Josef Cyrys

Estimating long-term average particulate air pollution concentrations: application of traffic indicators and geographic information systems.

Background. As part of a multicenter study relating traffic-related air pollution with incidence of asthma in three birth cohort studies (TRAPCA), we used a measurement and modelling procedure to estimate long-term average exposure to traffic-related particulate air pollution in communities throughout the Netherlands; in Munich, Germany; and in Stockholm County, Sweden. Methods. In each of the three locations, 40–42 measurement sites were selected to represent rural, urban background and urban traffic locations. At each site and fine particles and filter absorbance (a marker for diesel exhaust particles) were measured for four 2-week periods distributed over approximately 1-year periods between February 1999 and July 2000. We used these measurements to calculate annual average concentrations after adjustment for temporal variation. Traffic-related variables (eg, population density and traffic intensity) were collected using Geographic Information Systems and used in regression models predicting annual average concentrations. From these models we estimated ambient air concentrations at the home addresses of the cohort members. Results. Regression models using traffic-related variables explained 73%, 56% and 50% of the variability in annual average fine particle concentrations for the Netherlands, Munich and Stockholm County, respectively. For filter absorbance, the regression models explained 81%, 67% and 66% of the variability in the annual average concentrations. Cross-validation to estimate the model prediction errors indicated root mean squared errors of 1.1–1.6 &mgr;g/m3 for PM2.5 and 0.22–0.31 *10−5m−1 for absorbance. Conclusions. A substantial fraction of the variability in annual average concentrations for all locations was explained by traffic-related variables. This approach can be used to estimate individual exposures for epidemiologic studies and offers advantages over alternative techniques relying on surrogate variables or traditional approaches that utilize ambient monitoring data alone.

Atopic Diseases, Allergic Sensitization, and Exposure to Traffic-related Air Pollution in Children

RATIONALE In vitro studies, animal experiments, and human exposure studies have shown how ambient air pollution increases the risk of atopic diseases. However, results derived from observational studies are inconsistent. OBJECTIVES To assess the relationship between individual-based exposure to traffic-related air pollutants and allergic disease outcomes in a prospective birth cohort study during the first 6 years of life. METHODS We studied 2,860 children at the age of 4 years and 3,061 at the age of 6 years to investigate atopic diseases and allergic sensitization. Long-term exposure to particulate matter (PM(2.5)), PM(2.5) absorbance, and long-term exposure to nitrogen dioxide (NO(2)) was assessed at residential addresses using geographic information systems based regression models and air pollution measurements. The distance to the nearest main road was used as a surrogate for traffic-related air pollutants. MEASUREMENTS AND MAIN RESULTS Strong positive associations were found between the distance to the nearest main road and asthmatic bronchitis, hay fever, eczema, and sensitization. A distance-dependent relationship could be identified, with the highest odds ratios (ORs) for children living less than 50 m from busy streets. For PM(2.5) absorbance, statistically significant effects were found for asthmatic bronchitis (OR, 1.56; 95% confidence interval [CI], 1.03-2.37), hay fever (OR, 1.59; 95% CI, 1.11-2.27), and allergic sensitization to pollen (OR, 1.40; 95% CI, 1.20-1.64). NO(2) exposure was associated with eczema, whereas no association was found for allergic sensitization. CONCLUSIONS This study provides strong evidence for increased risk of atopic diseases and allergic sensitization when children are exposed to ambient particulate matter.

Health effects of particulate air pollution: A review of epidemiological evidence

Health effects of air pollution Everyone is exposed to ambient air pollution every day, some to a more and some to a lesser extent. When the first scientist examined the effect of air pollution on health after the Meuse Valley fog in 1930 (Firket, 1936) or the London smog in 1952 (Ministry of health, 1954), no one could have known what an extended field of research they started. Today, a lot of research is done on various aspects of air pollution. As shown in Figure 1, human health can be affected in all stages of life—from conception to old age. This review seeks to give an overview on the variety of health risks air pollution poses with a focus on epidemiological studies. Due to the vastness of the field, this review cannot go into too much detail in each section. However, it will give the reader a comprehensive impression on the large number of health effects of air pollution. Where available, the authors refer to existing reviews that might offer more depth in a certain field for the interested reader. The first six sections deal with different health outcomes in respect to ambient air pollution. Section 7 explains potential mechanisms that may lead from the inhalation of particles to adverse health outcomes. The last section finally gives an overview on research gaps that exist in the field and possible directions that research might take.

Traffic-related air pollution and respiratory health during the first 2 yrs of life

As part of an international collaborative study on the impact of Traffic-Related Air Pollution on Childhood Asthma (TRAPCA), the health effects associated with long-term exposure to particles with a 50% cut-off aerodynamic diameter of 2.5 µm (PM2.5), PM2.5 absorbance, and nitrogen dioxide (NO2) were analysed. The German part of the TRAPCA study used data from subpopulations of two ongoing birth cohort studies (German Infant Nutrition Intervention Programme (GINI) and Influences of Lifestyle Related Factors on the Human Immune System and Development of Allergies in Children (LISA)) based in the city of Munich. Geographic information systems (GIS)-based exposure modelling was used to estimate traffic-related air pollutants at the birth addresses of 1,756 infants. Logistic regression was used to analyse possible health effects and potential confounding factors were adjusted for. The ranges in estimated exposures to PM2.5, PM2.5 absorbance, and NO2 were 11.9–21.9 µg·m−3, 1.38–4.39×10−5 m−1, and 19.5–66.9 µg·m3, respectively. Significant associations between these pollutants and cough without infection (odds ratio (OR) (95% confidence interval (CI)): 1.34 (1.11–1.61), 1.32 (1.10–1.59), and 1.40 (1.12–1.75), respectively) and dry cough at night (OR (95% CI): 1.31 (1.07–1.60), 1.27 (1.04–1.55), and 1.36 (1.07–1.74), respectively) in the first year of life were found. In the second year of life, these effects were attenuated. There was some indication of an association between traffic-related air pollution and symptoms of cough. Due to the very young age of the infants, it was too early to draw definitive conclusions from this for the development of asthma.

Ultrafine particles and platelet activation in patients with coronary heart disease – results from a prospective panel study

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

Daily mortality and particulate matter in different size classes in Erfurt, Germany

The link between elevated concentrations of ambient particulate matter (PM) and increased mortality has been investigated in numerous studies. Here we analyzed the role of different particle size fractions with respect to total and cardio-respiratory mortality in Erfurt, Germany, between 1995 and 2001.Number concentrations (NC) of PM were measured using an aerosol spectrometer consisting of a Differential Mobility Particle Sizer and a Laser Aerosol Spectrometer to characterize particles between 0.01 and 0.5 and between 0.1 and 2.5 μm, respectively. We derived daily means of particle NC for ultrafine (0.01–0.1 μm) and for fine particles (0.01–2.5 μm). Assuming spherical particles of a constant density, we estimated the mass concentrations (MC) of particles in these size ranges. Concurrently, data on daily total and cardio-respiratory death counts were obtained from local health authorities. The data were analyzed using Poisson Generalized Additive Models adjusting for trend, seasonality, influenza epidemics, day of the week, and meteorology using smooth functions or indicator variables. We found statistically significant associations between elevated ultrafine particle (UFP; diameter: 0.01–0.1 μm) NC and total as well as cardio-respiratory mortality, each with a 4 days lag. The relative mortality risk (RR) for a 9748 cm−3 increase in UFP NC was RR=1.029 and its 95% confidence interval (CI)=1.003–1.055 for total mortality. For cardio-respiratory mortality we found: RR=1.031, 95% CI: 1.003–1.060. No association between fine particle MC and mortality was found.This study shows that UFP, representing fresh combustion particles, may be an important component of urban air pollution associated with health effects.

Comparison between different traffic-related particle indicators: elemental carbon (EC), PM2.5 mass, and absorbance.

Here we compare PM2.5 (particles with aerodynamic diameter less than 2.5 μm) mass and filter absorbance measurements with elemental carbon (EC) concentrations measured in parallel at the same site as well as collocated PM2.5 and PM10 (particles with aerodynamic diameter less than 10 μm) mass and absorbance measurements. The data were collected within the Traffic-Related Air Pollution on Childhood Asthma (TRAPCA) study in Germany, The Netherlands and Sweden. The study was designed to assess the health impact of spatial contrasts in long-term average concentrations. The measurement sites were distributed between background and traffic locations. Annual EC and PM2.5 absorbance measurements were at traffic sites on average 43–84% and 26–76% higher, respectively, compared to urban background sites. The contrast for PM2.5 mass measurements was lower (8–35%). The smaller contrast observed for PM2.5 mass in comparison with PM2.5 absorbance and EC documents that PM2.5 mass underestimates exposure contrasts related to motorized traffic emissions. The correlation between PM10 and PM2.5 was high, documenting that most of the spatial variation of PM10 was because of PM2.5. The measurement of PM2.5 absorbance was highly correlated with EC measurements and suggests that absorbance can be used as a simple, inexpensive and non-destructive method to estimate motorized traffic-related particulate air pollution. The EC/absorbance relation differed between countries and site type (background/traffic), supporting the need for site-specific calibrations of the simple absorbance method. While the ratio between PM2.5 and PM10 mass ranged from 0.54 to 0.68, the ratio of PM2.5 absorbance and PM10 absorbance was 0.96–0.97, indicating that PM2.5 absorbance captures nearly all of the particle absorbance.

Traffic-related atmospheric pollutants levels during pregnancy and offspring's term birth weight: a study relying on a land-use regression exposure model.

Background Some studies have suggested that particulate matter (PM) levels during pregnancy may be associated with birth weight. Road traffic is a major source of fine PM (PM with aero-dynamic diameter < 2.5 μm; PM2.5). Objective We determined to characterize the influence of maternal exposure to atmospheric pollutants due to road traffic and urban activities on offspring term birth weight. Methods Women from a birth cohort [the LISA (Influences of Lifestyle Related Factors on the Human Immune System and Development of Allergies in Children) cohort] who delivered a non-premature baby with a birth weight > 2,500 g in Munich metropolitan area were included. We assessed PM2.5, PM2.5 absorbance (which depends on the blackness of PM2.5, a marker of traffic-related air pollution), and nitrogen dioxide levels using a land-use regression model, taking into account the type and length of roads, population density, land coverage around the home address, and temporal variations in pollution during pregnancy. Using Poisson regression, we estimated prevalence ratios (PR) of birth weight < 3,000 g, adjusted for gestational duration, sex, maternal smoking, height, weight, and education. Results Exposure was defined for 1,016 births. Taking the lowest quartile of exposure during pregnancy as a reference, the PR of birth weight < 3,000 g associated with the highest quartile was 1.7 for PM2.5 [95% confidence interval (CI), 1.2–2.7], 1.8 for PM2.5 absorbance (95% CI, 1.1–2.7), and 1.2 for NO2 (95% CI, 0.7–1.7). The PR associated with an increase of 1 μg/m3 in PM2.5 levels was 1.13 (95% CI, 1.00–1.29). Conclusion Increases in PM2.5 levels and PM2.5 absorbance were associated with decreases in term birth weight. Traffic-related air pollutants may have adverse effects on birth weight.

Air Pollution Exposure and Lung Function in Children: The ESCAPE Project.

Background: There is evidence for adverse effects of outdoor air pollution on lung function of children. Quantitative summaries of the effects of air pollution on lung function, however, are lacking due to large differences among studies. Objectives: We aimed to study the association between residential exposure to air pollution and lung function in five European birth cohorts with a standardized exposure assessment following a common protocol. Methods: As part of the European Study of Cohorts for Air Pollution Effects (ESCAPE) we analyzed data from birth cohort studies situated in Germany, Sweden, the Netherlands, and the United Kingdom that measured lung function at 6–8 years of age (n = 5,921). Annual average exposure to air pollution [nitrogen oxides (NO2, NOx), mass concentrations of particulate matter with diameters < 2.5, < 10, and 2.5–10 μm (PM2.5, PM10, and PMcoarse), and PM2.5 absorbance] at the birth address and current address was estimated by land-use regression models. Associations of lung function with estimated air pollution levels and traffic indicators were estimated for each cohort using linear regression analysis, and then combined by random effects meta-analysis. Results: Estimated levels of NO2, NOx, PM2.5 absorbance, and PM2.5 at the current address, but not at the birth address, were associated with small decreases in lung function. For example, changes in forced expiratory volume in 1 sec (FEV1) ranged from –0.86% (95% CI: –1.48, –0.24%) for a 20-μg/m3 increase in NOx to –1.77% (95% CI: –3.34, –0.18%) for a 5-μg/m3 increase in PM2.5. Conclusions: Exposure to air pollution may result in reduced lung function in schoolchildren. Citation: Gehring U, Gruzieva O, Agius RM, Beelen R, Custovic A, Cyrys J, Eeftens M, Flexeder C, Fuertes E, Heinrich J, Hoffmann B, de Jongste JC, Kerkhof M, Klümper C, Korek M, Mölter A, Schultz ES, Simpson A, Sugiri D, Svartengren M, von Berg A, Wijga AH, Pershagen G, Brunekreef B. 2013. Air pollution exposure and lung function in children: the ESCAPE project. Environ Health Perspect 121:1357–1364; http://dx.doi.org/10.1289/ehp.1306770

Air Temperature and the Occurrence of Myocardial Infarction in Augsburg, Germany

Background— Air temperature changes have been associated with cardiovascular mortality and morbidity. The objective of this study was to examine in detail the registry-based myocardial infarction (MI) rates and coronary deaths in relation to air temperature in the area of Augsburg, Germany. Methods and Results— Between 1995 and 2004, the Monitoring Trends and Determinants on Cardiovascular Diseases/Cooperative Health Research in the Region of Augsburg (MONICA/KORA) registry recorded 9801 cases of MI and coronary deaths. Over the same period, meteorological parameters and air pollutant concentrations were measured in the study region. Poisson regression analyses adjusting for time trend, relative humidity, season, and calendar effects were used to estimate immediate, delayed, and cumulative temperature effects on the occurrence of MIs. The daily rates of total MI, nonfatal and fatal events, and incident and recurrent events were analyzed. For the total MI cases, a 10°C decrease in 5-day average temperature was associated with a relative risk of 1.10 (95% confidence interval, 1.04 to 1.15). The effect of temperature on the occurrence of nonfatal events showed a delayed pattern, whereas the association with fatal MI was more immediate. No association could be observed for recurrent events. The effects of temperature decreases on total MI cases were more pronounced in years with higher average temperatures and were visible in summer. Conclusions— We observed an inverse relationship between temperature and MI occurrence not only during winter but also during summer. Thus, our results suggest not a pure “cold effect” but an influence of unusual temperature decreases.