Laura Bouso

Aerosol Particle Number Concentration Measurements in Five European Cities Using TSI-3022 Condensation Particle Counter over a Three-Year Period during Health Effects of Air Pollution on Susceptible Subpopulations

Abstract In this study, long-term aerosol particle total number concentration measurements in five metropolitan areas across Europe are presented. The measurements have been carried out in Augsburg, Barcelona, Helsinki, Rome, and Stockholm using the same instrument, a condensation particle counter (TSI model 3022). The results show that in all of the studied cities, the winter concentrations are higher than the summer concentrations. In Helsinki and in Stockholm, winter concentrations are higher by a factor of two and in Augsburg almost by a factor of three compared with summer months. The winter maximum of the monthly average concentrations in these cities is between 10,000 cm-3 and 20,000 cm-3, whereas the summer min is ˜;5000–6000 cm-3. In Rome and in Barcelona, the winters are more polluted compared with summers by as much as a factor of 4–10. The winter maximum in both Rome and Barcelona is close to 100,000 cm-3, whereas the summer minimum is >10,000 cm-3. During the weekdays the maximum of the hourly average concentrations in all of the cities is detected during the morning hours between 7 and 10 a.m. The evening maxima were present in Barcelona, Rome, and Augsburg, but these were not as pronounced as the morning ones. The daily maxima in Helsinki and Stockholm are close or even lower than the daily minima in the more polluted cities. The concentrations between these two groups of cities are different with a factor of about five during the whole day. The study pointed out the influence of the selection of the measurement site and the configuration of the sampling line on the observed concentrations.

Child exposure to indoor and outdoor air pollutants in schools in Barcelona, Spain

Proximity to road traffic involves higher health risks because of atmospheric pollutants. In addition to outdoor air, indoor air quality contributes to overall exposure. In the framework of the BREATHE study, indoor and outdoor air pollution was assessed in 39 schools in Barcelona. The study quantifies indoor and outdoor air quality during school hours of the BREATHE schools. High levels of fine particles (PM2.5), nitrogen dioxide (NO2), equivalent black carbon (EBC), ultrafine particle (UFP) number concentration and road traffic related trace metals were detected in school playgrounds and indoor environments. PM2.5 almost doubled (factor of 1.7) the usual urban background (UB) levels reported for Barcelona owing to high school-sourced PM2.5 contributions: [1] an indoor-generated source characterised mainly by organic carbon (OC) from organic textile fibres, cooking and other organic emissions, and by calcium and strontium (chalk dust) and; [2] mineral elements from sand-filled playgrounds, detected both indoors and outdoors. The levels of mineral elements are unusually high in PM2.5 because of the breakdown of mineral particles during playground activities. Moreover, anthropogenic PM components (such as OC and arsenic) are dry/wet deposited in this mineral matter. Therefore, PM2.5 cannot be considered a good tracer of traffic emissions in schools despite being influenced by them. On the other hand, outdoor NO2, EBC, UFP, and antimony appear to be good indicators of traffic emissions. The concentrations of NO2 are 1.2 times higher at schools than UB, suggesting the proximity of some schools to road traffic. Indoor levels of these traffic-sourced pollutants are very similar to those detected outdoors, indicating easy penetration of atmospheric pollutants. Spatial variation shows higher levels of EBC, NO2, UFP and, partially, PM2.5 in schools in the centre than in the outskirts of Barcelona, highlighting the influence of traffic emissions. Mean child exposure to pollutants in schools in Barcelona attains intermediate levels between UB and traffic stations.

Local determinants of road traffic noise levels versus determinants of air pollution levels in a Mediterranean city.

BACKGROUND Both traffic-related noise and air pollution have been associated with cardiovascular disease (CVD). Spatial correlations between these environmental stressors may entail mutual confounding in epidemiological studies investigating their long-term effects. Few studies have investigated their correlation - none in Spain - and results differ among cities. OBJECTIVES We assessed the contribution of urban land-use and traffic variables to the noise-air pollution correlation in Girona town, where an investigation of the chronic effects of air pollution and noise on CVD takes place (REGICOR-AIR). METHODOLOGY Outdoor annual mean concentrations of nitrogen dioxide (NO(2)) derived from monthly passive sampler measurements were obtained at 83 residential locations. Long-term average traffic-related noise levels from a validated model were assigned to each residence. Linear regression models were fitted both for NO(2) and noise. RESULTS The correlation between NO(2) and noise (L(24h)) was 0.62. However, the correlation differed across the urban space, with lower correlations at sites with higher traffic density and in the modern downtown. Traffic density, distance from the location to the sidewalk and building density nearby explained 35.6% and 73.2% of the variability of NO(2) and noise levels, respectively. The correlation between the residuals of the two models suggested the presence of other unmeasured common variables. CONCLUSIONS The substantial correlation between traffic-related noise and NO(2), endorsed by common determinants, and the dependence of this correlation on complex local characteristics call for careful evaluations of both factors to ultimately assess their cardiovascular effects.

Sources of indoor and outdoor PM2.5 concentrations in primary schools.

Children spend a third of their day in the classroom, where air pollution levels may differ substantially from those outdoors due to specific indoor sources. Air pollution exposure assessments based on atmospheric particle mass measured outdoors may therefore have little to do with the daily PM dose received by school children. This study aims to investigate outdoor and indoor sources of PM2.5 measured at 39 primary schools in Barcelona during 2012. On average 47% of indoor PM2.5 measured concentrations was found to be generated indoors due to continuous resuspension of soil particles (13%) and a mixed source (34%) comprising organic (skin flakes, clothes fibers, possible condensation of VOCs) and Ca-rich particles (from chalk and building deterioration). Emissions from seven outdoor sources penetrated easily indoors being responsible for the remaining 53% of measured PM2.5 indoors. Unpaved playgrounds were found to increase mineral contributions in classrooms by 5-6 μg/m(3) on average with respect to schools with paved playgrounds. Weekday traffic contributions varied considerably across Barcelona within ranges of 1-14 μg/m(3) outdoor and 1-10 μg/m(3) indoor. Indoors, traffic contributions were significantly higher (more than twofold) for classrooms with windows oriented directly to the street, rather than to the interior of the block or to playgrounds. This highlights the importance of urban planning in order to reduce childrens exposure to traffic emissions.

Association between Long-Term Exposure to Traffic-Related Air Pollution and Subclinical Atherosclerosis: The REGICOR Study

Background: Epidemiological evidence of the effects of long-term exposure to air pollution on the chronic processes of atherogenesis is limited. Objective: We investigated the association of long-term exposure to traffic-related air pollution with subclinical atherosclerosis, measured by carotid intima media thickness (IMT) and ankle–brachial index (ABI). Methods: We performed a cross-sectional analysis using data collected during the reexamination (2007–2010) of 2,780 participants in the REGICOR (Registre Gironí del Cor: the Gerona Heart Register) study, a population-based prospective cohort in Girona, Spain. Long-term exposure across residences was calculated as the last 10 years’ time-weighted average of residential nitrogen dioxide (NO2) estimates (based on a local-scale land-use regression model), traffic intensity in the nearest street, and traffic intensity in a 100 m buffer. Associations with IMT and ABI were estimated using linear regression and multinomial logistic regression, respectively, controlling for sex, age, smoking status, education, marital status, and several other potential confounders or intermediates. Results: Exposure contrasts between the 5th and 95th percentiles for NO2 (25 µg/m3), traffic intensity in the nearest street (15,000 vehicles/day), and traffic load within 100 m (7,200,000 vehicle-m/day) were associated with differences of 0.56% (95% CI: –1.5, 2.6%), 2.32% (95% CI: 0.48, 4.17%), and 1.91% (95% CI: –0.24, 4.06) percent difference in IMT, respectively. Exposures were positively associated with an ABI of > 1.3, but not an ABI of < 0.9. Stronger associations were observed among those with a high level of education and in men ≥ 60 years of age. Conclusions: Long-term traffic-related exposures were associated with subclinical markers of atherosclerosis. Prospective studies are needed to confirm associations and further examine differences among population subgroups.

High blood pressure and long-term exposure to indoor noise and air pollution from road traffic

Background: Traffic noise has been associated with prevalence of hypertension, but reports are inconsistent for blood pressure (BP). To ascertain noise effects and to disentangle them from those suspected to be from traffic-related air pollution, it may be essential to estimate people’s noise exposure indoors in bedrooms. Objectives: We analyzed associations between long-term exposure to indoor traffic noise in bedrooms and prevalent hypertension and systolic (SBP) and diastolic (DBP) BP, considering long-term exposure to outdoor nitrogen dioxide (NO2). Methods: We evaluated 1,926 cohort participants at baseline (years 2003–2006; Girona, Spain). Outdoor annual average levels of nighttime traffic noise (Lnight) and NO2 were estimated at postal addresses with a detailed traffic noise model and a land-use regression model, respectively. Individual indoor traffic Lnight levels were derived from outdoor Lnight with application of insulations provided by reported noise-reducing factors. We assessed associations for hypertension and BP with multi-exposure logistic and linear regression models, respectively. Results: Median levels were 27.1 dB(A) (indoor Lnight), 56.7 dB(A) (outdoor Lnight), and 26.8 μg/m3 (NO2). Spearman correlations between outdoor and indoor Lnight with NO2 were 0.75 and 0.23, respectively. Indoor Lnight was associated both with hypertension (OR = 1.06; 95% CI: 0.99, 1.13) and SBP (β = 0.72; 95% CI: 0.29, 1.15) per 5 dB(A); and NO2 was associated with hypertension (OR = 1.16; 95% CI: 0.99, 1.36), SBP (β = 1.23; 95% CI: 0.21, 2.25), and DBP (β⊇= 0.56; 95% CI: –0.03, 1.14) per 10 μg/m3. In the outdoor noise model, Lnight was associated only with hypertension and NO2 with BP only. The indoor noise–SBP association was stronger and statistically significant with a threshold at 30 dB(A). Conclusion: Long-term exposure to indoor traffic noise was associated with prevalent hypertension and SBP, independently of NO2. Associations were less consistent for outdoor traffic Lnight and likely affected by collinearity. Citation: Foraster M, Künzli N, Aguilera I, Rivera M, Agis D, Vila J, Bouso L, Deltell A, Marrugat J, Ramos R, Sunyer J, Elosua R, Basagaña X. 2014. High blood pressure and long-term exposure to indoor noise and air pollution from road traffic. Environ Health Perspect 122:1193–1200; http://dx.doi.org/10.1289/ehp.1307156

Association of long-term exposure to traffic-related air pollution with blood pressure and hypertension in an adult population-based cohort in Spain (the REGICOR study).

Background: Long-term exposure to traffic-related air pollution may increase blood pressure (BP) and induce hypertension. However, evidence supporting these associations is limited, and they may be confounded by exposure to traffic noise and biased due to inappropriate control for use of BP-lowering medications. Objectives: We evaluated the associations of long-term traffic-related air pollution with BP and prevalent hypertension, adjusting for transportation noise and assessing different methodologies to control for BP-lowering medications. Methods: We measured systolic (SBP) and diastolic BP (DBP) at baseline (years 2003–2005) in 3,700 participants, 35–83 years of age, from a population-based cohort in Spain. We estimated home outdoor annual average concentrations of nitrogen dioxide (NO2) with a land-use regression model. We used multivariate linear and logistic regression. Results: A 10-μg/m3 increase in NO2 levels was associated with 1.34 mmHg (95% CI: 0.14, 2.55) higher SBP in nonmedicated individuals, after adjusting for transportation noise. Results were similar in the entire population after adjusting for medication, as commonly done, but weaker when other methods were used to account for medication use. For example, when 10 mmHg were added to the measured SBP levels of medicated participants, the association was β = 0.78 (95% CI: –0.43, 2.00). NO2 was not associated with hypertension. Associations of NO2 with SBP and DBP were stronger in participants with cardiovascular disease, and the association with SBP was stronger in those exposed to high traffic density and traffic noise levels ≥ 55 dB(A). Conclusions: We observed a positive association between long-term exposure to NO2 and SBP, after adjustment for transportation noise, which was sensitive to the methodology used to account for medication. Citation: Foraster M, Basagaña X, Aguilera I, Rivera M, Agis D, Bouso L, Deltell A, Marrugat J, Ramos R, Sunyer J, Vila J, Elosua R, Künzli N. 2014. Association of long-term exposure to traffic-related air pollution with blood pressure and hypertension in an adult population–based cohort in Spain (the REGICOR study). Environ Health Perspect 122:404–411; http://dx.doi.org/10.1289/ehp.1306497

Respiratory and inflammatory responses to short-term exposure to traffic-related air pollution with and without moderate physical activity.

Objectives Exposure to traffic-related air pollution (TRAP) has been associated with adverse respiratory and systemic outcomes. Physical activity (PA) in polluted air may increase pollutant uptake and thereby health effects. The authors aimed to determine the short-term health effects of TRAP in healthy participants and any possible modifying effect of PA. Methods Crossover real-world exposure study comparing in 28 healthy participants pulmonary and inflammatory responses to four different exposure scenarios: 2 h exposure in a high and low TRAP environment, each at rest and in combination with intermittent moderate PA, consisting of four 15 min rest and cycling intervals. Data were analysed using mixed effect models for repeated measures. Results Intermittent PA compared to rest, irrespective of the TRAP exposure status, increased statistically significant (p≤0.05) pulmonary function (forced expiratory volume in 1 s (34 mL), forced vital capacity (29 mL), forced expiratory flow (FEF25–75%) (91 mL)), lung inflammation (fraction of exhaled nitric oxide, FeNO, (0.89 ppb)), and systemic inflammation markers interleukin-6 (52.3%), leucocytes (9.7%) and neutrophils count (18.8%). Interquartile increases in coarse particulate matter were statistically significantly associated with increased FeNO (0.80 ppb) and neutrophil count (5.7%), while PM2.5 and PM10 (particulate matter smaller than 2.5 and 10 µm in diameter, respectively) increased leucocytes (5.1% and 4.0%, respectively). We found no consistent evidence for an interaction between TRAP and PA for any of the outcomes of interest. Conclusions In a healthy population, intermittent moderate PA has beneficial effects on pulmonary function even when performed in a highly polluted environment. This study also suggests that particulate air pollution is inducing pulmonary and systemic inflammatory responses.

Effect of fireworks events on urban background trace metal aerosol concentrations: is the cocktail worth the show?

We report on the effect of a major firework event on urban background atmospheric PM(2.5) chemistry, using 24-h data collected over 8 weeks at two sites in Girona, Spain. The firework pollution episode (Sant Joan fiesta on 23rd June 2008) measured in city centre parkland increased local background PM(2.5) concentrations as follows: Sr (x86), K (x26), Ba (x11), Co (x9), Pb (x7), Cu (x5), Zn (x4), Bi (x4), Mg (x4), Rb (x4), Sb (x3), P (x3), Ga (x2), Mn (x2), As (x2), Ti (x2) and SO(4)(2-) (x2). Marked increases in these elements were also measured outside the park as the pollution cloud drifted over the city centre, and levels of some metals remained elevated above background for days after the event as a reservoir of metalliferous dust persisted within the urban area. Transient high-PM pollution episodes are a proven health hazard, made worse in the case of firework combustion because many of the elements released are both toxic and finely respirable, and because displays commonly take place in an already polluted urban atmosphere.

Arterial blood pressure responses to short-term exposure to low and high traffic-related air pollution with and without moderate physical activity:

Background Short-term exposure to traffic-related air pollution (TRAP) has been associated with adverse cardiovascular outcomes. Physical activity (PA) in polluted air may increase pollutant uptake and increase these effects. Methods Crossover real-world exposure study in 28 healthy participants comparing systolic (SBP) and diastolic blood pressure (DBP) responses to four different exposure scenarios: 2 h exposure in high or low-TRAP environment, each at rest and combined with intermittent moderate PA consisting of 15 min intervals alternating rest and cycling on a stationary bicycle. Data was analyzed using mixed effect models for repeated measures. Results Exposure to high TRAP was associated with higher DBP (1.1 mm/Hg, p = 0.002) post-exposure, irrespective of exercise status. Ultrafine particles (UFP) increased DBP post-exposure (0.9 mm/Hg, p = 0.004). Interquartile increases in black carbon (BC), fine particulate matter (PM10 and PMcoarse), UFP, and nitric oxides (NOx) were associated with statistically significantly higher SBP post-exposure (1.2, 1.0, 1.1, and 1.1 mm/Hg, respectively). Intermittent PA compared with rest was associated with lower SBP post-exposure (−2.4 mm/Hg, p < 0.001). PA lowered SBP more after exposure to the low-TRAP site (−2.3 mm/Hg) compared with the high-TRAP site (−1.6 mm/Hg). We only found evidence of an interaction between PA and both PM10 and PMcoarse, increasing SBP. Conclusion Both SBP and DBP increase after exposure to TRAP. Intermittent PA attenuates the TRAP-related increases in SBP, with the exception of PM10 and PMcoarse, which potentiate these increases. We showed that in low-TRAP environments intermittent PA has stronger beneficial effects on SBP than in high-TRAP environments.