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Aims: To assess the relation between ambient, indoor, and personal levels of PM2.5 and its elemental composition for elderly subjects with cardiovascular disease. Methods: In the framework of a European Union funded study, panel studies were conducted in Amsterdam, the Netherlands and Helsinki, Finland. Outdoor PM2.5 concentrations were measured at a fixed site. Each subject’s indoor and personal PM2.5 exposure was measured biweekly for six months, during the 24 hour period preceding intensive health measurements. The absorbance of PM2.5 filters was measured as a marker for diesel exhaust. The elemental content of more than 50% of the personal and indoor samples and all corresponding outdoor samples was measured using energy dispersive x ray fluorescence. Results: For Amsterdam and Helsinki respectively, a total of 225 and 238 personal, and 220 and 233 indoor measurements, were analysed from 36 and 46 subjects. For most elements, personal and indoor concentrations were lower than and highly correlated with outdoor concentrations. The highest correlations (median r>0.9) were found for sulfur and particle absorbance, which both represent fine mode particles from outdoor origin. Low correlations were observed for elements that represent the coarser part of the PM2.5 particles (Ca, Cu, Si, Cl). Conclusions: The findings of this study provide support for using fixed site measurements as a measure of exposure to particulate matter in time series studies linking the day to day variation in particulate matter to the day to day variation in health endpoints, especially for components of particulate matter that are generally associated with fine particles and have few indoor sources. The high correlation for absorbance of PM2.5 documents that this applies to particulate matter from combustion sources, such as diesel vehicles, as well.

Background Particulate matter air pollution has been associated with adverse health effects. The fraction of ambient particles that are mainly responsible for the observed health effects is still a matter of controversy. Better characterization of the health relevant particle fraction will have major implications for air quality policy since it will determine which sources should be controlled. The RUPIOH study, an EU-funded multicentre study, was designed to examine the distribution of various ambient particle metrics in four European cities (Amsterdam, Athens, Birmingham, Helsinki) and assess their health effects in participants with asthma or COPD, based on a detailed exposure assessment. In this paper the association of central site measurements with respiratory symptoms and restriction of activities is examined. Methods At each centre a panel of participants with either asthma or COPD recorded respiratory symptoms and restriction of activities in a diary for six months. Exposure assessment included simultaneous measurements of coarse, fine and ultrafine particles at a central site. Data on gaseous pollutants were also collected. The associations of the 24-hour average concentrations of air pollution indices with the health outcomes were assessed in a hierarchical modelling approach. A city specific analysis controlling for potential confounders was followed by a meta-analysis to provide overall effect estimates. Results A 10 μg/m 3 increase in previous day coarse particles concentrations was positively associated with most symptoms (an increase of 0.6 to 0.7% in average) and limitation in walking (OR= 1.076, 95% CI: 1.026-1.128). Same day, previous day and previous two days ozone concentrations were positively associated with cough (OR= 1.061, 95% CI: 1.013-1.111; OR= 1.049, 95% CI: 1.016-1.083 and OR= 1.059, 95% CI: 1.027-1.091, respectively). No consistent associations were observed between fine particle concentrations, nitrogen dioxide and respiratory health effects. As for particle number concentrations negative association (mostly non-significant at the nominal level) was observed with most symptoms whilst the positive association with limitation of activities did not reach the nominal level of significance. Conclusions The observed associations with coarse particles are in agreement with the findings of toxicological studies. Together they suggest it is prudent to regulate also coarse particles in addition to fine particles.

Objectives:Misclassification of exposure related to the use of central sites may be larger for ultrafine particles than for particulate matter ⩽2.5 μm and ⩽10 μm (PM2.5 and PM10) and may result in underestimation of health effects. This paper describes the relative strength of the association between outdoor and indoor exposure to ultrafine particles, PM2.5 and PM10 and lung function.Methods:In four European cities (Helsinki, Athens, Amsterdam and Birmingham), lung function (forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1) and peak expiratory flow (PEF)) was measured three times a day for 1 week in 135 patients with asthma or chronic obstructive pulmonary disease (COPD), covering study periods of >1 year. Daily concentrations of particle number, PM2.5 and PM10 were measured at a central site in each city and both inside and outside the subjects’ homes.Results:Daily average particle number concentrations ranged between 2100 and 66 100 particles/cm3. We found no association between 24 h average particle number or particle mass concentrations and FVC, FEV1 and PEF. Substituting home outdoor or home indoor concentrations of particulate air pollution instead of the central site measurements did not change the observed associations. Analyses restricted to asthmatics also showed no associations.Conclusions:No consistent associations between lung function and 24 h average particle number or particle mass concentrations were found in panels of patients with mild to moderate COPD or asthma. More detailed exposure assessment did not change the observed associations. The lack of association could be due to the high prevalence of medication use, limited ability to assess lagged effects over several days or absence of an effect.

Background Exposure to fine ambient particulate matter (PM) has consistently been associated with increased morbidity and mortality. The relationship between exposure to ultrafine particles (UFP) and health effects is less firmly established. If UFP cause health effects independently from coarser fractions, this could affect health impact assessment of air pollution, which would possibly lead to alternative policy options to be considered to reduce the disease burden of PM. Therefore, we organized an expert elicitation workshop to assess the evidence for a causal relationship between exposure to UFP and health endpoints. Methods An expert elicitation on the health effects of ambient ultrafine particle exposure was carried out, focusing on: 1) the likelihood of causal relationships with key health endpoints, and 2) the likelihood of potential causal pathways for cardiac events. Based on a systematic peer-nomination procedure, fourteen European experts (epidemiologists, toxicologists and clinicians) were selected, of whom twelve attended. They were provided with a briefing book containing key literature. After a group discussion, individual expert judgments in the form of ratings of the likelihood of causal relationships and pathways were obtained using a confidence scheme adapted from the one used by the Intergovernmental Panel on Climate Change. Results The likelihood of an independent causal relationship between increased short-term UFP exposure and increased all-cause mortality, hospital admissions for cardiovascular and respiratory diseases, aggravation of asthma symptoms and lung function decrements was rated medium to high by most experts. The likelihood for long-term UFP exposure to be causally related to all cause mortality, cardiovascular and respiratory morbidity and lung cancer was rated slightly lower, mostly medium. The experts rated the likelihood of each of the six identified possible causal pathways separately. Out of these six, the highest likelihood was rated for the pathway involving respiratory inflammation and subsequent thrombotic effects. Conclusion The overall medium to high likelihood rating of causality of health effects of UFP exposure and the high likelihood rating of at least one of the proposed causal mechanisms explaining associations between UFP and cardiac events, stresses the importance of considering UFP in future health impact assessments of (transport-related) air pollution, and the need for further research on UFP exposure and health effects.

ObjectivesStudies of individual inflammatory responses to exposure to air pollution are few but are important in defining the most sensitive markers in better understanding pathophysiological pathways in the lung. The goal of this study was to assess whether exposure to airborne particles is associated with oxidative stress in an epidemiological setting.MethodsThe authors assessed exposure to particulate matter air pollution in four European cities in relation to levels of nitrite plus nitrate (NOx) in exhaled breath condensate (EBC) measurements in 133 subjects with asthma or chronic obstructive pulmonary disease using an EBC capture method developed for field use. In each subject, three measurements were collected. Exposure measurements included particles smaller than 10 μm (PM10), smaller than 2.5 μm (PM2.5) and particle number counts at a central site, outdoors near the subject's home and indoors.ResultsThere were positive and significant relationships between EBC NOx and coarse particles at the central sampling sites (increase of 20.4% (95% CI 6.1% to 36.6%) per 10 μg/m3 increase of coarse particles of the previous day) but not between EBC NOx and other particle measures. Associations tended to be stronger in subjects not taking steroid medication.ConclusionsAn association was found between exposure to ambient coarse particles at central sites and EBC NOx, a marker of oxidative stress. The lack of association between PM measures more indicative of personal exposures (particularly indoor exposure) means interpretation should be cautious. However, EBC NOx may prove to be a marker of PM-induced oxidative stress in epidemiological studies.

The associations between residential outdoor and ambient particle mass, fine particle absorbance, particle number (PN) concentrations, and residential and traffic determinants were investigated in four European urban areas (Helsinki, Athens, Amsterdam, and Birmingham). A total of 152 nonsmoking participants with respiratory diseases, not exposed to occupational pollution, were included in the study, which comprised a 7-day intensive exposure monitoring period of both indoor and home outdoor particle mass and number concentrations. The same pollutants were also continuously measured at ambient fixed sites centrally located to the studied areas (fixed ambient sites). Relationships between concentrations measured directly outside the homes (residential outdoor) and at the fixed ambient sites were pollutant-specific, with substantial variations among the urban areas. Differences were more pronounced for coarse particles due to resuspension of road dust and PN, which is strongly related to traffic emissions. Less significant outdoor-to-fixed variation for particle mass was observed for Amsterdam and Birmingham, predominantly due to regional secondary aerosol. On the contrary, a strong spatial variation was observed for Athens and to a lesser extent for Helsinki. This was attributed to the overwhelming and time-varied inputs from traffic and other local sources. The location of the residence and traffic volume and distance to street and traffic light were important determinants of residential outdoor particle concentrations. On average, particle mass levels in suburban areas were less than 30% of those measured for residences located in the city center. Residences located less than 10 m from a street experienced 133% higher PN concentrations than residences located further away. Overall, the findings of this multi-city study, indicated that (1) spatial variation was larger for PN than for fine particulate matter (PM) mass and varied between the cities, (2) vehicular emissions in the residential street and location in the center of the city were significant predictors of spatial variation, and (3) the impact of traffic and location in the city was much larger for PN than for fine particle mass.

Epidemiologic studies have shown that ambient particulate matter (PM) has adverse effects on cardiovascular health. Effective mitigation of the health effects requires identification of the most harmful PM sources. The objective of our study was to evaluate relative effects of fine PM [aerodynamic diameter $\\leq 2.5 \\mu m (PM_{2.5})$] from different sources on exercise-induced ischemia. We collected daily outdoor PM2.5 samples between autumn 1998 and spring 1999 in Helsinki, Finland. The mass of PM2.5 was apportioned between five sources. Forty-five elderly nonsmoking persons with stable coronary heart disease visited a clinic biweekly for submaximal exercise testing, during which the occurrence of ST segment depressions was recorded. Levels of PM2.5 originating from local traffic and long-range transport were associated with ST segment depressions > 0.1 mV, with odds ratios at 2-day lag of 1.53 [95% confidence interval (CI), 1.19-1.97] and 1.11 (95% CI, 1.02-1.20) per $1 \\mu g/m^3$, respectively. In multipollutant models, where we used indicator elements for sources instead of source-specific PM2.5, only absorbance (elemental carbon), an indicator of local traffic and other combustion, was associated with ST segment depressions. Our results suggest that the PM fraction originating from combustion processes, notably traffic, exacerbates ischemic heart diseases associated with PM mass.

Background: Daily variations in ambient particulate air pollution have been associated with respiratory mortality and morbidity. Aims: To assess the associations between urinary concentration of lung Clara cell protein CC16, a marker for lung damage, and daily variation in fine and ultrafine particulate air pollution. Methods: Spot urinary samples (n = 1249) were collected biweekly for six months in subjects with coronary heart disease in Amsterdam, Netherlands (n = 37), Erfurt, Germany (n = 47), and Helsinki, Finland (n = 47). Ambient particulate air pollution was monitored at a central site in each city. Results: The mean 24 hour number concentration of ultrafine particles was 17.3×103 cm−3 in Amsterdam, 21.1×103 cm−3 in Erfurt, and 17.0×103 cm−3 in Helsinki. The mean 24 hour PM2.5 concentrations were 20, 23, and 13 μg/m3, respectively. Daily variation in ultrafine particle levels was not associated with CC16. In contrast, CC16 concentration seemed to increase with increasing levels of PM2.5 in Helsinki, especially among subjects with lung disorders. No clear associations were observed in Amsterdam and Erfurt. In Helsinki, the CC16 concentration increased by 20.2% (95% CI 6.9 to 33.5) per 10 μg/m3 increase in PM2.5 concentration (lag 2). The respective pooled effect estimate was 2.1% (95% CI −1.3 to 5.6). Conclusion: The results suggest that exposure to particulate air pollution may lead to increased epithelial barrier permeability in lungs.

The contribution of motorized traffic to air pollution is widely recognized, but relatively few studies have looked at the respiratory health status of subjects living near busy roads. We studied children in six areas located near major motorways in the Netherlands. We measured lung function in the children, and we assessed their exposure to traffic-related air pollution using separate traffic counts for automobiles and trucks. We also measured air pollution in the children's schools. Lung function was associated with truck traffic density but had a lesser association with automobile traffic density. The association was stronger in children living closest (<300 m) to the motorways. Lung function was also associated with the concentration of black smoke, measured inside the schools, as a proxy for diesel exhaust particles. The associations were stronger in girls than in boys. The results indicate that exposure to traffic-related air pollution, in particular diesel exhaust particles, may lead to reduced lung function in children living near major motorways.

Epidemiological studies have established an association between outdoor levels of fine particles (PM 2.5 ) and cardiovascular health. However, there is little information on the determinants of PM 2.5 exposures among persons with cardiovascular disease, a potentially susceptible population group. Daily outdoor, indoor and personal PM 2.5 and absorbance (proxy for elemental carbon) concentrations were measured among elderly subjects with cardiovascular disease in Amsterdam, the Netherlands, and Helsinki, Finland, during the winter and spring of 1998–1999 within the framework of the ULTRA study. There were 37 non-smoking subjects in Amsterdam and 47 in Helsinki. In Amsterdam, where there were enough exposure events for analyses, exposure to environmental tobacco smoke (ETS) indoors was a major source of between-subject variation in PM 2.5 exposures, and a strong determinant of PM 2.5 and absorbance exposures. When the days with ETS were excluded, within-subject variation accounted for 89% of the total variation in personal PM 2.5 and 97% in absorbance in Amsterdam. The respective figures were 66% and 61% in Helsinki. In both cities, outdoor levels of PM 2.5 and absorbance were major determinants of personal and indoor levels. Traffic was also an important determinant of absorbance: living near a major street increased exposure by 22%, and every hour spent in a motor vehicle by 13% in Amsterdam. The respective increases were 37% and 9% in Helsinki. Cooking was associated with increased levels of both absorbance and PM 2.5 . Our results demonstrate that by using questionnaires in connection with outdoor measurements, exposure estimation of PM 2.5 and its combustion originating fraction can be improved among elderly persons with compromised health.