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To update the current state of evidence and assess its quality, we conducted a systematic review on the effects of environmental noise exposure on the cardio-metabolic systems as input for the new WHO environmental noise guidelines for the European Region. We identified 600 references relating to studies on effects of noise from road, rail and air traffic, and wind turbines on the cardio-metabolic system, published between January 2000 and August 2015. Only 61 studies, investigating different end points, included information enabling estimation of exposure response relationships. These studies were used for meta-analyses, and assessments of the quality of evidence using the Grading of Recommendations Assessment, Development and Evaluation (GRADE). A majority of the studies concerned traffic noise and hypertension, but most were cross-sectional and suffering from a high risk of bias. The most comprehensive evidence was available for road traffic noise and Ischeamic Heart Diseases (IHD). Combining the results of 7 longitudinal studies revealed a Relative Risk (RR) of 1.08 (95% CI: 1.01–1.15) per 10 dB (LDEN) for the association between road traffic noise and the incidence of IHD. We rated the quality of this evidence as high. Only a few studies reported on the association between transportation noise and stroke, diabetes, and/or obesity. The quality of evidence for these associations was rated from moderate to very low, depending on transportation noise source and outcome. For a comprehensive assessment of the impact of noise exposure on the cardiovascular and metabolic system, we need more and better quality evidence, primarily based on longitudinal studies.

Road traffic noise is a prevalent and known health hazard. However, little is known yet about its effect on children's cognition. We aimed to study the association between exposure to road traffic noise and the development of working memory and attention in primary school children, considering school-outdoor and school-indoor annual average noise levels and noise fluctuation characteristics, as well as home-outdoor noise exposure. We followed up a population-based sample of 2,680 children aged 7 to 10 years from 38 schools in Barcelona (Catalonia, Spain) between January 2012 to March 2013. Children underwent computerised cognitive tests 4 times (n = 10,112), for working memory (2-back task, detectability), complex working memory (3-back task, detectability), and inattentiveness (Attention Network Task, hit reaction time standard error, in milliseconds). Road traffic noise was measured indoors and outdoors at schools, at the start of the school year, using standard protocols to obtain A-weighted equivalent sound pressure levels, i.e., annual average levels scaled to human hearing, for the daytime (daytime LAeq, in dB). We also derived fluctuation indicators out of the measurements (noise intermittency ratio, %; and number of noise events) and obtained individual estimated indoor noise levels (LAeq) correcting for classroom orientation and classroom change between years. Home-outdoor noise exposure at home (Lden, i.e., EU indicator for the 24-hour annual average levels) was estimated using Barcelona's noise map for year 2012, according to the European Noise Directive (2002). We used linear mixed models to evaluate the association between exposure to noise and cognitive development adjusting for age, sex, maternal education, socioeconomical vulnerability index at home, indoor or outdoor traffic-related air pollution (TRAP) for corresponding school models or outdoor nitrogen dioxide (NO2) for home models. Child and school were included as nested random effects. The median age (percentile 25, percentile 75) of children in visit 1 was 8.5 (7.8; 9.3) years, 49.9% were girls, and 50% of the schools were public. School-outdoor exposure to road traffic noise was associated with a slower development in working memory (2-back and 3-back) and greater inattentiveness over 1 year in children, both for the average noise level (e.g., ‒4.83 points [95% CI: ‒7.21, ‒2.45], p-value < 0.001, in 2-back detectability per 5 dB in street levels) and noise fluctuation (e.g., ‒4.38 [‒7.08, ‒1.67], p-value = 0.002, per 50 noise events at street level). Individual exposure to the road traffic average noise level in classrooms was only associated with inattentiveness (2.49 ms [0, 4.81], p-value = 0.050, per 5 dB), whereas indoor noise fluctuation was consistently associated with all outcomes. Home-outdoor noise exposure was not associated with the outcomes. Study limitations include a potential lack of generalizability (58% of mothers with university degree in our study versus 50% in the region) and the lack of past noise exposure assessment. We observed that exposure to road traffic noise at school, but not at home, was associated with slower development of working memory, complex working memory, and attention in schoolchildren over 1 year. Associations with noise fluctuation indicators were more evident than with average noise levels in classrooms.

Air pollution is a suspected developmental neurotoxicant. Many schools are located in close proximity to busy roads, and traffic air pollution peaks when children are at school. We aimed to assess whether exposure of children in primary school to traffic-related air pollutants is associated with impaired cognitive development. We conducted a prospective study of children (n = 2,715, aged 7 to 10 y) from 39 schools in Barcelona (Catalonia, Spain) exposed to high and low traffic-related air pollution, paired by school socioeconomic index; children were tested four times (i.e., to assess the 12-mo developmental trajectories) via computerized tests (n = 10,112). Chronic traffic air pollution (elemental carbon [EC], nitrogen dioxide [NO2], and ultrafine particle number [UFP; 10-700 nm]) was measured twice during 1-wk campaigns both in the courtyard (outdoor) and inside the classroom (indoor) simultaneously in each school pair. Cognitive development was assessed with the n-back and the attentional network tests, in particular, working memory (two-back detectability), superior working memory (three-back detectability), and inattentiveness (hit reaction time standard error). Linear mixed effects models were adjusted for age, sex, maternal education, socioeconomic status, and air pollution exposure at home. Children from highly polluted schools had a smaller growth in cognitive development than children from the paired lowly polluted schools, both in crude and adjusted models (e.g., 7.4% [95% CI 5.6%-8.8%] versus 11.5% [95% CI 8.9%-12.5%] improvement in working memory, p = 0.0024). Cogently, children attending schools with higher levels of EC, NO2, and UFP both indoors and outdoors experienced substantially smaller growth in all the cognitive measurements; for example, a change from the first to the fourth quartile in indoor EC reduced the gain in working memory by 13.0% (95% CI 4.2%-23.1%). Residual confounding for social class could not be discarded completely; however, the associations remained in stratified analyses (e.g., for type of school or high-/low-polluted area) and after additional adjustments (e.g., for commuting, educational quality, or smoking at home), contradicting a potential residual confounding explanation. Children attending schools with higher traffic-related air pollution had a smaller improvement in cognitive development.

Introduction: Cities often experience high air pollution and noise levels and lack of natural outdoor environments, which may be detrimental to health. The aim of this study was to evaluate the effects of air pollution, noise, and blue and green space on premature all-cause mortality in Barcelona using a mega cohort approach. Methods: Both men and women of 18 years and above registered on 1 January 2010 by the Sistema d’Informació pel Desenvolupament de la Investigació en Atenció Primària (SIDIAP) and living in the city of Barcelona were included in the cohort and followed up until 31 December 2014 or until death (n = 2,939,067 person years). The exposure assessment was conducted at the census tract level (n = 1061). We assigned exposure to long term ambient levels of nitrogen dioxides (NO2), nitrogen oxides (NOx), particulate matter with aerodynamic diameter less than 2.5 µm (PM2.5), between 2.5 µm and 10 µm (PM2.5–10, i.e., coarse particulate matter), less than 10 µm (PM10) and PM2.5 light absorption (hereafter referred to as PM2.5 absorbance) based on land use regressions models. Normalized Difference Vegetation Index (NDVI) was assigned based on remote sensing data, percentage green space and blue space were calculated based on land use maps and modelled road traffic noise was available through the strategic noise map for Barcelona. Results: In this large prospective study (n = 792,649) in an urban area, we found a decreased risk of all-cause mortality with an increase in green space measured as NDVI (hazard ratio (HR) = 0.92, 95% CI 0.89–0.97 per 0.1) and increased risks of mortality with an increase in exposure to blue space (HR = 1.04, 95% CI 1.01–1.06 per 1%), NO2 (HR = 1.01, 95% CI 1.00–1.02 per 5 ug/m3) but no risk with noise (HR = 1.00, 95% CI 0.98–1.02 per 5 dB(A)). The increased risks appeared to be more pronounced in the more deprived areas. Results for NDVI, and to a lesser extent NO2, remained most consistent after mutual adjustment for other exposures. The NDVI estimate was a little attenuated when NO2 was included in the model. The study had some limitations including e.g., the assessment of air pollution, noise, green space and socioeconomic status (SES) on census tract level rather than individual level and residual confounding. Conclusion: This large study provides new insights on the relationship between green and blue space, noise and air pollution and premature all-cause mortality.

The available evidence of the effects of air pollution and noise on behavioral development is limited, and it overlooks exposure at schools, where children spend a considerable amount of time. We aimed to investigate the associations of exposure to traffic-related air pollutants (TRAPs) and noise at school on behavioral development of schoolchildren. We evaluated children 7-11 years of age in Barcelona (Catalonia, Spain) during 2012-2013 within the BREATHE project. Indoor and outdoor concentrations of elemental carbon (EC), black carbon (BC), and nitrogen dioxide (NO2) were measured at schools in two separate 1-week campaigns. In one campaign we also measured noise levels inside classrooms. Parents filled out the strengths and difficulties questionnaire (SDQ) to assess child behavioral development, while teachers completed the attention deficit/hyperactivity disorder criteria of the DSM-IV (ADHD-DSM-IV) list to assess specific ADHD symptomatology. Negative binomial mixed-effects models were used to estimate associations between the exposures and behavioral development scores. Interquartile range (IQR) increases in indoor and outdoor EC, BC, and NO2 concentrations were positively associated with SDQ total difficulties scores (suggesting more frequent behavioral problems) in adjusted multivariate models, whereas noise was significantly associated with ADHD-DSM-IV scores. In our study population of 7- to 11-year-old children residing in Barcelona, exposure to TRAPs at school was associated with increased behavioral problems in schoolchildren. Noise exposure at school was associated with more ADHD symptoms. Forns J, Dadvand P, Foraster M, Alvarez-Pedrerol M, Rivas I, López-Vicente M, Suades-Gonzalez E, Garcia-Esteban R, Esnaola M, Cirach M, Grellier J, Basagaña X, Querol X, Guxens M, Nieuwenhuijsen MJ, Sunyer J. 2016. Traffic-related air pollution, noise at school, and behavioral problems in Barcelona schoolchildren: a cross-sectional study. Environ Health Perspect 124:529-535; http://dx.doi.org/10.1289/ehp.1409449.

The association between long-term exposure to ambient air pollutants and severe COVID-19 is uncertain. We followed 4,660,502 adults from the general population in 2020 in Catalonia, Spain. Cox proportional models were fit to evaluate the association between annual averages of PM 2.5 , NO 2 , BC, and O 3 at each participant’s residential address and severe COVID-19. Higher exposure to PM 2.5, NO 2, and BC was associated with an increased risk of COVID-19 hospitalization, ICU admission, death, and hospital length of stay. An increase of 3.2 µg/m 3 of PM 2.5 was associated with a 19% (95% CI, 16–21) increase in hospitalizations. An increase of 16.1 µg/m 3 of NO 2 was associated with a 42% (95% CI, 30–55) increase in ICU admissions. An increase of 0.7 µg/m 3 of BC was associated with a 6% (95% CI, 0–13) increase in deaths. O 3 was positively associated with severe outcomes when adjusted by NO 2 . Our study contributes robust evidence that long-term exposure to air pollutants is associated with severe COVID-19. In this study, the authors investigate the relationship between exposure to air pollutants and severe COVID-19 disease using data from a cohort of ~5 million people in Catalonia, Spain. They find that long-term exposure to pollutants is associated with a higher risk of COVID-19-related hospitalization, death, intensive care admission, and length of hospital stay.

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. 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). 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. 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). 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.

Air pollutants (AP) play a role in subclinical inflammation, and are associated with cardiovascular morbidity and mortality. Metabolic syndrome (MetS) is inflammatory and precedes cardiovascular morbidity and type 2 diabetes. Thus, a positive association between AP and MetS may be hypothesized. We explored this association, (taking into account, pathway-specific MetS definitions), and its potential modifiers in Swiss adults. We studied 3769 participants of the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults, reporting at least four-hour fasting time before venepuncture. AP exposures were 10-year mean residential PM10 (particulate matter <10μm in diameter) and NO2 (nitrogen dioxide). Outcomes included MetS defined by World Health Organization (MetS-W), International Diabetes Federation (MetS-I) and Adult Treatment Panel-III (MetS-A) using four- and eight-hour fasting time limits. We also explored associations with individual components of MetS. We applied mixed logistic regression models to explore these associations. The prevalence of MetS-W, MetS-I and MetS-A were 10%, 22% and 18% respectively. Odds of MetS-W, MetS-I and MetS-A increased by 72% (51-102%), 31% (11-54%) and 18% (4-34%) per 10μg/m3 increase in 10-year mean PM10. We observed weaker associations with NO2. Associations were stronger among physically-active, ever-smokers and non-diabetic participants especially with PM10 (p<0.05). Associations remained robust across various sensitivity analyses including ten imputations of missing observations and exclusion of diabetes cases. The observed associations between AP exposure and MetS were sensitive to MetS definitions. Regarding the MetS components, we observed strongest associations with impaired fasting glycemia, and positive but weaker associations with hypertension and waist-circumference-based obesity. Cardio-metabolic effects of AP may be majorly driven by impairment of glucose homeostasis, and to a less-strong extent, visceral adiposity. Well-designed prospective studies are needed to confirm these findings.

Whether differences in lifestyle between co-twins are reflected in differences in their internal or external exposome profiles remains largely underexplored. We therefore investigated whether within-pair differences in lifestyle were associated with within-pair differences in exposome profiles across four domains: the external exposome, proteome, metabolome and epigenetic age acceleration (EAA). For each domain, we assessed the similarity of co-twin profiles using Gaussian similarities in up to 257 young adult same-sex twin pairs (54% monozygotic). We additionally tested whether similarity in one domain translated into greater similarity in another. Results suggest that a lower degree of similarity in co-twins' exposome profiles was associated with greater differences in their behavior and substance use. The strongest association was identified between excessive drinking behavior and the external exposome. Overall, our study demonstrates how social behavior and especially substance use are connected to the internal and external exposomes, while controlling for familial confounders.

Arterial stiffness, and its progression with age, is an important indicator of cardiovascular aging. Greenspace exposure may protect against arterial stiffness by promoting physical activity, fostering social cohesion, and reducing stress and exposure to air pollution and noise. The aim of this study was to investigate the association of long-term exposure to outdoor greenspace with arterial stiffness and its progression over time. This prospective cohort study was based on 4,349 participants (55-83 years of age) of the Whitehall II Study, United Kingdom. Arterial stiffness was assessed in two medical examinations (2007-2009 and 2012-2013) by measuring the carotid-femoral pulse wave velocity (cf-PWV). Residential surrounding greenspace was characterized using satellite-based indices of greenspace including normalized difference vegetation index (NDVI), enhanced vegetation index (EVI), and vegetation continuous fields (VCF) across buffers of 500 and surrounding the participants' residential locations at each follow-up. The association between the greenspace indicators and baseline cf-PWV and 4-year progression of cf-PWV was assessed using linear mixed-effects models with the participant as a random effect, controlling for demographic, lifestyle, and (individual and area) socioeconomic factors. No statistically significant associations were observed between residential surrounding greenspace and baseline or 4-y progression of cf-PWV; interquartile range (IQR) increases in NDVI, EVI, and VCF in the buffer were associated with [95% confidence interval (CI): , 0.04], (95% CI: , 0.05), and (95% CI: , 0.04) in baseline cf-PWV and (95% CI: , 0.14), (95% CI: , 0.14), and (95% CI: , 0.09) in 4-y progression in cf-PWV, respectively. The associations were similar when using buffers. We did not observe any consistent association between residential surrounding greenspace and arterial stiffness. https://doi.org/10.1289/EHP6159.