Search

At city level, personal monitoring is the best way to assess people's exposure. However, it is usually estimated from a few monitoring stations. Our aim was to determine the exposure to black carbon (BC) and BC dose for 45 schoolchildren with portable microaethalometers and to evaluate the relationship between personal monitoring and fixed stations at schools (indoor and outdoor) and in an urban background (UB) site. Personal BC concentra-tions were 20% higher than in fixed stations at schools. Linear mixed-effect models showed low R2 between personal measurements and fixed stations at schools (R2 ≤ 0.28), increasing to R2 ≥ 0.70 if considering only periods when children were at schools. For the UB station, the respective R2 were 0.18 and 0.45, indicating the importance of the distance to the monitoring station when assessing exposure. During the warm season, the fixed stations agreed better with personal measurements than during the cold one. Children spent 6% of their time on commuting but received 20% of their daily BC dose, due to co-occurrence with road traffic rush hours and the close proximity to the source. Children received 37% of their daily-integrated BC dose at school. Indoor environments (classroom and home) were responsible for the 56% BC dose. © 2016 John Wiley & Sons A/S.

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 ß = 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., Peer Reviewed, Postprint (published version)

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 (ß = 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 (ß = 1.23; 95% CI: 0.21, 2.25), and DBP (ß¿= 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 Lnig, Peer Reviewed, Postprint (published version)

Postprint (published version)

Outdoor road traffic noise levels are associated with hypertension (HT). Studies on blood pressure (BP) are inconsistent and the true indoor traffic noise exposure may differ due to protections against noise. We analysed the effects of long-term exposure to outdoor and indoor traffic noise levels on HT, systolic (SBP) and diastolic BP (DBP, mmHg), adjusting for outdoor annual average concentrations of near-road traffic-related air pollution (nitrogen dioxide, NO2) among 1926 participants (aged 36-82) from the Catalan REGICOR study. Long-term outdoor residential levels of traffic noise at night (Lnight, in A-weighted dB) and annual averages of NO2 (in µg/m3 ) were estimated at the postal addresses’ façades with a city-specific noise model and a land-use regression model, respectively. Indoor traffic noise was calculated from outdoor noise levels subtracting the attenuations in dB according to reported noise protections. Median noise levels were 56.7 dB outdoors and 27.1 dB indoors. Spearman correlations between outdoor and indoor noise with NO2 were 0.75 and 0.23, respectively. Outdoor noise was only associated with HT (OR=1.19, 95%CI: 1.02, 1.40), whereas there was a suggestive association of indoor noise with both HT (OR=1.06, 95%CI: 0.99, 1.13) and SBP (ß=0.38, 95%CI: -0.08, 0.83) per 5 dB increase in outdoor noise levels. NO2 was also associated with both outcomes after adjustment for indoor noise. Findings for indoor traffic noise levels are more plausible than those for outdoor traffic noise. The use of indoor traffic noise estimates help to disentangle the effects from those of traffic-related air pollution., Postprint (author's final draft)

Epidemiological evidence of the effects of long-term exposure to air pollution on the chronic processes of atherogenesis is limited. 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). 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. 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. 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., Peer Reviewed, Postprint (published version)

Peer Reviewed, Postprint (author's final draft)

Peer Reviewed, Postprint (published version)

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. © Elsevier B.V.