Skip to main content
Open access
Research
14 August 2007

Characterization of Source-Specific Air Pollution Exposure for a Large Population-Based Swiss Cohort (SAPALDIA)

Publication: Environmental Health Perspectives
Volume 115, Issue 11
Pages 1638 - 1645

Abstract

Background

Although the dispersion model approach has been used in some epidemiologic studies to examine health effects of traffic-specific air pollution, no study has evaluated the model predictions vigorously.

Methods

We evaluated total and traffic-specific particulate matter < 10 and < 2.5 μm in aero-dynamic diameter (PM10, PM2.5), nitrogren dioxide, and nitrogen oxide concentrations predicted by Gaussian dispersion models against fixed-site measurements at different locations, including traffic-impacted, urban-background, and alpine settings between and across cities. The model predictions were then used to estimate individual subjects’ historical and cumulative exposures with a temporal trend model.

Results

Modeled PM10 and NO2 predicted at least 55% and 72% of the variability of the measured PM10 and NO2, respectively. Traffic-specific pollution estimates correlated with the NOx measurements (R2 ≥0.77) for background sites but not for traffic sites. Regional background PM10 accounted for most PM10 mass in all cities. Whereas traffic PM10 accounted for < 20% of the total PM10, it varied significantly within cities. The modeling error for PM10 was similar within and between cities. Traffic NOx accounted for the majority of NOx mass in urban areas, whereas background NOx accounted for the majority of NOx in rural areas. The within-city NO2 modeling error was larger than that between cities.

Conclusions

The dispersion model predicted well the total PM10, NOx, and NO2 and traffic-specific pollution at background sites. However, the model underpredicted traffic NOx and NO2 at traffic sites and needs refinement to reflect local conditions. The dispersion model predictions for PM10 are suitable for examining individual exposures and health effects within and between cities.
Long-term exposure to air pollution, especially particulate matter (PM), has been linked to reduced lung capacity (Ackermann-Liebrich et al. 1997; Gauderman et al. 2004), elevated mortality (Dockery et al. 1993; Filleul et al. 2005; Jerrett et al. 2005; Krewski et al. 2005; Künzli et al. 2000; Lipfert et al. 2006), lung cancer (Nyberg et al. 2000; Vineis et al. 2006), and cardiopulmonary mortality (Gehring et al. 2006; Pope et al. 2002; Rosenlund et al. 2006). Except for the Stockholm, Sweden, studies (Nyberg et al. 2000; Rosenlund et al. 2006), exposure assessment in most air pollution epidemiologic studies generally have used central-site measurements to represent community-wide cohort exposure. This has attracted critiques on inadequate characterization of the long-term exposure of study subjects. The availability of the PM measurements, the types of PM monitors deployed, differences in PM sources, and various degrees of spatial variability in PM could also result in different types of bias in allocating exposure to subjects in separate cities.
To minimize exposure misclassification and in some cases to focus on traffic-related air pollution, recent cohort studies improved previous exposure assessment methodologies by assigning individual exposure indices, including subjective traffic assessment (Heinrich et al. 2005), distance between a major road and residences (Bayer-Oglesby et al. 2006; Garshick et al. 2003; Venn et al. 2001; Vineis et al. 2006), and traffic density/counts near residences (Nicolai et al. 2003; Zmirou et al. 2004). Individual and/or residential outdoor nitrogen dioxide measurements from a subset of cohort were also used for health assessment (Schindler et al. 1998; Sunyer et al. 2006). Other studies constructed statistical models by regressing home outdoor nitrogen oxides or NO2 measurements against traffic characteristics (Carr et al. 2002) or local geographic characteristics related to traffic (Brauer et al. 2006; Hochadel et al. 2006; Hoek et al. 2002) for estimating individual residential outdoor concentrations. These statistical models provide improvements over the earlier qualitative indices. However, they used short-term measurements (usually 1- to 2-week averages in 2–4 seasons) to attain annual averages in a specific year. Models constructed from such measurements implicitly assumed that temporal variation is homogeneous within a given area. In addition, the spatial pattern was assumed to hold over the years when such models were applied to long-term exposure estimation.
The dispersion modeling approach is an alternative for assigning individual exposure indices based on both physical and stochastic processes. It is seldom used because detailed emission and meteorologic data are required. Although the dispersion modeling approach has been applied to the Stockholm and Oslo, Norway, cohorts (Bellander et al. 2001; Nafstad et al. 2003, 2004; Nyberg et al. 2000; Pierse et al. 2006; Rosenlund et al. 2006), model evaluation has been limited to comparisons of the modeled NO2 against measurements at six monitoring sites (Nyberg et al. 2000). Cyrys et al. (2005) compared dispersion and stochastic model estimates using NO2 and PM2.5 (particulate matter with aero-dynamic diameter < 2.5 μm) measurements at 40 sites in Munich, Germany, and reported that NO2 dispersion predictions overestimated the measured values but were highly correlated with stochastic model estimates. However, the dispersion model used by Cyrys et al. was run without source-specific emission data and predicted total suspended particulate (TSP) which could not be validated directly against PM2.5 measurements.
We used a dispersion model to estimate individual exposure to source-specific PM10 (particulate matter with aerodynamic diameter < 10 μm), NOx, and NO2 for subjects in the Swiss Cohort Study on Air Pollution and Lung Diseases in Adults (SAPALDIA) (Ackermann-Liebrich et al. 2005). In this article we provide a detailed evaluation of the dispersion model predictions against fixed-site measurements between and across cities and estimate individual historical exposure to source-specific PM10.

Methods

Monitoring sites

The SAPALDIA cohort included 9,651 subjects in Switzerland, with the first health examination (SAPALDIA 1) conducted in 1991 (Martin et al. 1997) and a follow-up assessment (SAPALDIA 2) of 8,047 subjects in 2002 (Ackermann-Liebrich et al. 2005). The study areas included two large cities (Basel, Geneva), two medium-sized cities (Aarau, Lugano), two rural areas (Payerne, Wald), and two alpine areas (Davos, Montana). Each area was monitored with up to three fixed monitoring sites for PM, NO2, and NOx. For dispersion model evaluation, we used measurements from all available Swiss sites, including up to 57 PM10 sites, 103 NO2 sites, and 17 NOx sites [Supplemental Table 1 (online at http://www.ehponline.org/docs/2007/10177/suppl.pdf)].

Fixed-site PM measurements

At most central sties, 24-hr PM was measured using the Digitel monitor (High Volume Sampler DHA80; Digitel Elektronik, Hegnau, Switzerland) for TSP between 1990 and 1996 and for PM10 afterward. At Davos an FAG β-attenuation monitor was used for TSP and the Harvard impactor (Marple et al. 1987) for PM10 (Monn et al. 1995), and a custom-made PM10 sampler was used in Aarau between 1990 and 1998. Since 1999, all sites have used the Digitel monitor for PM10. A conversion factor of 0.86 was used to estimate PM10 from TSP measurements based on a collocation study (Gehrig and Hofer 1999).

Black smoke measurements

In 2000–2002, black smoke (BS) from PM2.5, a marker for traffic exhaust (Brunekreef et al. 1997; Zhu et al. 2002), was measured at nine sites using the Digitel monitor with glass fiber filters. Filters were analyzed gravimetrically and for light reflectance using a Smoke Stain reflectometer (M43D EEL; Diffusion Systems Ltd., London, UK). The absorption coefficient (m−1) was calculated using ISO (International Standard) 9835 (Götschi et al. 2002).

NO2 and NOx measurements

NO2 and NOx were measured with the Monitor Labs 8840 (Environment SA, Englewood, CO, USA), the Tecan CLD 502 (Tecan, Hombrechtikon, Switzerland), and the Horiba monitor (model APNA-350E; Horiba Europe, Leichlingen, Germany). In 2003, NO2 was also measured outside residences with the passive Palmes tubes (Monn et al. 1998; Palmes et al. 1976), integrated over three 2-week periods from 335 residences (Hazenkampvon Arx et al. 2004). These home outdoor measurements in 2003 were used to calibrate the within- and between-city variations from the dispersion model that used emission data in 2000.

Dispersion modeling

We modeled annual average concentrations of PM10, PM2.5, NOx, and NO2 in 1990 and 2000 using the PolluMap Gaussian dispersion model (version 2.0) [Swiss Agency for the Environment, Forests, and Landscape (SAEFL) 2003, 2004]. PolluMap used transfer functions to represent the impact of a source to the neighboring areas. The dispersion was performed for each emission inventory, including road, rail, and air transports, industrial and commercial, construction, household (heating), and agricultural activities, and forestry. For 1990 and 2000, we computed traffic emissions for the road network for passenger cars, light-duty vehicles, motorcycles, and buses (SAEFL 1997). Emissions from heavy-duty vehicles were computed separately from an updated road network and a new relative distribution of traffic loads. We obtained emissions from other sources from the Swiss inventory data (SAEFL 2003, 2004). The emission strengths were allowed to vary by season and hour of the day for stationary sources, and with the day of the week and the hour of the day for transport sources. We computed road transport emissions for all major roads individually and then projected onto the 200 ×200-m grids. For all other source categories, the total emission load was estimated and then spatially disaggregated by distributing it equally to all grid cells with certain land use characteristics. We used different transfer functions for three Swiss regions (alpine, plateau, and others) and for different source types (area vs. line) and heights (0–2, 2–20, and > 20 m). The dispersion modeling was performed for up to 5 km for NOx and 200 km for PM. Dispersion of primary particles was modeled with hourly emission and meteorologic parameters and outputs were averaged for the year.
We calculated secondary inorganic particles, including nitrate, sulfate, and ammonium, by applying a transformation function (European Union, Directorates-General XI 1997) to the smoothed annual average concentrations of NO2, NH3, and SO2. We computed secondary organic matter from 32 classes of anthropogenic and biogenic volatile organic compounds, each from a detailed emission inventory (Bundesamtes für Bildung und Wissenschaft 1995; SAEFL 1995), multiplied by a fractional aerosol yield coefficient and dispersed by the Gaussian model. The concentrations of the secondary particles were averaged over a 12-km radius area around the source to account for the transition time from gaseous precursor to secondary particles.
We added a background concentration to all computed primary and secondary PM10 concentrations originating from Swiss sources in the emission inventory data, which captured most emissions except for road transport in ventilated tunnels, air transport at 200 m above ground or higher, water transport, and biogenic particles. The effect of these noninventoried emissions, albeit negligible [< 1.0 μg/m3 (SAEFL 2003)], was implicitly included in the background concentration, which primarily accounted for imported primary and secondary particles. The primary background PM10 included Sahara desert sand events, biogenic materials, mineral dust and sea salt aerosols, noninventoried Swiss emissions, and other anthropogenic particles from abroad. The background primary and secondary concentrations were not dispersed with the dispersion model. They were first determined from the difference between the modeled results from Swiss emissions only and the measurements at Basel, Bern, Payerne, and Zurich, with the differences representing the sum of the background emissions and the model errors. The total background concentration for any given location was then computed using an elevation and region dependent empirical nonlinear function [Supplemental Material, Equation 1 (online at http://www.ehponline.org/docs/2007/10177/suppl.pdf)].
For NOx, the background concentration covered the natural sources, the far-reaching impact of Swiss emission sources, the total impact of any NOx sources not covered by the emission inventory, and the regional anthropogenic background. Thus, the background concentrations included both long-range transported pollutants from abroad (including possibly traffic exhaust) and within Switzerland, whereas the traffic-specific concentrations covered exclusively emissions from urban sources.
We modeled the PM2.5 concentrations separately based on the PM10 emissions and source-specific factors describing the share of the fine fraction on the total PM10. Separate transfer functions for the fine fractions with different particle deposition velocity were used. For the background PM2.5 concentration, we estimated a weighted mean of 93% of the background PM10. We calculated concentrations of NO2 from the total NOx estimates using the plume volume molar ratio method (Hanrahan 1999a) with the conversion coefficients derived from actual NO2/ NOx observations across Switzerland.

Analysis

We evaluated the dispersion model results for PM10, NOx, and NO2 against measurements in 1990 and 2000. The PM2.5 predictions were not evaluated because few measurements were available. The modeled city means of PM10 and NO2 were examined against the measured city means. We examined the within-city modeling error by calculating the Pearson’s and Spearman’s correlation coefficients (rP and rS) between the deviations of modeled and measured values from their city means from cities with at least two monitoring sites. For NO2, we evaluated modeling error against the central-site and home outdoor measurements, respectively. Model predictions for traffic-specific PM10, PM2.5, NOx, and NO2 were evaluated against NOx measurements. Because of the significant correlations among sources, we used principal component analysis (PCA) to identify principal components (or the source groups) that explained most of the variability in the predicted outdoor PM10. Source-specific NO2 was not examined because the dispersion model only computed total NO2 based on total NOx.

Estimating annual means

To estimate the annual PM10 averages between 1990 and 2000 for individual residences, we used the modeled values at individual residences in 1990 and 2000, and the 1990–2000 historical trends of central-site measurements to develop an algorithm to interpolate dispersion modeled values. To assess historical trends, we defined areas with comparable sources or climatic characteristics, including the catchment areas of the eight study centers, Zurich, and Bern; each area is represented by at least one monitoring station. Residences outside these areas were grouped into four “other” areas based on similarities in meteorology and pollution sources. PM10 in any year t at station i, PMi10(t), was expressed as:
where the interpolation term ci(t) represents relative deviations from the simple linear interpolation:
ci(t) vanishes if and only if the respective annual means lie on the straight line connecting the 1990 and the 2000 annual means. To obtain more robust estimates of ci(t), local interpolation terms were shrunk using an empirical Bayes methodology. For this purpose, all available PM10 and TSP annual means from all stations with complete data between 1990 and 2000 were used (n = 18). Correlation analyses suggested that the interpolation term ci(t) exhibited a similar longitudinal pattern for most of the 16 stations north of the Alps with complete PM10 data since 1990. For these sites, we averaged all local interpolation terms to obtain an annual mean interpolation term, c(t) (t = 1990,…,2000). For shrinkage, we decomposed the variance of the local interpolation term ci(t) of a given year t into an across-areas variance ρt2 and a within-areas variance σt2 and estimated σt2 using the data from the four areas (Aarau, Berne, Geneva, and Zurich) with at least two stations. We then shrunk local interpolation term ci(t) toward the average interpolation term c(t) using the formula:
The assignment of cis(t) is based on the area assignment of individual residences.

Results

Summary of measurements

Table 1 summarizes available annual averages of PM10, PM2.5, NOx, NO2, and BS measurements at the eight SAPALDIA areas in 1990 and 2000. A significant decrease in PM10, NOx, and NO2 levels between 1990 and 2000 was observed in all areas, with a larger reduction in more polluted areas. PM2.5 was not monitored until 1998. Lugano had the highest levels for all measurements in 2000.
Table 1 Annual averages (± SD) of air pollution measurements in the eight SAPALDIA study areas.
  1990a2000a
AreaAltitude (m)PM10 (μg/m3)NOx (ppb)NO2 (μg/m3)PM10 (μg/m3)PM2.5 (μg/m3)NOx (ppb)NO2 (μg/m3)BSb (m−1)
Basel32033.2 ± 18.739.3 ± 28.540.5 ± 18.420.5 ± 11.515.8 ± 10.420.4 ± 15.124.8 ± 12.11.0 ± 0.5
Wald64015.7 ± 8.611.7 ± 7.0c9.5 ± 6.93.6 ± 7.40.8 ± 0.3
Davos1,63713.816.4 ± 12.323.1 ± 13.114.0 ± 7.96.9 ± 3.8c11.6 ± 11.95.1 ± 12.9
Lugano28141.7 ± 22.153.7 ± 38.751.9 ± 19.033.8 ± 23.624.9 ± 19.139.1 ± 25.938.9 ± 15.21.5 ± 0.6
Montana1,35010.4 ± 6.2c8.1 ± 4.9c0.5 ± 0.3
Payerne49029.0 ± 17.114.6 ± 9.018.3 ± 8.719.8 ± 12.314.7 ± 10.312.5 ± 8.915.9 ± 8.50.9 ± 0.4
Aarau41741.436.728.7 ± 15.321.6 ± 13.31.2 ± 0.5
Geneva37551.659.9 ± 21.121.7 ± 12.436.9 ± 12.8
—, no data. Mean values without SD in 1990 were annual means reported by SAEFL, where daily values were no longer available.
a
Sample size (no.) ranges between 302 (83% of possible samples) and 366 for all reported annual averages except for those noted below.
b
BS, presented as absorption coefficient, was taken 1 in 3 days. No. ranges between 84 and 122.
c
No. ranges between 180 and 183 (every other day samples), except for Montana where n = 124.

Evaluation of dispersion model predictions

For PM10 in 2000, the dispersion model predicted at least 55% of the variability in the measurements (Figure 1A). The dispersion model generally underestimated PM10 in the alpine region, due partially to the oversimplified alpine meteorology. For PM10 in 1990, the model underestimated most measurements, due potentially to the less accurate emission inventory data. In 2000, the model performed equally for background and traffic sites (e.g., sites located within 20 m of a major road and shown as up or down triangles) (Figure 1A, Table 2).
Figure 1 Measured versus modeled annual PM10 concentrations for all Swiss sites including those in the SAPALDIA areas (in white) in (A) 2000 [SAPALDIA areas: y = 1.9 + 0.87x (R2 = 0.68, n = 15); all sites: y = 5.2 + 0.72x (R2 = 0.55, n = 57] and (B) 1990 [SAPALDIA areas: y = 8.6 + 0.6x (R2 = 0.45, n = 8); all sites: y = 8.6 + 0.61x (R2 = 0.63, n = 25)]. Traffic sites are within 20 m of a major road.
Table 2 Ratios of the dispersion modeled to measured pollutant values and the differences (μg/m3).
  Ratio (modeled – measured)Difference (modeled – measured)
Pollutant (year)SiteMeanSDMinMaxNo.MeanSDMinMaxNo.
PM10 2000All0.970.200.611.4557−1.03.9−10.25.357
 Background0.980.210.611.4547−1.04.0−10.25.347
 Traffic0.960.150.741.1410−1.33.8−6.73.410
PM10 1990All0.930.290.602.0525−4.47.2−20.95.325
 Background0.980.300.622.0520−2.15.7−14.25.320
 Traffic0.710.070.600.785−13.55.2−20.9−7.35
NOx 2000All1.100.470.452.24170.931.1−60.475.617
 Background1.160.340.491.67117.713.2−10.035.011
 Traffic0.980.660.452.246−11.549.5−60.475.66
NOx 1990All1.170.530.462.571117.342.0−19.3130.311
 Background0.980.260.461.2970.49.8−15.017.77
 Traffic1.510.750.842.57446.762.3−19.3130.34
 Traffica1.160.310.841.46318.934.1−19.346.13
NO2 2000All1.010.290.532.99103−1.16.0−18.912.3103
 Background1.030.310.532.9986−0.76.2−18.912.386
 Traffic0.920.110.651.0917−3.14.1−12.83.217
NO2 1990All0.910.280.461.9538−5.37.5−22.46.638
 Background0.950.320.461.9524−3.86.0−15.36.624
 Traffic0.860.170.591.0714−7.79.4−22.43.214
Abbreviations: Max, maximum; Min, minimum.
a
Without Lugano.
The NOx model generally overestimated measured NOx and did not predict well at some traffic sites (Figure 2, Table 2). For non-traffic sites, the R2 was 0.88 (n = 11) and 0.91 (n = 7) in 1990 and 2000, respectively. Although traffic sites were distinguishable by elevated NOx measurements, they were indistinguishable in the modeled values in 2000 (Figure 2A). The outliers marked in Figure 2 were partially attributed to the approximately 100-m inaccuracy in the geographic information system (GIS) codes against the actual distance from the closest major street. For NO2, the model predicted well the measured values with an R2 of ≥0.72 (Figure 3). NO2 measurements at traffic sites were not necessarily higher than those at background sites. The dispersion model on average underestimated the NO2 measurements at the traffic sites by 3.1 and 7.7 μg/m3 in 2000 and 1999, respectively, and less so for background sites (Table 2).
Figure 2 Measured vs. modeled annual NOx concentrations for all Swiss sites including those in the SAPALDIA areas (in white) in (A) 2000 [SAPALDIA: y = 17.1 + 0.68x (R2 = 0.43, n = 10); all sites: y = 18.6 + 0.67x (R2 = 0.48, n = 17)] and (B) 1990 [SAPALDIA areas: y = −39 + 2.4x (R2 = 0.79, n = 6); all sites: y = −0.1 + 1.2x (R2 = 0.66, n = 11)]. Traffic sites are shown as triangles.
Figure 3 Measured vs. modeled annual NO2 concentrations for all Swiss sites including those in the SAPALDIA areas (in white) in (A) 2000 [SAPALDIA areas: y = 3.3 + 0.81x (R2 = 0.79, n = 24); all sites: y = 5.8 + 0.73x (R2 = 0.72, n = 103)] and (B) 1990 [SAPALDIA areas: y = 1.8 + 0.78x (R2 = 0.80, n = 12); all sites: y = 6.0 + 0.69x (R2 = 0.75, n = 38)]. Two blue triangles are airport sites.
The predicted and measured city means of PM10 were comparable, with a Spearman correlation coefficient of 0.71 (rP = 0.71, n = 57) [Supplemental Figure 1A (online at http://www.ehponline.org/docs/2007/10177/suppl.pdf)]. The modeled within-city residuals were comparable to and correlated with the measured values (rS = 0.60; rP = 0.79), indicating that the dispersion model was able to distinguish locations with higher concentrations from those with lower concentrations within a city. For NO2, the predicted city means correlated with those from the central-site measurements (n = 103, up to four sites per city) with an rS of 0.88 (rP = 0.85), larger than that for the within-city residuals (rS = 0.44, rP = 0.80). Comparing the modeled values with those from the home outdoor NO2 measurements (n = 335, up to 54 sites per city), the rS was 0.87 (rP = 0.91) for city means and 0.52 (rP = 0.59) for within-city residuals. These results distinguished the differences in the modeling error between PM10 and NO2 predictions. The PM10 predictions demonstrated consistency with the measured values across- and within-cities. Although the NO2 predictions were able to match the measured city means, the predicted within-city residuals were less consistent with those measured.

Evaluation of predictions of traffic-specific pollutants

BS correlated extremely well with the NOx measurements with an R2 of 0.99 [Supplemental Figure 2A (online at http://www.ehponline.org/docs/2007/10177/suppl.pdf)], higher than those for NO2, PM10, and PM2.5 (Supplemental Figure 2B–D). This near-perfect correlation between BS and NOx indicated that NOx and BS shared a common source. Because the number of available BS measurements was limited, we thus used NOx as the reference to evaluate traffic-related pollutant predictions.
Figure 4 shows the predicted versus measured traffic exhaust pollutants. Measured NOx levels clearly distinguished traffic from background sites, but the modeled values could not. Similar prediction profiles were observed for NOx and NO2 and for PM10 and PM2.5 because the dispersion model estimated NO2 and PM2.5 from NOx and PM10, respectively. The model clearly predicted better at the background sites than at the traffic sites.
Figure 4 Relationship in 2000 between measured NOx and modeled traffic-related (A) NOx [background sites: y = −14 + 0.98x (R2 = 0.77, n = 11); traffic sites: y = 41 + 0.13x (R2 = 0.01, n = 6); all sites: y = 2 + 0.50x (R2 = 0.41, n = 17)]; (B) PM10 [background: y = −2 + 0.16x (R 2 = 0.84, n = 11); traffic sites: y = 0.4 + 0.06x (R2 = 0.35, n = 6); all sites: y = 1 + 0.06x (R2 = 0.54, n = 17)]; (C) NO2 [background: y = −7 + 0.59x (R 2 = 0.85, n = 11); traffic sites: y = 20 + 0.08x (R2 = 0.04, n = 6); all sites: y = 4 + 0.24x (R2 = 0.50, n = 17)]; and (D) PM2.5 [background: y = −0.7 + 0.07x (R2 = 0.86, n = 11); traffic sites: y = 0.4 + 0.03x (R2 = 0.34, n = 6); all sites: y = 0.6 + 0.03x (R2 = 0.53, n = 17)]. SAPALDIA sites are in white.

Time trend of emissions

The three largest local PM10 emission sources included industry, traffic, and household [Supplemental Table 2 (online at http://www.ehponline.org/docs/2007/10177/suppl.pdf)]. Emissions from all sources decreased between 1990 and 2000. For PM10, the largest reduction (43%) occurred in the industrial source. For NOx, traffic was the largest source, with emissions approximately three times higher than those of other two large sources, household and industry [Supplemental Table 3 (online at http://www.ehponline.org/docs/2007/10177/suppl.pdf)]. The largest reduction of 43% between 1990 and 2000 occurred in traffic emissions.
The dispersion results produced concentrations of PM10, PM2.5, NOx, and NO2 for all of Switzerland and were spatially interpreted to coordinates of individual addresses (e.g., Figure 5). Table 3 shows the average individual source-specific concentrations of PM10 in each area for those who did not move between SAPALDIA 1 and 2. Home outdoor concentrations of PM10 were the highest in urban areas and lowest in the Alpine areas. The major emission contributors of PM10 are not necessarily the major contributors of the predicted concentrations due to the interplay among the dispersion process, long-range transport, atmospheric chemical processes, and the home locations. Background PM10 accounted for an average of 54% of the PM10 mass concentrations, followed by secondary PM10 except for Basel and Geneva. The spatial variation of total PM10 within each area, expressed as the coefficient of variation (CV), was small (range, 2–11%) (Table 3). Background and secondary PM10 were generally homogeneous within areas except for Montana and Lugano (Table 3) due to the elevation-dependent background influence. Although the contribution of traffic-originated PM10 from urban sources accounted for < 20% of the total PM10 mass concentrations, it was highly variable within areas (range of CV, 16–35%). Similar results were found for the predicted 1990 PM10 (results not shown).
Figure 5 Dispersion modeling predictions for PM10 concentrations outside residences of the SAPALDIA 2 cohort.
Table 3 Source-specific PM10 (μg/m3), percentage of the total, and the CV within each source in 2000 among nonmovers.
AreaTrafficSecondaryBackgroundAgriculturalIndustrialHouseholdTotalNo.
Basel4.44.012.90.92.31.125.5515
 % total171651394100 
 CV (%)3213610267 
Wald1.43.18.21.32.00.316.3669
 % total919508122100 
 CV (%)223555105 
Davos0.81.34.90.40.80.28.3294
 % total101659492100 
 CV (%)29331610234 
Lugano3.03.922.20.52.10.732.4559
 % total91268272100 
 CV (%)359109182911 
Montana0.82.05.90.81.40.211.0381
 % total718537132100 
 CV (%)1651112788 
Payerne1.72.99.51.82.20.418.4582
 % total9165210122100 
 CV (%)240132112 
Aarau3.63.710.11.63.00.622.6523
 % total1616457133100 
 CV (%)16113363 
Geneva4.13.311.50.62.01.322.7335
 % total181450396100 
 CV (%)230135195 
Overall2.53.111.11.12.10.620.53,858
 % total1215545103100 
 CV (%)61254647276435 
The highest and most variable NOx predictions were found in larger cities (Table 4). NOx from traffic emissions accounted for most of the NOx mass concentration in all four urban areas (Basel, Geneva, Aarau, and Lugano) and had the highest CVs within all areas (range, 30–86%) (Table 4). Background NOx was the next largest contributor to total NOx.
Table 4 Source-specific NOx (μg/m3), percentage of the total, and the CV within each source in 2000 among nonmovers.
AreaTrafficBackgroundAgriculturalIndustrialHouseholdTotalNo.
Basel31.818.91.66.17.665.9515
 % total48292911100 
 CV (%)42363201325 
Wald4.011.41.41.91.019.8669
 % total20587105100 
 CV (%)81399241523 
Davos2.23.01.01.71.18.9294
 % total2434111912100 
 CV (%)864210311726 
Lugano51.817.62.65.35.082.3559
 % total6321366100 
 CV (%)55339231737 
Montana5.64.92.32.50.816.1381
 % total353114165100 
 CV (%)723229183633 
Payerne9.114.51.92.71.429.7582
 % total3149695100 
 CV (%)5441214419 
Aarau19.015.91.54.62.443.4523
 % total44374115100 
 CV (%)3223316715 
Geneva36.115.82.26.712.172.9335
 % total50223917100 
 CV (%)3023381617 
Overall20.313.51.83.93.643.13,858
 % total4731498100 
 CV (%)10510437493268 
The PCA analysis identified two principal components (PCs) accounting for 82% of the variability in the predicted PM10 concentrations. The most important PC was the “urban mixture” including secondary, traffic, household, background, and industrial PM10, accounting for 56% of the variability (Figure 6A). The second PC was a mixture of agricultural and industrial PM10 and to a lesser extent secondary PM10, which accounted for 26% of the variability. The scores of these two PCs at individual residences were then averaged over each area (Figure 6B). Residences in Basel, Geneva, and Lugano scored positively (above the average) on the “urban mixture” and negatively on the “agricultural/industrial mixture.” Two rural areas, Payerne and Wald, scored positively on “agricultural/industrial mixture” and negatively on the “urban mixture.” The alpine areas, Davos and Montana, scored negatively on both mixtures, whereas Aarau scored positively on both mixtures. Those who moved out of our study areas (“other”) scored near the average (zero) on both mixtures.
Figure 6 (A) Two principal components of sources which are presented by their loadings on these two components. (B) Source characteristics of the SAPALDIA areas given by the two component scores. “Other” includes subjects who have moved out of the SAPALDIA areas.

Cumulative versus differences in exposure

We evaluated the interpolated yearly PM10 predictions between 1990 and 2000 against PM10 measurements from Basel, Lugano, and Payerne, where measurements were available throughout the 11 years. The predicted yearly PM10 agreed well with the measured annual means with an R2 value between 0.74 and 0.80. Based on model predictions, we reconstructed annual exposures for every subject and calculated the cumulative exposure and the changes in exposure between 1990 and 2000. There was a clear inverse relationship between the cumulative exposure and the exposure reduction between 1990 and 2000 (r = −0.99) [Supplemental Figure 3 (online at http://www.ehponline.org/docs/2007/10177/suppl.pdf)]. Although the variability in the cumulative exposure and exposure reduction is large within larger cities, general linear model results for nonmovers indicated that the between-cities variance accounted for 88% and 92% of the variability in the estimated individual cumulative and changes in exposures to PM10 between 1990 and 2000, respectively.

Discussion

We assessed the performance of the dispersion model for total PM10, NOx, and NO2 based on the agreement between the total predictions and measurements, between traffic-specific predictions and NOx measurements (a traffic marker), and between the predicted and measured variations within and between cities. PM10 concentrations at background locations were appropriately predicted by the model. PM10 and NO2 concentrations at traffic sites, especially those with heavy traffic, were underestimated. NOx, a better traffic marker than NO2, was more difficult to predict locally due to its reactivity and thus the large spatial gradient within an area (Hanrahan 1999a, 1999b). At the current spatial resolution (200 × 200 m), the model could not accurately predict NO2 and NOx at locations that are strongly affected by local conditions. On further examination, we discovered that the imprecision of the GIS data, such as the address codes and thus the distance to major roads, could be as large as 100 m, depending on the geocoding algorithm. This would result in an imprecision of our spatially interpreted dispersion model predictions in neighborhoods with a high spatial variability in pollutant concentrations.
For PM10, the modeled and measured city means and within-city residuals were comparable due to the small spatial variability of PM10. Our results indicated that the PM10 dispersion model was able to distinguish locations with higher concentrations from those with lower concentrations within and between cities. In contrast, the within-city residuals for NO2 were less consistent with the measured values, stressing the need for further model refinement to take into account local geographic and emission characteristics. Although our analysis of within-city modeling error for PM10 was performed with a limited numberof monitoring sites within cities, our results agreed with those of Cyrys et al. (2005), who reported small and very agreeable CVs for the measured PM2.5 (13.2%) at 40 sites and the dispersion modeled TSP (12.9%).
Although PM emissions from industry and traffic were the largest among all domestic sources, the dispersion model predictions indicated that background particles accounted for the largest share (mean = 54%) of the ambient PM mass concentration. This large background contribution might have been inflated by the implicit inclusion of the model error. However, the magnitude of the background contribution agreed with those (50–65% at European urban background-sites) reported by Querol et al. (2004), who used a source apportionment method. Model predictions demonstrated a clear within-area spatial variation for traffic-specific PM10 and for total and traffic-specific NOx (Tables 3 and 4). As in most cohort studies, health effect estimates for SAPALDIA 1 subjects were based on the central-site measurements (Ackermann-Liebrich et al. 1997). Without taking into account these differences in individual exposures, misclassification of exposures among subjects might weaken the association with the health effects. The bias in the health effect estimates also may vary by source-specific exposure as indicated by their different variances. Health effect assessment using these improved source-specific and historical individual exposure estimates should shed further insights to the effects of long-term air pollution exposure.
With these source-specific exposure estimates, the SAPALDIA areas were clearly distinguished by the relative impacts of urban sources and a mixture of agriculture and industrial sources. Thus, PM constituents may differ by area. Although effects by area were demonstrated previously (Samet et al. 2000), no studies had the tools to examine health effects by source over a long period. We devised methods to reconstruct individual exposure history and observed a strong negative correlation between cumulative exposure and exposure reduction [Supplemental Figure 3 (online at http://www.ehponline.org/docs/2007/10177/suppl.pdf)]. We believe that this reflects a situation typical in many areas of the world where air pollution abatement policies were implemented during the last decades with a focus on more polluted areas (i.e., high cumulative exposure). As a result, changes (or improvements) are larger in these areas. This paradox needs to be considered in long-term air pollution studies because it may seriously influence the ability to observe health effects and the interpretation of findings. Depending on the health outcomes, the more recent changes in air quality may be more important than the long-term cumulative exposure, or vice versa.
The strengths of this study include the evaluation of the model predictions based on actual measurements over 2 separate years at up to 103 sites of various geographic characteristics. We are not aware of any studies that provided such comprehensive evaluation for assessing dispersion model predictions due partially to the difficulties of data collection. Bellander et al. (2001) modeled NO2 from road traffic and SO2 from house heating, with no source-specific measurements to evaluate their predictions. Wu et al. (2005) predicted time-location weighted exposure estimates from transport without measurements to evaluate their predictions.
No epidemiologic studies thus far have used the dispersion model approach to estimate and examine PM exposure from various sources. Few studies have focused on dispersion model predictions from traffic or home heating sources (Gauderman et al. 2005; Künzli et al. 2000; Pierse et al. 2006), with limited or no validation of the model predictions. Other studies have used the receptor modeling approach to apportion sources of central-site PM2.5 to represent the average population exposure (Laden et al. 2000; Mar et al. 2000; Tsai et al. 2000). Such an approach is subject to the availability of the speciated data at few receptor sites, and misses the substantial spatial variation of traffic-specific exposure within a city. The dispersion modeling approach described in this article uses emissions from different source categories and local meteorologic parameters to predict source-specific exposures outside residences and provides spatially resolved exposure for examining source-specific health effects.
One disadvantage of the dispersion model is its dependence on the availability and quality of the emission inventory data, which continue to become more available as required by the regulatory agencies. As the GIS evolves, we expect the accuracy and precision of GIS and traffic emission data to improve over time. One weakness of our dispersion model is the conversion of NO2 from total NOx based on a general first-level conversion equation for all Swiss locations. The NOx–NO2 conversion depends on temperature, solar radiation, zenith angle, background ozone, and sources (Hanrahan 1999a,b). Although the spatial resolution of our current model was one of the finest, as compared with the 5 × 5-km resolution described by Wu et al. (2005) and Hoffmann et al. (2006), and between 100 × 100 m to 2 × 2 km by Bellander et al. (2001), it still did not provide sufficient resolution to clearly distinguish traffic exposures. Improvements of the dispersion model could be achieved with better traffic emission data, location and source-specific NOx–NO2 conversion factors, a higher spatial resolution, and/or the inclusion of a traffic emission submodule (Pierse et al. 2006).

Conclusions

In this article we provide a comprehensive evaluation of the dispersion modeling estimates for all and for traffic-specific sources. For PM10, the dispersion model is suitable for estimating and comparing individual exposures between and within cities. Individual estimates for NO2 within a city, however, need further refinement. As better emission and high-resolution GIS data become more available, the dispersion modeling approach employing both physical and stochastic processes should provide a great tool for individual source-specific exposure estimates in air pollution health assessment studies.

Article Notes

Supplemental Material is available online at http://www.ehponline.org/docs/2007/10177/suppl.pdf
This study was supported by the National Science Foundation of Switzerland (grants 32 65896.01, NF32 59302.99, NF32 47BO 104283, NF32 47BO 104288), the Swiss Agency for the Environment, Forests, and Landscape, the Federal Office of Public Health, the Federal Office of Roads and Transport, the Cantons Basel-City, Basel-Land, Geneva, Zurich, Ticino, Aargau, Luzern, the Swiss Lung League and the Lung Leagues of Ticino, Zurich, Geneva and Basel City and Basel Land.

References

Ackermann-Liebrich U, Kuna-Dibbert B, Probst-Hensch NM, Schindler C, Felber Dietrich D, Stutz EZet al. 2005. Follow-up of the Swiss Cohort Study on Air Pollution and Lung Diseases in Adults (SAPALDIA 2) 1991–2003: methods and characterization of participants. Soz Praventivmed 50(4):245-263 https://pubmed.ncbi.nlm.nih.gov/16167509/.
Ackermann-Liebrich U, Leuenberger P, Schwartz J, Schindler C, Monn C, Bolognini Get al. 1997. Lung function and long term exposure to air pollutants in Switzerland. Am J Respir Crit Care Med 155(1):122-129 https://pubmed.ncbi.nlm.nih.gov/9001300/.
Bayer-Oglesby L, Schindler C, Hazenkamp-von Arx ME, Braun-Fahrlander C, Keidel D, Rapp Ret al. 2006. Living near Main Streets and Respiratory Symptoms in Adults. Am J Epidemiol 164:1190-1198 https://pubmed.ncbi.nlm.nih.gov/17032694/.
Bellander T, Berglind N, Gustavsson P, Jonson T, Nyberg F, Pershagen Get al. 2001. Using geographic information systems to assess individual historical exposure to air pollution from traffic and house heating in Stockholm. Environ Health Perspect 109:633-639 https://pubmed.ncbi.nlm.nih.gov/11445519/.
Brauer M, Gehring U, Brunekreef B, de Jongste J, Gerritsen J, Rovers Met al. 2006. Traffic-related air pollution and otitis media. Environ Health Perspect 114:1414-1418 https://pubmed.ncbi.nlm.nih.gov/16966098/.
Brunekreef B, Janssen NA, de Hartog J, Harssema H, Knape M, van Vliet P. 1997. Air pollution from truck traffic and lung function in children living near motorways. Epidemiology 8(3):298-303 https://pubmed.ncbi.nlm.nih.gov/9115026/.
Bundesamtes für Bildung und Wissenschaft. 1995. TRACT Emission Model Switzerland. Bern:Schlussbericht METEOTEST/Carbotech im Auftrag des Bundesamtes für Bildung und Wissenschaft.
Carr D, von Ehrenstein O, Weiland S, Wagner C, Wellie O, Nicolai Tet al. 2002. Modeling annual benzene, toluene, NO2, and soot concentrations on the basis of road traffic characteristics. Environ Res 90(2):111-118 https://pubmed.ncbi.nlm.nih.gov/12483801/.
Cyrys J, Hochadel M, Gehring U, Hoek G, Diegmann V, Brunekreef Bet al. 2005. GIS-based estimation of exposure to particulate matter and NO2 in an urban area: stochastic versus dispersion modeling. Environ Health Perspect 113:987-992 https://pubmed.ncbi.nlm.nih.gov/16079068/.
Dockery DW, Pope CA, Xu X, Spengler JD, Ware JH, Fay MEet al. 1993. An association between air pollution and mortality in six U.S. cities. N Engl J Med 329(24):1753-1759 https://pubmed.ncbi.nlm.nih.gov/8179653/.
European Union, Directorates-General XI. 1997. Economic Evaluation of Air Quality Targets for SO2, NO2, PM10 and Pb. Final report Amsterdam Institute for Environmetal Studies, Vrije Universiteit.
Filleul L, Rondeau V, Vandentorren S, Le Moual N, Cantagrel A, Annesi-Maesano Iet al. 2005. Twenty five year mortality and air pollution: results from the French PAARC survey. Occup Environ Med 62(7):453-460 https://pubmed.ncbi.nlm.nih.gov/15961621/.
Garshick E, Laden F, Hart JE, Caron A. 2003. Residence near a major road and respiratory symptoms in U.S. Veterans. Epidemiology 14(6):728-736 https://pubmed.ncbi.nlm.nih.gov/14569190/.
Gauderman WJ, Avol E, Gilliland F, Vora H, Thomas D, Berhane Ket al. 2004. The effect of air pollution on lung development from 10 to 18 years of age. N Engl J Med 351:1057-1067 https://pubmed.ncbi.nlm.nih.gov/15356303/.
Gauderman WJ, Avol E, Lurmann F, Kuenzli N, Gilliland F, Peters Jet al. 2005. Childhood asthma and exposure to traffic and nitrogen dioxide. Epidemiology 16(6):737-743 https://pubmed.ncbi.nlm.nih.gov/16222162/.
Gehrig R, Hofer P. 1999. Vergleich von TSP-, PM10- und PM2.5-Schwebestaubmessungen im NABEL 1997 und 1998. Nr. 200’039/168’107.8600 Dübendorf EMPA.
Gehring U, Heinrich J, Kramer U, Grote V, Hochadel M, Sugiri Det al. 2006. Long-term exposure to ambient air pollution and cardiopulmonary mortality in women. Epidemiology 17(5):545-551 https://pubmed.ncbi.nlm.nih.gov/16755270/.
Götschi T, Oglesby L, Mathys P, Monn C, Manalis N, Koistinen Ket al. 2002. Comparison of black smoke and PM2.5 levels in indoor and outdoor environments of four European cities. Environ Sci Technol 36(6):1191-1197 https://pubmed.ncbi.nlm.nih.gov/11944668/.
Hanrahan PL. 1999a. The plume volume molar ratio method for determining NO2/NOx ratios in modeling. Part I: Methodology. J Air Waste Manag Assoc 49:1324-1331.
Hanrahan PL. 1999b. The plume volume molar ratio method for determining NO2 /NOx ratios in modeling. Part II: Evaluation studies. J Air Waste Manag Assoc 49:1332-1338.
Hazenkamp-von Arx ME, Thomas G, Ackermann-Liebrich U, Bonoc R, Burney P, Cyrys Jet al. 2004. PM2.5 and NO2 assessment in 21 European study centres of ECRHS II: annual means and seasonal differences. Atmos Environ 38:1943-1953.
Heinrich J, Topp R, Gehring U, Thefeld W. 2005. Traffic at residential address, respiratory health, and atopy in adults: the National German Health Survey 1998. Environ Res 98(2):240-249 https://pubmed.ncbi.nlm.nih.gov/15820731/.
Hochadel M, Heinrich J, Gehring U, Morgenstern V, Kuhlbusch T, Link Eet al. 2006. Predicting long-term average concentrations of traffic-related air pollutants using GIS-based information. Atmos Environ 40:542-553.
Hoek G, Meliefste K, Cyrys J, Lewne M, Bellander T, Brauer Met al. 2002. Spatial variability of fine particle concentrations in three European areas. Atmos Environ 36:4077-4088.
Hoffmann B, Moebus S, Stang A, Beck EM, Dragano N, Mohlenkamp Set al. 2006. Residence close to high traffic and prevalence of coronary heart disease. Eur Heart J 27(22):2696-2702 https://pubmed.ncbi.nlm.nih.gov/17003049/.
Jerrett M, Burnett RT, Ma R, Pope CAI, Krewski D, Newbold KBet al. 2005. Spatial analysis of air pollution and mortality in Los Angeles. Epidemiology 16(6):727-736 https://pubmed.ncbi.nlm.nih.gov/16222161/.
Krewski D, Burnett R, Jarrett M, Pope CA, Rainham D, Calle Eet al. 2005. Mortality and long-term exposure to ambient air pollution: ongoing analyses based on the American Cancer Society cohort. J Toxicol Environ Health 68(part A):1093-1109.
Künzli N KR, Medina S, Studnicka M, Chanel O, Filliger P, Herry Met al. 2000. Public-health impact of outdoor and traffic-related air pollution: a European assessment. Lancet 356:795-801 https://pubmed.ncbi.nlm.nih.gov/11022926/.
Laden F, Neas LM, Dockery DW, Schwartz J. 2000. Association of fine particulate matter from different sources with daily mortality in six U.S. cities. Environ Health Perspect 108:941-947 https://pubmed.ncbi.nlm.nih.gov/11049813/.
Lipfert FW, Baty JD, Miller JP, Wyzga RE. 2006. PM2.5 constituents and related air quality variables as predictors of survival in a cohort of U.S. military veterans. Inhal Toxicol 18(9):645-657 https://pubmed.ncbi.nlm.nih.gov/16864555/.
Mar TF, Norris GA, Koenig JQ, Larson TV. 2000. Associations between air pollution and mortality in Phoenix, 1995–1997. Environ Health Perspect 108:347-353 https://pubmed.ncbi.nlm.nih.gov/10753094/.
Marple VA, Rubow KL, Turner W, Spengler JD. 1987. Low flow rate sharp cut impactors for indoor air sampling: design and calibration. JAPCA 37(11):1303-1307 https://pubmed.ncbi.nlm.nih.gov/3443863/.
Martin BW, Ackermann-Liebrich U, Leuenberger P, Künzli N, Zemp Stutz EZ, Keller Ret al. 1997. SAPALDIA: methods and participation in the cross-sectional part of the Swiss Study on Air Pollution and Lung Diseases in Adults. Soz Praventivmed 42(2):67-84 https://pubmed.ncbi.nlm.nih.gov/9151378/.
Monn C, Brändli O, Schindler C, Ackermann-Liebrich U, Leuenberger P. 1998. Personal exposure to nitrogen dioxide in Switzerland. SAPALDIA team. Swiss Study on Air Pollution and Lung Diseases in Adults. Sci Total Environ 215(3):243-251 https://pubmed.ncbi.nlm.nih.gov/9606945/.
Monn C, Brändli O, Schaeppi G, Schindler C, Ackermann-Liebrich U, Leuenberger Pet al. 1995. Particulate matter < 10 um (PM10) and total suspended particulates (TSP) in urban, rural and alpine air in Switzerland. Atmos Environ 29:2565-2573.
Nafstad P, Haheim LL, Oftedal B, Gram F, Holme I, Hjermann Iet al. 2003. Lung cancer and air pollution: a 27 year follow up of 16,209 Norwegian men. Thorax 58(12):1071-1076 https://pubmed.ncbi.nlm.nih.gov/14645978/.
Nafstad P, Haheim LL, Wisloff T, Gram F, Oftedal B, Holme Iet al. 2004. Urban air pollution and mortality in a cohort of Norwegian men. Environ Health Perspect 112:610-615 https://pubmed.ncbi.nlm.nih.gov/15064169/.
Nicolai T, Carr D, Weiland SK, Duhme H, von Ehrenstein O, Wagner Cet al. 2003. Urban traffic and pollutant exposure related to respiratory outcomes and atopy in a large sample of children. Eur Respir J 21(6):956-963 https://pubmed.ncbi.nlm.nih.gov/12797488/.
Nyberg F, Gustavsson P, Jarup L, Bellander T, Berglind N, Jakobsson Ret al. 2000. Urban Air Pollution and Lung Cancer in Stockholm. Epidemiology 11(5):487-495 https://pubmed.ncbi.nlm.nih.gov/10955399/.
Palmes ED, Gunnison AF, Dimattio J, Tomczyk C. 1976. Personal samplers for nitrogen dioxide. Am Ind Hyg Assoc J 37(10):570-577 https://pubmed.ncbi.nlm.nih.gov/983946/.
Pierse N, Rushton L, Harris RS, Kuehni CE, Silverman M, Grigg J. 2006. Locally generated particulate pollution and respiratory symptoms in young children. Thorax 61(3):216-220 https://pubmed.ncbi.nlm.nih.gov/16396948/.
Pope CA, Burnett RT, Thun MJ, Calle EE, Krewski D, Ito Ket al. 2002. Lung cancer, cardiopulmonary mortality, and long-term exposure to fine particulate air pollution. JAMA 287(9):1132-1141 https://pubmed.ncbi.nlm.nih.gov/11879110/.
Querol X, Alastuey A, Ruiz CR, Artinano B, Hansson HC, Harrison RMet al. 2004. Speciation and origin of PM10 and PM2.5 in selected European cities. Atmos Environ 38(38):6547-6555.
Rosenlund M, Berglind N, Pershagen G, Hallqvist J, Jonson T, Bellander T. 2006. Long-term exposure to urban air pollution and myocardial infarction. Epidemiology 17(4):383-390 https://pubmed.ncbi.nlm.nih.gov/16699471/.
SAEFL. 1995. Vom Menschen verursachte Luftschadstoff-Emissionen in der Schweiz von 1950 bis 2010. Schriftenreihe Umwelt Nr 256 [available in German and in French]. Dokumentationsdienst 3003 Berne Swiss Agency for the Environment, Forests, and Landscape.
SAEFL. 1997. NO2-Immisssionen in der Schweiz 1990–2010. Dokumentationsdienst 3003. [German, with abstracts in English, French, and Italian] Berne Swiss Agency for the Environment, Forests, and Landscape.
SAEFL. 2003. Modelling of PM10 and PM2.5 ambient concentrations in Switzerland 2000 and 2010. Environmental Documentation No 169 Air Berne Swiss Agency for the Environment, Forests, and Landscape.
SAEFL. 2004. Modelling of NO2 and benzene ambient concentrations in Switzerland 2000 to 2020. Environmental Documentation No 188 Air Berne Swiss Agency for the Environment, Forests, and Landscape.
Samet JM, Dominici F, Curriero FC, Coursac I, Zeger SL. 2000. Fine particulate air pollution and mortality in 20 U.S. Cities, 1987–1994. N Engl J Med 343:1742-1749 https://pubmed.ncbi.nlm.nih.gov/11114312/.
Schindler C, Ackermann-Liebrich U, Leuenberger P, Monn C, Rapp R, Bolognini Get al. 1998. Associations between lung function and estimated average exposure to NO2 in eight areas of Switzerland. The SAPALDIA Team. Swiss Study of Air Pollution and Lung Diseases in Adults. Epidemiology 9(4):405-411 https://pubmed.ncbi.nlm.nih.gov/9647904/.
Sunyer J, Jarvis D, Gotschi T, Garcia-Esteban R, Jacquemin B, Aguilera Iet al. 2006. Chronic bronchitis and urban air pollution in an international study. Occup Environ Med 63:836-843 https://pubmed.ncbi.nlm.nih.gov/16847030/.
Tsai FC, Apte MG, Daisey JM. 2000. An exploratory analysis of the relationship between mortality and the chemical composition of airborne particulate matter. Inhal Toxicol 12(suppl 2):121-135 https://pubmed.ncbi.nlm.nih.gov/10715620/.
Venn AJ, Lewis SA, Cooper M, Hubbard R, Britton J. 2001. Living near a main road and the risk of wheezing illness in children. Am J Respir Crit Care Med 164:2177-2180 https://pubmed.ncbi.nlm.nih.gov/11751183/.
Vineis P, Hoek G, Krzyzanowski M, Vigna-Taglianti F, Veglia F, Airoldi Let al. 2006. Air pollution and risk of lung cancer in a prospective study in Europe. Int J Cancer 119(1):169-174 https://pubmed.ncbi.nlm.nih.gov/16463382/.
Wu J, Lurmann F, Winer A, Lu R, Turco R, Funk T. 2005. Development of an individual exposure model for application to the southern California children’s health study. Atmos Environ 39(2):259-273.
Zhu Y, Hinds W, Kim S, Shen S, Sioutas C. 2002. Study of ultra-fine particles near a major highway with heavy-duty diesel traffic. Atmos Environ 36(27):4323-4335.
Zmirou D, Gauvin S, Pin I, Momas I, Sahraoui F, Just Jet al. 2004. Traffic related air pollution and incidence of childhood asthma: results of the Vesta case-control study. J Epidemiol Community Health 58:18-23 https://pubmed.ncbi.nlm.nih.gov/14684722/.

Information & Authors

Information

Published In

Environmental Health Perspectives
Volume 115Issue 11November 2007
Pages: 1638 - 1645
PubMed: 18007997

History

Received: 16 February 2007
Accepted: 14 August 2007
Published online: 14 August 2007

Keywords

  1. cohort study
  2. cumulative exposure
  3. dispersion model
  4. exposure assessment
  5. long-term exposure

Authors

Affiliations

L.-J. Sally Liu [email protected]
Institute of Social and Preventive Medicine, University of Basel, Basel, Switzerland
Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, Washington, USA
Ivan Curjuric
Institute of Social and Preventive Medicine, University of Basel, Basel, Switzerland
Dirk Keidel
Institute of Social and Preventive Medicine, University of Basel, Basel, Switzerland
Jürg Heldstab
Infras, Zürich, Switzerland
Nino Künzli
ICREA (Institució Catalana de Recerca i Estudis Avançats) and Center for Research in Environmental Epidemiology (CREAL) at Institut Municipal d’Investigació Mèdica (IMIM), Barcelona, Spain
Lucy Bayer-Oglesby
Institute of Social and Preventive Medicine, University of Basel, Basel, Switzerland
Ursula Ackermann-Liebrich
Institute of Social and Preventive Medicine, University of Basel, Basel, Switzerland
Christian Schindler
Institute of Social and Preventive Medicine, University of Basel, Basel, Switzerland

Notes

Address correspondence to L.-J.S. Liu, Institute of Social and Preventive Medicine, University of Basel, Steinengraben 49, CH-4051 Basel, Switzerland. Telephone: 41 61 267 6500. Fax: 41 61 267 6190. E-mail: [email protected]
The authors declare they have no competing financial interests.

Metrics & Citations

Metrics

About Article Metrics


Citations

Download citation

If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Simply select your manager software from the list below and click DOWNLOAD.

Cited by

  • High spatial-resolved source-specific exposure and risk in the city scale: Influence of spatial interrelationship between PM2.5 sources and population on exposure, Science of The Total Environment, 10.1016/j.scitotenv.2024.171873, 926, (171873), (2024).
  • The impact of Cold-start emissions on air pollution exposure during active travel, Transportation Research Part D: Transport and Environment, 10.1016/j.trd.2022.103469, 112, (103469), (2022).
  • Role of Traffic Emission on Temporal and Spatial Characteristics of Pollutant Concentration on Urban Road Network: A Case of Beijing, Journal of Advanced Transportation, 10.1155/2020/8883697, 2020, (1-21), (2020).
  • Comparison of PM2.5 Chemical Components over East Asia Simulated by the WRF-Chem and WRF/CMAQ Models: On the Models’ Prediction Inconsistency, Atmosphere, 10.3390/atmos10100618, 10, 10, (618), (2019).
  • The mediating effect of immune markers on the association between ambient air pollution and adult-onset asthma, Scientific Reports, 10.1038/s41598-019-45327-4, 9, 1, (2019).
  • Association of long-term exposure to traffic-related PM10 with heart rate variability and heart rate dynamics in healthy subjects, Environment International, 10.1016/j.envint.2019.01.031, 125, (107-116), (2019).
  • Transportation noise exposure, noise annoyance and respiratory health in adults: A repeated-measures study, Environment International, 10.1016/j.envint.2018.10.006, 121, (741-750), (2018).
  • Is physical activity a modifier of the association between air pollution and arterial stiffness in older adults: The SAPALDIA cohort study, International Journal of Hygiene and Environmental Health, 10.1016/j.ijheh.2017.06.001, 220, 6, (1030-1038), (2017).
  • Development of land use regression models for nitrogen dioxide, ultrafine particles, lung deposited surface area, and four other markers of particulate matter pollution in the Swiss SAPALDIA regions, Environmental Health, 10.1186/s12940-016-0137-9, 15, 1, (2016).
  • A common functional variant on the pro-inflammatory Interleukin-6 gene may modify the association between long-term PM10 exposure and diabetes, Environmental Health, 10.1186/s12940-016-0120-5, 15, 1, (2016).

View Options

View options

PDF

View PDF

Get Access

Restore your content access

Enter your email address to restore your content access:

Note: This functionality works only for purchases done as a guest. If you already have an account, log in to access the content to which you are entitled.

Media

Figures

Other

Tables

Share

Share

Copy the content Link

Share on social media