (NO2) in Montreal, Quebec, Canada. These estimates of concentrations of NO2 will be subsequently used to assess exposure in epidemiologic studies on the health effects of traffic-related air pollution. In May 2003, NO2 was measured for 14 consecutive days at 67 sites across the city using Ogawa passive diffusion samplers. Concentrations ranged from 4.9 to 21.2 ppb (median 11.8 ppb). Linear regression analysis was used to assess the association between logarithmic concentrations of NO2 and land-use variables derived using the ESRI Arc 8 geographic information system. In univariate analyses, NO2 was negatively associated with the area of open space and positively associated with traffic count on nearest highway, the length of highways within any radius from 100 to 750 m, the length of major roads within 750 m, and population density within 2000 m. Industrial land-use and the length of minor roads showed-no association with NO2. In multiple regression analyses, distance from the nearest highway, traffic count on the nearest highway, length of highways and major roads within 100 m, and population density showed significant associations with NO2; the best-fitting regression model had a R2 of 0.54. These analyses confirm the value of land-use regression modeling to assign exposures in large-scale epidemiologic studies.

Although progress has been made in the last few decades at reducing ambient concentrations of air pollutants, scientific evidence suggests that there remains a risk to human health from exposure to these pollutants at current levels in Canada. Much of the motivation for air pollution reduction efforts is to protect population health. This article presents a method of monitoring changes in air pollution-related health outcomes over time in conjunction with temporal changes in ambient pollution concentrations. The progress measure is a function of temporal changes in location-specific ambient concentrations and the potentially time-dependent association between those concentrations and daily deaths. The progress measure can be determined for a single location or at a national level. The measure can also be extended to include several pollutants. The progress measure is illustrated with an example of how changes in nitrogen dioxide levels in 12 Canadian cities from 1981 to 1999 have translated into changes in the percent of nonaccidental mortality burden attributable to this pollutant over time.

An ensemble-trajectory analysis technique known as Quantitative Transport Bias Analysis was applied to determine which geographic areas systematically contributed to above- and below-average fine particle mass (PM2.5) over eastern North America. Six-hour average measurements from 12 rural or suburban locations in eastern North America collected using a tapered element oscillating microbalance were individually associated with corresponding 3-day back-trajectories for the warm seasons (May-September) of 2000 and 2001. Much of the populated areas of northeastern North America were implicated in the build-up of PM2.5 to above-average concentrations. The finer structure of the Quantitative Transport Bias Analysis pattern indicated that transport from the Ohio River Valley, particularly the eastern portion of this area, was most often associated with the highest PM2.5 concentrations. In addition, air masses originating over a relatively large area from southeast Ohio to the western part of Virginia and the western Kentucky to central Tennessee area tended to result in relatively high PM2.5 concentrations over northeastern North America. These observation-based findings were consistent with the spatial distribution of the main sulfur dioxide emissions sources and the major oxides of nitrogen point sources.

We assessed the in vitro toxicity of various particles on three murine macrophage cell lines, (J774A.1, WR19M.1, RAW264.7). The cells were exposed to aqueous suspensions (0-100 microg/30 mm2 well) of urban particulate matter (SRM-1648, SRM-1649, EHC-93), fine particulate matter (PM2.5), titanium dioxide (SRM-154b), and respirable cristobalite (SRM-1879) for 2 h and were then stimulated with lipopolysaccharide (LPS, 100 ng/ml) and recombinant interferon-gamma (IFN, 100 U/ml). After overnight incubation with the particles and LPS/IFN, nitric oxide production was estimated from culture supernatant nitrite. Cell viability was determined by monitoring the rate of AlamarBlue reduction. The dose-effect relationships for nitrite and viability were modeled as a power function (Fold change = [Dose+1]beta), where beta represents the slope of the dose-response curve. Potency was defined as the rate of change in nitrite production corrected for cell viability (beta(POTENCY) = beta(NITRITE) - beta(VIABILITY)). Overall, the urban particles decreased nitric oxide production (beta(POTENCY) < 0), while exposure of the cells to fine particulate matter or cristobalite increased the production of nitric oxide (beta(POTENCY) > 0). Titanium dioxide (TiO2) was essentially inactive (beta(POTENCY) approximately to 0). The decrease in nitric oxide production seen in cells exposed to the urban particles was directly correlated to a decrease in the expression of inducible nitric oxide (iNOS) as determined by Western blot analysis. The results indicate that particles are modulators of nitric oxide production in murine macrophages and may directly disrupt expression of iNOS during concomitant pathogen exposure. Pathways leading to enhanced NO production causing cell injury, and to decreased NO release resulting in lower bacterial clearance, may both be relevant to the health effects of ambient particles.

The health effects of ambient fine particulate matter (PM(2.5)) and its potential impact on vascular endothelial function have not been thoroughly investigated. As endothelial dysfunction plays an important role in the pathogenesis of atherosclerosis and its complications, we examined the effects of concentrated fine ambient particles (CAPs) on the plasma level of asymmetric dimethylarginine (ADMA) in a pilot study. ADMA is a circulating endogenous inhibitor of nitric oxide synthase (NOS) that is associated with impaired vascular function and increased risk for cardiovascular events. A mobile air research laboratory (AirCARE 1) was used to provide "real-world" CAPs exposures for this study conducted in Detroit, MI. Fourteen Brown Norway rats were exposed to filtered air (FA) (n = 7) or CAPs (0.1-2.5 microm) (n = 7) for 3 consecutive days (8 h/day) in July 2002. Rats were exposed during these periods to average particle mass concentrations of 354 microg/m(3). Rat plasma samples were collected 24 h postexposure. Plasma concentrations of ADMA were significantly elevated in rats exposed to CAPs versus those exposed to FA (mean +/- standard deviation = 1.49 +/- 0.18 vs. 1.29 +/- 0.26 microM, p =.05 by one-tailed t-test). Analyses of meteorological data and CAPs trace element composition suggest that local particle emission sources contributed largely to overall mass of CAPs. Results of this pilot study suggest that exposure to PM(2.5) at high concentrations may trigger an acute increase in circulating ADMA level. This finding has implications for the regulation of vasomotor tone by particulate pollutants and the propensity for adverse cardiovascular events.

Studies have shown associations between acute ambient particulate matter (PM) levels and increases in morbidity and mortality from cardiovascular diseases. We have previously reported in 24 healthy adults that exposure to concentrated ambient particles plus ozone (CAP + O(3)) caused a mean decrease of 0.09 mm in brachial artery diameter (BAD), which was significantly larger than a mean increase of 0.01 mm among the same individuals exposed to filtered air (FA). Our current objective is to examine the relationship between total and constituent PM(2.5) mass concentrations and the acute vascular response. We have analyzed both ambient and exposure filters from the brachial artery study for major chemical constituents, allowing us to compare the strength of the associations between each constituent and an individual's arterial response. We determined gravimetric PM(2.5) mass concentration and inorganic ion content from exposure filters. Twenty-three-hour ambient PM(2.5) filters collected from the same site and on the same day were used to estimate exposure concentrations of trace elements and organic and elemental carbon. We performed linear regression analyses on the levels of measured or estimated PM constituents using each subject's FA exposure as a control. We found, from our regression analyses, a significant negative association between both the organic and elemental carbon concentrations and the difference in the postexposure change in the BAD (Delta BAD) between and CAP + O(3) and FA exposure days. An understanding of the PM constituents most responsible for adverse health outcomes is critical for efforts to develop pollution abatement strategies that maximize benefits to public health.

The association between daily variations in ambient concentrations of nitrogen dioxide (NO2) and mortality was examined in 12 of Canada's largest cities, using a 19-yr time-series analysis (from 1981-1999). The authors employed parametric statistical methods that are not subject to the recently discovered convergence and error estimation problems of generalized additive models. An increase in the 3-d moving average of NO2 concentrations equivalent to the population-weighted study mean of 22.4 ppb was associated with a 2.25% (t = 4.45) increase in the daily nonaccidental mortality rate and was insensitive to adjustment for ozone, sulfur dioxide, carbon monoxide, coefficient of haze, size-fractionated particulate mass, and the sulfate ion measured on an every-6th-day sampling schedule. The 3-d moving average of NO2 was sensitive to adjustment for fine particulate matter measured daily during the 1998-2000 time period.

Background: Uterine arteriovenous communications are uncommon lesions that may be associated with life-threatening postpartum and postinstrumentation hemorrhage., Case: A primigravida presented with infected retained products of conception. Excessive hemorrhage of unclear etiology occurred at dilation and curettage. After a second episode of bleeding, the patient received a diagnosis of uterine arteriovenous fistula., Conclusion: Uterine arteriovenous communications should be included in the differential diagnosis in patients with excessive postpartum or postinstrumentation bleeding. Color and spectral flow Doppler can aid diagnosis and clinical management.

Background: The risk of hospitalization for asthma caused by outdoor aeroallergens is largely unknown., Objective: The objective of this study was to determine the association between changes in outdoor aeroallergens and hospitalizations for asthma from the Pacific coast to the Atlantic coast of Canada., Methods: A daily time series analysis was done to test the association between daily changes in aeroallergens and daily changes in hospitalizations for asthma during a 7-year period between 1993 and 2000 in 10 of the largest cities in Canada. Results were adjusted for long-term trends, day of the week, climate, and air pollution., Results: A daily increase, equivalent to the mean value of each allergen, was associated with the following percentage increase in asthma hospitalizations: 3.3% (95% CI, 2.3 to 4.1) for basidiomycetes, 3.1% (95% CI, 2.8 to 5.7) for ascomycetes, 3.2% (95% CI, 1.6 to 4.8) for deuteromycetes, 3.0% (95% CI, 1.1 to 4.9) for weeds, 2.9% (95% CI, 0.9 to 5.0) for trees, and 2.0% (95% CI, 1.1 to 2.8) for grasses. After accounting for the independent effects of trees and ozone, the combination of the 2 was associated with an additional 0.22% increase in admissions averaged across cities (P <.05)., Conclusion: These findings provide evidence for the hypothesis that aeroallergens are an important cause of severe asthma morbidity across Canada, and in some situations there might be a modest synergistic adverse effect of ozone and aeroallergens combined.

The chemical composition of Toronto PM2.5 was measured daily from Feb 2000 to Feb 2001, and source apportionment was undertaken using positive matrix factorization (PMF). In Toronto, PM2.5 levels were influenced both by local urban activities and also by regional-scale transport. Although several PMF solutions were possible, an eight-source model for explaining the observed Toronto PM2.5 was found to provide realistic results and interesting insights into sources. The four main sources were coal combustion related to regional transport and secondary sulfate (26%), secondary nitrate related to both local and upwind sources of NOx and NH3 (36%), secondary organic aerosols (SOA) formed from a variety of precursor organic emissions (15%), and motor vehicle traffic (10%). The other detectable sources were road salt (winter) and three types of primary PM2.5 hypothesized to be associated with smelters, coal and oil combustion, industry, and local construction. Overall, motor vehicle-related emissions (including road salt and nitrate) were estimated to be responsible for about 40% of the PM2.5. In the summer, the SOA mass was estimated to contribute approximately 20% to the PM2.5. Inclusion of water-soluble, low-molecular-weight organic acids led to identification of this component, thus providing a significant improvement in PMF's ability to resolve sources. Without organic acid measurements the SOA portion of the observed PM2.5 was assigned to the secondary coal component, increasing its contribution and resulting in a source profile with an unrealistic amount of organic mass. This suggests that in the northeastern part of North America, there are physical and/or chemical processes that lead to close interaction between secondary organic and inorganic aerosols.

The NERAM International Colloquia series is a program of five annual meetings involving scientists, regulators, industry representatives, and other stakeholder groups to improve the linkage between emerging scientific evidence on the population health impacts of exposure to particulate matter and clean air policy decisions. Health and Air Quality 2001, the first meeting in the colloquium series, focused on the findings of prospective cohort studies of particulate air pollution and mortality and implications for risk management. A further objective of the colloquium was to identify research directions to reduce information gaps and uncertainties faced by policy makers. This article discusses priority themes for future research to generate evidence in support of policy decisions to improve air quality and population health. These research themes include development of population health indicators to characterize the public health burden of air pollution; individual exposure and outcome studies to the currently available database on the association between air pollution and adverse health effects; identification of sensitive subpopulations; techniques to assess the independent effects of individual pollutants on population health; comparative risk assessment; methods for characterization and communication of uncertainty in risk estimates; effectiveness of policy interventions to guide allocation of limited population health protection resources; improved predictions of the benefits of interventions through appropriate economic analyses: targeted interventions; and approaches for effective stakeholder engagement in risk management policy decisions. Future meetings in the NERAM Colloquium series will provide a forum for discussion of the current state of knowledge and policy implications of findings associated with these key research themes.

The primary objective of this pilot study was to measure the variation of ambient nitrogen dioxide (NO(2)) concentration with increasing distance from a major highway in Montréal, Canada, in order to assess the validity of distance from the roadways as a surrogate for exposure to traffic-related air pollution in epidemiologic studies. A total of 31 two-sided Ogawa passive samplers (using triethanolamine-impregnated filters as an absorbent) were installed for 7 days in groups of two or three along an axis perpendicular to a major highway where traffic density exceeds 100000 vehicles/day. Distances ranged from 0 to 1310 m from the highway. Concentrations of NO(2) ranged from 11.9 to 29.3 ppb, and decreased significantly with increasing logarithmic distance from the highway (P<0.0001). Concentrations of NO(2) were also significantly lower upwind than downwind relative to the highway (P=0.0012). These findings indicate that distance from highways may be a valid surrogate for traffic-related air pollution.

Measurement of particle-bound organic carbon (OC) may be complicated by sampling artifacts such as adsorption of gas-phase species onto particles or filters or evaporation of semivolatile compounds off the particles. A denuder-based integrated organic gas and particle sampler (IOGAPS), specifically designed to minimize sampling artifacts, has been developed to sample atmospheric carbonaceous aerosols. IOGAPS is designed to first remove gas-phase chemicals via sorption to the XAD-coated denuder, and subsequently particles are trapped on a quartz filter. A backup sorbent system consisting of sorbent- (XAD-4 resin) impregnated filters (SIFs) was used to capture the semivolatile OC that evaporates from the particles accumulated on the upstream quartz filter. A traditional filter pack (FP) air sampler, which uses a single quartz filter to collect the particles, was employed for comparison in this study. Elemental and organic carbon were determined from filter punches by a thermal optical transmittance aerosol carbon analyzer. Field measurements show that there was no significant difference between the elemental carbon concentrations determined by the FP and IOGAPS, indicating that particle loss during the transit through the denuder tube was negligible. Compared with the OC determined by FP (3.9-12.6 microg of C/m3), the lower OC observed on the quartz filter in the IOGAPS (2.2-6.0 microg of C/m3) was expected because of the removal of gas-phase organics by the denuder. Higher semivolatile organic carbon (SVOC) on the backup SIFs during the night (1.24-8.43 microg of C/m3) suggests that more SVOC, emitted from primary sources or formed as secondary organic compounds, partitions onto the particles during the night because of the decreased ambient temperature. These data illustrate the utility of an IOGAPS system to more accurately determine the particle-bound OC in comparison to FP-based systems.

Study Objectives: To document the existence and investigate the etiology of "thunderstorm asthma," which has been reported sporadically over the past 20 years., Design: We assessed the relationship between thunderstorms, air pollutants, aeroallergens, and asthma admissions to a children's hospital emergency department over a 6-year period., Results: During thunderstorm days (n = 151 days) compared to days without thunderstorms (n = 919 days), daily asthma visits increased from 8.6 to 10 (p < 0.05), and air concentrations of fungal spores doubled (from 1,512 to 2,749/m(3)), with relatively smaller changes in pollens and air pollutants. Daily time-series analyses across the 6 years of observation, irrespective of the presence or absence of thunderstorms, demonstrated that an increase in total spores, equivalent to its seasonal mean, was associated with a 2.2% (0.9% SE) increase in asthma visits., Conclusions: Our results support a relationship between thunderstorms and asthma, and suggest that the mechanism may be through increases in spores that exacerbate asthma. Replication in other climates is suggested to determine whether these findings can be generalized to other aeroallergen mixes.

Air pollution exposure is associated with an increased risk of acute and chronic cardiovascular mortality. Recent observations have implicated fine particulate matter (PM(2.5)) as one of the most important pollutants. Inhalation of PM(2.5) causes acute pulmonary inflammation and oxidative stress. The subsequent generation of a systemic inflammatory response could link air pollution exposure with the development of cardiovascular disease. Human experiments have demonstrated pro-arrhythmic alterations in cardiac autonomic tone, increased blood pressure, higher serum C-reactive protein levels, and alterations in blood rheology favoring coagulation following controlled pollution exposures or in relation to elevated ambient PM(2.5) levels. Recent studies have also uncovered several harmful impacts on the systemic vasculature, including the triggering of acute vasoconstriction and the enhanced development of atherosclerosis. Many questions, however, remain unanswered and future studies will be required to clarify the relevant biologic mechanisms and to identify the specific constituents responsible for mediating the adverse health impacts.

A 10-day winter sampling campaign was conducted in downtown Toronto for particulate matter (PM) air pollution in the fine (<2.5 microm) size range. An aerosol laser ablation mass spectrometer (LAMS), a tapered-element oscillating microbalance (TEOM), and an aerodynamic particle sizer (APS) were operated in parallel to characterize the PM on-line. In this study, the LAMS observed differences in the chemical composition between three separate episodes with higher PM2.5 mass and APS counts. LAMS results showed that in one instance of elevated PM, organic amines were present in the particulates. Temporal analyses of this episode revealed chemical transformations as the amines, characterized by m/z peaks 58(C3HeN)+, 86(C5H2N)+, and nitrates, increased in number concentration while Ca and hydrocarbon particle classes concurrently decreased. On another day, sulfates were found to have increased significantly. The third event was only 4 h in duration and exhibited an increase in the number of submicron-sized K/hydrocarbons and sulfate-containing particles. In this last event, the hydrocarbons and a K to Fe ratio enrichment indicated there was likely a contribution from a combustion source. This work offers some of the first insights into single particle size and chemistry in a cold winter climate.

The impact of various atmospheric transport directions on ambient fine particle (PM2.5) concentrations at several sites in southeastern Canada was estimated (for May-September) using back-trajectory analysis. Three-day back trajectories (four per day) were paired with 6-hr average PM2.5 mass concentrations measured using tapered element oscillating microbalances (TEOM). PM2.5 concentrations at rural locations in the region were affected by nonlocal sources originating in both Canada and the United States. Comparison of sites revealed that, on average, the local contribution to total PM2.5 in the greater Toronto area (GTA) is approximately 30-35%. At each location, average PM2.5 concentrations under south/southwesterly flow conditions were 2-4 times higher than under the corresponding northerly flow conditions. The chemical composition of both urban and rural PM2.5 was determined during two separate 2-week spring/summer measurement campaigns. Components identified included SO4(2-) NO3-, NH4+, black carbon and organic carbon (OC), and trace elements. Higher particle mass at the urban Toronto site was composed of a higher proportion of all components. However, black carbon, NO3-, NaCl, and trace elements were found to be the most enriched over the rural/regional background levels.

The influence of air pollution on disability days in Toronto during the period 1994-1999 was examined using data from Canada's National Population Health Survey. A model of disability days (the sum of days spent in bed and days when the respondent cut down on usual activities) during the 2 weeks prior to the interview was constructed by sequentially examining the influence of time period, personal characteristics, weather, and air pollution. After adjusting for these other factors, only the effects of carbon monoxide and particulate matter of median diameter less than 2.5 microm (PM2.5) were statistically significant (respectively, 30.8% (95% CI 1.2-69.0) and 21.9% (95% CI 3.8-43.0) increase in disability days for a change in concentration equal to the interquartile range of the 2-week average pollutant concentration). PM2.5 was more strongly associated with disability days in the warm season. Results of multipollutant models were difficult to interpret in that effect sizes appeared to be influenced by covariation among pollutants. With the exception of warm season results for PM2.5, findings were not sensitive to alternative analytical approaches. While these results are suggestive of significant effects of the urban air pollution mix at relatively low ambient concentrations, the precise contribution of individual pollutants could not be determined.

Background: Fine particulate air pollution and ozone are associated with increased cardiovascular events. To help explain the mechanism behind these observations, we investigated the effect of air pollution exposure on vascular function., Methods and Results: Twenty-five healthy adults underwent a randomized, double-blind, crossover study comparing the vascular response to the 2-hour inhalation of approximately 150 microg/m(3) of concentrated ambient fine particles (CAP) plus ozone (120 ppb) versus the response to the inhalation of filtered air. High-resolution vascular ultrasonography was used to measure alterations in brachial artery diameter, endothelial-dependent flow-mediated dilatation (FMD) and endothelial-independent nitroglycerin-mediated dilatation (NMD). Exposure to CAP plus ozone caused a significant brachial artery vasoconstriction compared with filtered air inhalation (-0.09+/-0.15 mm versus +0.01+/-0.18 mm, P=0.03). There were no significant differences in FMD (+0.29+/-4.11% versus -0.03+/-6.63%, P=0.88), NMD (+3.87+/-5.43% versus +3.46+/-7.92%, P=0.83), or blood pressure responses between exposures., Conclusions: Short-term inhalation of fine particulate air pollution and ozone at concentrations that occur in the urban environment causes acute conduit artery vasoconstriction.

To clarify the health effects of ozone exposure in young children, the authors studied the association between air pollution and hospital admissions for acute respiratory problems in children less than 2 years of age during the 15-year period from 1980 to 1994 in Toronto, Canada. The daily time series of admissions was adjusted for the influences of day of the week, season, and weather. A 35% (95% confidence interval: 19%, 52%) increase in the daily hospitalization rate for respiratory problems was associated with a 5-day moving average of the daily 1-hour maximum ozone concentration of 45 parts per billion, the May-August average value. The ozone effect persisted after adjustment for other ambient air pollutants or weather variables. Ozone was not associated with hospital admissions during the September-April period. Ambient ozone levels in the summertime should be considered a risk factor for respiratory problems in children less than 2 years of age.

The impact of ambient aeroallergens on morbidity from childhood asthma is largely unknown. To address this issue, we studied the association between daily emergency department visits for asthma to a children's hospital, and daily concentrations of both pollen grains and fungal spores during a 5-yr period between 1993 and 1997. Air pollution and meteorological data accounted for in the analyses included ozone, nitrogen dioxide, sulfur dioxide, sulfates, temperature, barometric pressure, and relative humidity. The daily number of asthma visits ranged from 0 to 36 per day with an average of 7.5. Fungal spores, but not pollen grains, were associated with visits (p < 0.05). The percentage increase associated with each group, independent of the others, was 1.9% (SE 0.9) for deuteromycetes, 4.1% (1.6) for basidiomycetes, 2.8% (1.0) for ascomycetes, and 8.8% for these spores combined. In summary, fungal spores account for a significant proportion of the asthma exacerbations in children that prompt an emergency department visit.

This study was undertaken in order to shed light on which groups of the general population may be susceptible to the effects of ambient particles. The objectives of the study were (1) to determine whether concentrations of particles in the ambient air of Montreal, Quebec, were associated with daily all-cause and cause-specific mortality in the period 1984 to 1993, and (2) to determine whether groups of the population had higher than average risks of death from exposure to particles. From the network of fixed-site air pollution monitors in Montreal we obtained daily mean levels of various measures of particles, gaseous pollutants, and weather variables measured at Dorval International Airport. We also used measurements of sulfate from an acid rain monitoring station 150 km southeast of the city (Sutton, Quebec). We estimated associations for particulate matter (PM) with an aerodynamic diameter of 10 microns or smaller (PM10), or 2.5 microns or smaller (PM2.5), total suspended particles (TSP), coefficient of haze (COH), an extinction coefficient, and sulfate. Because substantial data for fine particles were missing, we developed a regression model to predict PM2.5 and to predict sulfate from PM2.5. In the main body of the report, we present results for COH, predicted PM2.5, and sulfate. Detailed results for all pollutants are included in Appendices H through O, which are available on request from Health Effects Institute and from the HEI web site at www.healtheffects.org. To address the first objective, we made use of the underlying causes of death among all 140,939 residents of Montreal who died between 1984 and 1993. We regressed the logarithm of daily counts of cause-specific mortality on the daily mean levels for a variety of measures of particles, accounting for seasonal and subseasonal fluctuations in the mortality time series, overdispersion, and weather factors. To address the second objective, we developed algorithms to define conditions that subjects had prior to death, with the focus on cardiopulmonary diseases. These algorithms were based on information retained on the databases of the universal Quebec Health Insurance Plan (QHIP). The databases include records of all procedures (e.g., type of surgery), physician visits, and consultations carried out by all physicians in Quebec. For persons > or = 65 years and for all recipients of social assistance the prescription database contains records of all pharmaceuticals dispensed (type of medication, dose, quantity). For each group of conditions defined, we used the same statistical model that was used in the analyses of all nonaccidental causes of death. In the analyses of cause-specific mortality, we found evidence of associations for all nonaccidental causes of death and specific causes of death--cancer, coronary artery disease, respiratory diseases, and diabetes--that were consistent across most metrics of ambient air particle concentrations, evaluated as the 3-day mean of particle concentrations measured on the day of death (lag 0) and on each of the two days before death (lag 1, lag 2). Associations for all cardiovascular diseases combined were found only with sulfate. As well, we generally found increased daily mortality for persons 65 years of age and over. The results for all nonaccidental causes of death are similar to findings from other studies; the mean percent increase in mortality for a 100 micrograms/m3 increase in daily TSP at lag 0 was 6.7%. In the analyses of the groups defined from the QHIP data, there was little evidence of associations with air pollutants among persons who before death were classified as having acute or chronic upper respiratory diseases, airways diseases, hypertension, acute coronary artery diseases, and cerebrovascular diseases. On the other hand, we found consistent increases across most types of ambient particles for persons who had cancer, acute lower respiratory diseases, any form of cardiovascular disease, chronic coronary artery diseases, and congestive heart failure. As well, we found an association for individuals who did not have any cardiovascular disease, lower respiratory diseases, and cancer. This latter group consisted of persons who had no interactions with the health care system one year before death (12%) and individuals with a wide variety of potentially fatal diseases (52%), including neurological conditions (12%), diabetes (8%), cardiac dysrhythmias (8%), dementia (6%), organic psychotic disorders (6%), and anemias (4%). As statistical power was reduced in the analyses presented above, differences between groups (e.g., < 65 and > or = 65 year age groups) were not usually statistically significant. The association with diabetes has not been reported previously, and this needs to be replicated in other studies. (ABSTRACT TRUNCATED)

Existing studies of the association between air pollution, aeroallergens and emergency department (ED) visits have generally examined the effects of a few pollutants or aeroallergens on individual conditions such as asthma or chronic obstructive pulmonary disease. In this study, we considered a wide variety of respiratory and cardiac conditions and an extensive set of pollutants and aeroallergens, and utilized prospectively collected information on possible effect modifiers which would not normally be available from purely administrative data. The association between air pollution, aeroallergens and cardiorespiratory ED visits (n = 19,821) was examined for the period 1992 to 1996 using generalized additive models. ED visit, air pollution and aeroallergen time series were prefiltered using LOESS smoothers to minimize temporal confounding, and a parsimonious model was constructed to control for confounding by weather and day of week. Multipollutant and multi-aeroallergen models were constructed using stepwise procedures and sensitivity analyses were conducted by season, diagnosis, and selected individual characteristics or effect modifiers. In single-pollutant models, positive effects of all pollutants but NO2 and COH were observed on asthma visits, and positive effects on all respiratory diagnosis groups were observed for O3, SO2, PM10, PM2.5, and SO4(2-). Among cardiac conditions, only dysrhythmia visits were positively associated with all measures of particulate matter. In the final year-round multipollutant models, a 20.9% increase in cardiac ED visits was attributed to the combination of O3 (16.0%, 95% CI 2.8-30.9) and SO2 (4.9%, 95%CI 1.7-8.2) at the mean concentration of each pollutant. In the final multipollutant model for respiratory visits, O3 accounted for 3.9% of visits (95% CI 0.8-7.2), and SO2 for 3.7% (95% CI 1.5-6.0), whereas a weak, negative association was observed with NO2. In multi-aeroallergen models of warm season asthma ED visits, Ascomycetes, Alternaria and small round fungal spores accounted for 4.5% (95% CI 1.8-7.4), 4.7% (95% CI 1.0-8.6) and 3.0% (95% CI 0.8-5.1), respectively, of visits at their mean concentrations, and these effects were not sensitive to adjustment for air pollution effects. In conclusion, we observed a significant influence of the air pollution mix on cardiac and respiratory ED visits. Although in single-pollutant models, positive associations were noted between ED visits and some measures of particulate matter, in multipollutant models, pollutant gases, particularly ozone, exhibited more consistent effects. Aeroallergens were also significantly associated with warm season asthma ED visits.

Canadian particle monitoring programs examining PM10, PM2.5, and particle composition have been in operation for over 10 years. Until recently, the measurements were manual/filter-based with 24-hr sample collection varying in frequency from daily to every sixth day, using GrasebyAnderson dichotomous samplers. In the past few years, these monitoring activities have been expanded to include hourly measurements using tapered element oscillating microbalances (TEOMs). This continuous monitoring program started operation focusing on PM 10, but now emphasizes PM 2.5 through the addition of more TEOMs and switching of the inlets of some of the existing units. The data from all of these measurement activities show that there are broad geographical differences and also local- to regional-scale spatial differences in mass and composition of PM2.5. Due to variations in sources, significantly different PM2.5 concentrations are not uncommon within the same city. Comparison of nearby urban and rural sites indicates that 30 and 40% of the PM 2.5 is from local urban sources in Montreal and Toronto, respectively. Hourly PM 2.5 measurements in Toronto suggest that vehicular emissions are an important contributor to urban PM 2.5. There has been a decreasing trend in urban PM 2.5, with annual average concentrations between the 1987-1990 and 1993-1995 periods decreasing by 11 to 39%, depending upon the site. The largest declines were in Montreal and Halifax, and the smallest decline was in Toronto. Comparison of 24-hr TEOM and manual dichotomous sampler PM 2.5 measurements from a site in Toronto indicates that the TEOM results in lower concentrations. The magnitude of this difference is relatively small in the warmer months, averaging about 12%. During the colder months the difference averages about 23%, but can be as large as 50%.

We obtained data on daily numbers of admissions to hospital in Toronto, Canada, from 1980 to 1994 for respiratory, cardiac, cerebral vascular, and peripheral vascular diseases. We then linked the data to daily measures of particulate mass less than 10 microns in aerodynamic diameter (PM10), particulate mass less than 2.5 microns in aerodynamic diameter (PM2.5), and particulate mass between 2.5 and 10 microns in aerodynamic diameter (PM10-2.5), ozone, carbon monoxide, nitrogen dioxide, and sulfur dioxide. Air pollution was only associated weakly with hospitalization for cerebral vascular and peripheral vascular diseases. We controlled for temporal trends and climatic factors, and we found that increases of 10 microg/m3 in PM10, PM2.5, and PM10-2.5 were associated with 1.9%, 3.3%, and 2.9% respective increase in respiratory and cardiac hospital admissions. We further controlled for gaseous pollutants, and the percentages were reduced to 0.50%, 0.75%, and 0.77%, respectively. Of the 7.72 excess daily hospital admissions in Toronto attributable to the atmospheric pollution mix, 11.8% resulted from PM2.5, 8.2% to PM10-2.5, 17% to carbon monoxide, 40.4% to nitrogen dioxide, 2.8% to sulfur dioxide, and 19.8% to ozone.

At a variety of Canadian monitoring sites, carbonaceous compounds were estimated to account for an average of 50% of fine particle mass. These estimates were determined by subtracting the total fine particle mass associated with inorganic compounds from the total fine mass determined gravimetrically. This approach, which yields an upper limit estimate of the total amount of carbon-related mass was necessary since particulate carbon was not measured in the Canadian National Air Pollution Surveillance (NAPS) network. In this paper, total carbon estimates are evaluated against organic and elemental carbon measurements at locations in the Greater Vancouver area and Toronto. In addition, particle nitrate measurements at seven Canadian locations are used to determine the importance of nitrate relative to total mass and to examine the sampling artifacts due to the loss of particle nitrate from Teflon filters used in the NAPS di-chotomous samplers. Measurements of organic and elemental carbon indicated that the total carbon estimation approach provides representative estimates of the average contribution by carbonaceous material to the total fine and coarse mass. The average total carbon among all Vancouver area measurements (N = 225) was 4.28 μg m -3 , while the estimated value was 4.34 μg m -3 . There was a larger discrepancy between Toronto total carbon measurements (12.1 μg m -3 ) and estimates (8.8 μg m -3 ), which is attributed in part to sampling of particles above 10 mm in diameter. However, the R 2 relating the measurements and estimates was about 0.71 for both areas. Linear regression slopes of 0.98 for Vancouver and 0.78 for Toronto (nonsignificant intercepts) indicate little bias in the Vancouver estimates, but a tendency for underestimation as the observed total carbon concentration increased in Toronto. Annually, nitrate was responsible for 17% and 12% of the fine mass in the Vancouver area and Ontario, respectively. In contrast, at two rural locations in southern Quebec and Nova Scotia, only 6% of fine mass was associated with nitrate. Due to filter losses, nitrate concentrations determined through the NAPS dichot sampling were much lower than actual concentrations (0.44 μg m -3 vs. 2.63 μg m -3 ). As a result of these losses (attributed mostly to loss during laboratory storage), previous total carbon estimates for the Canadian NAPS sites were likely to have been overestimated on average by about 10%.

The role of ambient levels of carbon monoxide (CO) in the exacerbation of heart problems in individuals with both cardiac and other diseases was examined by comparing daily variations in CO levels and daily fluctuations in nonaccidental mortality in metropolitan Toronto for the 15-year period 1980-1994. After adjusting the mortality time series for day-of-the-week effects, nonparametic smoothed functions of day of study and weather variables, statistically significant positive associations were observed between daily fluctuations in mortality and ambient levels of carbon monoxide, nitrogen dioxide, sulfur dioxide, coefficient of haze, total suspended particulate matter, sulfates, and estimated PM2.5 and PM10. However, the effects of this complex mixture of air pollutants could be almost completely explained by the levels of CO and total suspended particulates (TSP). Of the 40 daily nonaccidental deaths in metropolitan Toronto, 4.7% (95% confidence interval of 3.4%-6.1%) could be attributable to CO while TSP contributed an additional 1.0% (95% confidence interval of 0.2-1.9%), based on changes in CO and TSP equivalent to their average concentrations. Statistically significant positive associations were observed between CO and mortality in all seasons, age, and disease groupings examined. Carbon monoxide should be considered as a potential public health risk to urban populations at current ambient exposure levels.

This paper compares three analytical methods that are often used to analyze composition of atmospheric aerosol: Ion Chromatography (IC), Proton Induced X-ray Emission (PIXE), and X-ray Fluorescence (XRF). Three monitoring studies are discussed: (1) a comparison of air particulate data collected by several independent sampler/analytical technique suites run by different laboratories; (2) a study involving two identical samplers and a single suite of analytical techniques; and (3) analysis of identical aerosol samples by two different techniques (XRF vs. PIXE). While the XRF versus PIXE project shows a very good agreement for most elements, the first interlaboratory study demonstrates the "real-life" noise introduced into the final data set by various sampling complications and different collection characteristics of the samplers used. The XRF versus PIXE study also revealed an unexplained deviation in measured sulphur concentrations for very lightly loaded samples. In the five-sampler comparison, two data sets provided by IC were approximately 20% lower than the three data sets obtained by PIXE and XRF. When two identical IMPROVE-compatible samplers were used and samples were subjected to similar procedures and the same analytical techniques, the variability between the two air concentration data sets significantly decreased.

Objective: Determine the risk of premature mortality due to the urban ambient air pollution mix in Canada., Methods: The number of daily deaths for non-accidental causes were obtained in 11 cities from 1980 to 1991 and linked to concentrations of ambient gaseous air pollutants using relative risk regression models for longitudinal count data., Results: Nitrogen dioxide had the largest effect on mortality with a 4.1% increased risk (p < 0.01), followed by ozone at 1.8% (p < 0.01), sulphur dioxide at 1.4% (p < 0.01), and carbon monoxide at 0.9% (p = 0.04) in multiple pollutant regression models. A 0.4% reduction in premature mortality was attributed to achieving a sulphur content of gasoline of 30 ppm in five Canadian cities, a risk reduction 12 times greater than previously reported., Conclusions: Ambient air pollution generated from the burning of fossil fuels is a risk factor for premature mortality in 11 Canadian cities.

A panel of HepG2-derived cell lines (CAT-Tox [L] assay, Xenometrix), harboring stress genes consisting of a sequence for chloramphenicol acetyltransferase (CAT) under the transcriptional regulation from mammalian promoters and response elements, was exposed for 18-24 hr to aqueous suspensions of urban dusts (SRM-1648, SRM-1649, EHC-93) or PM2.5 particles (particulate matter < 2.5 micron). Expression of CAT protein was measured by enzyme-linked immunosorbent assay. Induction of the CAT genes was verified with benzo[a]pyrene (CYP1A1, cytochrome P450 1A1 promoter; GSTYa, glutathione transferase subunit Ya promoter; XRE, xenobiotic response element), cadmium sulfate, and copper sulfate (HMTIIa, metallothionein IIa promoter; HSP70, heat shock protein 70 promoter). The urban dust suspensions were active on CYP1A1, GSTYa, and XRE cell lines. SRM-1648 and SRM-1649 were twice as potent as EHC-93 per unit mass in inducing the xenobiotic-dependent responses, which correlated with contents in polycyclic aromatic hydrocarbons. These three reference particles, as well as six PM2.5 preparations collected on hi-vol filters in the Great Lakes basin, were also found to induce HMTIIa and HSP70, the magnitude of the responses correlating closely with the amount of soluble copper in the particulate preparations. The results indicate that bioavailable chemical species in the unfractionated particles can directly and quantitatively induce xenobiotic, metal, and stress-dependent responses in a target cell model, resulting in patterns of gene induction consistent with the chemical compositions of the environmental materials. We propose that cell culture models could be helpful for toxicodynamic inferences in adjunct to environmental monitoring and exposure assessments., (Copyright 1997 Society of Toxicology.)