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Background: Road-traffic noise may influence the development of cardiovascular events such as stroke and myocardial infarction, but etiological mechanisms remain unclear. This study aimed to assess the relationship between long-term road-traffic noise exposure and coronary atherosclerosis in Sweden. Methods: In the Swedish CArdioPulmonary bioImage Study (SCAPIS) cohort, including 30,154 subjects aged 50-65 years, recruited between 2013 and 2018, coronary atherosclerosis was measured based on computer tomography (CT) scans as coronary artery calcium score, segment involvement score (SIS), and non-calcified plaques (NCP) at enrollment. Based on modified Nordic model, road-traffic noise exposure was modeled for 2000, 2013, and 2018 with interpolation for intermediate years. We investigated the association between time-weighted long-term exposure to road-traffic noise (Lden) and the prevalence of atherosclerosis using ordinal logistic regression models adjusting for potential socioeconomic, behavioral, and environmental confounders, including air pollution. Results: No clear associations were found between road-traffic noise and coronary atherosclerosis. The odds ratio for coronary artery calcium score was 1.00 (95% confidence interval [CI] = 0.96, 1.04), SIS 0.99 (0.96, 1.03), and NCP 0.98 (0.90, 1.03) per interquartile range (9.4 dB Lden) for road-traffic noise exposure during 10 years before enrollment. No consistent associations were observed in site-specific analyses or using shorter exposure periods. Furthermore, exposure-response analyses revealed no clear trends, and there were no strong interactions between road-traffic noise and cardiovascular risk factors in relation to the atherosclerosis markers. Conclusions: Long-term exposure to road-traffic noise was not linked to coronary atherosclerosis or calcification in relatively healthy, middle-aged populations in Sweden.
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Background: Transportation noise has been linked with cardiometabolic outcomes, yet whether it is a risk factor for atrial fibrillation (AF) remains inconclusive. We aimed to assess whether transportation noise was associated with AF in a large, pooled Nordic cohort. Methods: We pooled data from 11 Nordic cohorts, totaling 161,115 participants. Based on address history from five years before baseline until end of follow-up, road, railway, and aircraft noise was estimated at a residential level. Incident AF was ascertained via linkage to nationwide patient registries. Cox proportional hazards models were utilized to estimate associations between running 5-year time-weighted mean transportation noise (Lden) and AF after adjusting for sociodemographics, lifestyle, and air pollution. Findings: We identified 18,939 incident AF cases over a median follow-up of 19.6 years. Road traffic noise was associated with AF, with a hazard ratio (HR) and 95% confidence interval (CI) of 1.02 (1.00-1.04) per 10-dB of 5-year mean time-weighted exposure, which changed to 1.03 (1.01-1.06) when implementing a 53-dB cut-off. In effect modification analyses, the association for road traffic noise and AF appeared strongest in women and overweight and obese participants. Compared to exposures ≤40 dB, aircraft noise of 40.1-50 and > 50 dB were associated with HRs of 1.04 (0.93-1.16) and 1.12 (0.98-1.27), respectively. Railway noise was not associated with AF. We found a HR of 1.19 (1.02-1.40) among people exposed to noise from road (≥45 dB), railway (>40 dB), and aircraft (>40 dB) combined. Interpretation: Road traffic noise, and possibly aircraft noise, may be associated with elevated risk of AF. Funding: NordForsk.
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Growing evidence suggests that extreme heat events affect both pregnant women and their infants, but few studies are available from sub-Saharan Africa. Using data from 138,015 singleton births in 16 hospitals in Benin, Malawi, Tanzania and Uganda, we investigated the association between extreme heat and early perinatal deaths, including antepartum and intrapartum stillbirths, and deaths within 24 h after birth using a time-stratified case-crossover design. We observed an association between an increase from the 75th to the 99th percentile in mean temperature 1 week (lag 0-6 d) before childbirth and perinatal mortality (odds ratio (OR) = 1.34 (95% confidence interval (CI) 1.01-1.78)). The estimates for stillbirths were similarly positive, but CIs included unity: OR = 1.29 (95% CI 0.95-1.77) for all stillbirths, OR = 1.18 (95% CI 0.71-1.95) for antepartum stillbirths and OR = 1.64 (95% CI 0.74-3.63) for intrapartum stillbirths. The cumulative exposure-response curve suggested that the steepest slopes for heat for intrapartum stillbirths and associations were stronger during the hottest seasons. We conclude that short-term heat exposure may increase mortality risks, particularly for intrapartum stillbirths, raising the importance of improved intrapartum care.
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Socioeconomic inequalities in the exposome have been found to be complex and highly context-specific, but studies have not been conducted in large population-wide cohorts from multiple countries. This study aims to examine the external exposome, encompassing individual and environmental factors influencing health over the life course, and to perform dimension reduction to derive interpretable characterization of the external exposome for multicountry epidemiological studies. Analyzing data from over 25 million individuals across seven European countries including 12 administrative and traditional cohorts, we utilized domain-specific principal component analysis (PCA) to define the external exposome, focusing on air pollution, the built environment, and air temperature. We conducted linear regression to estimate the association between individual- and area-level socioeconomic position and each domain of the external exposome. Consistent exposure patterns were observed within countries, indicating the representativeness of traditional cohorts for air pollution and the built environment. However, cohorts with limited geographical coverage and Southern European countries displayed lower temperature variability, especially in the cold season, compared to Northern European countries and cohorts including a wide range of urban and rural areas. The individual- and area-level socioeconomic determinants (i.e., education, income, and unemployment rate) of the urban exposome exhibited significant variability across the European region, with area-level indicators showing stronger associations than individual variables. While the PCA approach facilitated common interpretations of the external exposome for air pollution and the built environment, it was less effective for air temperature. The diverse socioeconomic determinants suggest regional variations in environmental health inequities, emphasizing the need for targeted interventions across European countries.
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Exposoma , Factores Socioeconómicos , Europa (Continente) , Humanos , Contaminación del Aire , Exposición a Riesgos Ambientales , Estudios de CohortesRESUMEN
BACKGROUND: Lower air temperature and cold spells have been associated with an increased risk of various diseases. However, the short-term effect of lower air temperature and cold spells on myocardial infarction (MI) remains incompletely understood. OBJECTIVES: The purpose of this study was to investigate the short-term effects of lower air temperature and cold spells on the risk of hospitalization for MI in Sweden. METHODS: This population-based nationwide study included 120,380 MI cases admitted to hospitals in Sweden during the cold season (October to March) from 2005 to 2019. Daily mean air temperature (1 km2 resolution) was estimated using machine learning, and percentiles of daily temperatures experienced by individuals in the same municipality were used as individual exposure indicators to account for potential geographic adaptation. Cold spells were defined as periods of at least 2 consecutive days with a daily mean temperature below the 10th percentile of the temperature distribution for each municipality. A time-stratified case-crossover design incorporating conditional logistic regression models with distributed lag nonlinear models using lag 0 to 1 (immediate) and 2 to 6 days (delayed) was used to evaluate the short-term effects of lower air temperature and cold spells on total MI, non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). RESULTS: A decrease of 1-U in percentile temperature at a lag of 2 to 6 days was significantly associated with increased risks of total MI, NSTEMI, and STEMI, with ORs of 1.099 (95% CI: 1.057-1.142), 1.110 (95% CI: 1.060-1.164), and 1.076 (95% CI: 1.004-1.153), respectively. Additionally, cold spells at a lag of 2 to 6 days were significantly associated with increased risks for total MI, NSTEMI, and STEMI, with ORs of 1.077 (95% CI: 1.037-1.120), 1.069 (95% CI: 1.020-1.119), and 1.095 (95% CI: 1.023-1.172), respectively. Conversely, lower air temperature and cold spells at a lag of 0 to 1 days were associated with decreased risks for MI. CONCLUSIONS: This nationwide case-crossover study reveals that short-term exposures to lower air temperature and cold spells are associated with an increased risk of hospitalization for MI at lag 2 to 6 days.
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Frío , Hospitalización , Infarto del Miocardio , Humanos , Suecia/epidemiología , Masculino , Femenino , Frío/efectos adversos , Anciano , Infarto del Miocardio/epidemiología , Hospitalización/estadística & datos numéricos , Persona de Mediana Edad , Anciano de 80 o más Años , Factores de TiempoRESUMEN
BACKGROUND: Air pollution exposure has been linked with increased risk of preterm birth, which is one of the leading causes of infant mortality. Limited studies have attempted to explore these associations in low-polluted areas. In this study, we aimed to assess the association between short-term exposure to ambient air pollution and preterm birth in Sweden. METHOD: In this population-based study we included preterm births between 2014 and 2019 from the Swedish Pregnancy Register. We applied a spatiotemporal model to estimate daily levels of particulate matter <2.5 µm (PM2.5), PM < 10 µm (PM10), nitrogen dioxide (NO2), and ozone (O3) at the residential address of each participant. We applied a time-stratified case-crossover design with conditional logistic regression analysis to estimate odds ratios (OR) of preterm birth per 10 µg/m3 (PM10, NO2, O3) and 5 µg/m3 (PM2.5) increase in air pollution exposure at 0-6-day lag. Two-pollutant models were applied to evaluate the independent association of each exposure on preterm birth. We also stratified by maternal characteristics to identify potential effect modifiers. RESULTS: 28,216 (4.5%) preterm births were included. An increase in O3 exposure was associated with increased odds of preterm birth [OR = 1.06 per 10 µg/m3 (95% CI, 1.02; 1.10]. PM2.5 and PM10 were not significantly associated with preterm birth, and NO2 displayed a negative nonlinear association with preterm birth. We did not observe any notable effect modification, but we found suggestive larger associations between O3 and preterm birth when stratifying by male sex, spontaneous delivery, and spring season. CONCLUSIONS: Increased O3 exposure one week before delivery was associated with an increased risk of preterm birth in Sweden, a country with levels of air pollution below the current World Health Organization air quality guidelines. Increases in O3 levels with climate change make these findings especially concerning.
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Contaminantes Atmosféricos , Contaminación del Aire , Dióxido de Nitrógeno , Ozono , Material Particulado , Nacimiento Prematuro , Humanos , Suecia/epidemiología , Nacimiento Prematuro/epidemiología , Femenino , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Embarazo , Material Particulado/análisis , Material Particulado/efectos adversos , Adulto , Ozono/análisis , Ozono/efectos adversos , Dióxido de Nitrógeno/análisis , Dióxido de Nitrógeno/efectos adversos , Recién Nacido , Adulto Joven , Masculino , Exposición Materna/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisisRESUMEN
BACKGROUND: Despite accumulating evidence of an association between air pollution and renal disease, studies on the association between long-term exposure to air pollution and renal function are still contradictory. This study aimed to investigate this association in a large population with relatively low exposure and with improved estimation of renal function as well as renal injury biomarkers. METHODS: We performed a cross-sectional analysis in the middle-aged general population participating in the Swedish CardioPulmonary bioImaging Study (SCAPIS; n = 30 154). Individual 10-year exposure to total and locally emitted fine particulate matter (PM2.5), inhalable particulate matter (PM10), and nitrogen oxides (NOx) were modelled using high-resolution dispersion models. Linear regression models were used to estimate associations between exposures and estimated glomerular filtration rate (eGFR, combined creatinine and cystatin C) and serum levels of renal injury biomarkers (KIM-1, MCP-1, IL-6, IL-18, MMP-2, MMP-7, MMP-9, FGF-23, and uric acid), with consideration of potential confounders. RESULTS: Median long-term PM2.5 exposure was 6.2 µg/m3. Almost all participants had a normal renal function and median eGFR was 99.2 mL/min/1.73 m2. PM2.5 exposure was associated with 1.3% (95% CI 0.6, 2.0) higher eGFR per 2.03 µg/m3 (interquartile range, IQR). PM2.5 exposure was also associated with elevated serum matrix metalloproteinase 2 (MMP-2) concentration, with 7.2% (95% CI 1.9, 12.8) higher MMP-2 per 2.03 µg/m3. There was a tendency towards an association between PM10 and higher levels of uric acid, but no associations were found with the other biomarkers. Associations with other air pollutants were null or inconsistent. CONCLUSION: In this large general population sample at low exposure levels, we found a surprising association between PM2.5 exposure and a higher renal filtration. It seems unlikely that particle function would improve renal function. However, increased filtration is an early sign of renal injury and may be related to the relatively healthy population at comparatively low exposure levels. Furthermore, PM2.5 exposure was associated with higher serum concentrations of MMP-2, an early indicator of renal and cardiovascular pathology.
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Contaminantes Atmosféricos , Biomarcadores , Exposición a Riesgos Ambientales , Tasa de Filtración Glomerular , Enfermedades Renales , Material Particulado , Humanos , Biomarcadores/sangre , Persona de Mediana Edad , Masculino , Femenino , Material Particulado/efectos adversos , Material Particulado/análisis , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Suecia/epidemiología , Estudios Transversales , Exposición a Riesgos Ambientales/efectos adversos , Enfermedades Renales/inducido químicamente , Enfermedades Renales/epidemiología , Enfermedades Renales/sangre , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Anciano , Factor-23 de Crecimiento de Fibroblastos , Riñón/fisiopatología , Riñón/efectos de los fármacos , Óxidos de Nitrógeno/sangre , Óxidos de Nitrógeno/análisis , Óxidos de Nitrógeno/efectos adversos , AdultoRESUMEN
Background: Available evidence suggests a link between exposure to transportation noise and an increased risk of obesity. We aimed to assess exposure-response functions for long-term residential exposure to road traffic, railway and aircraft noise, and markers of obesity. Methods: Our cross-sectional study is based on pooled data from 11 Nordic cohorts, including up to 162,639 individuals with either measured (69.2%) or self-reported obesity data. Residential exposure to transportation noise was estimated as a time-weighted average Lden 5 years before recruitment. Adjusted linear and logistic regression models were fitted to assess beta coefficients and odds ratios (OR) with 95% confidence intervals (CI) for body mass index, overweight, and obesity, as well as for waist circumference and central obesity. Furthermore, natural splines were fitted to assess the shape of the exposure-response functions. Results: For road traffic noise, the OR for obesity was 1.06 (95% CI = 1.03, 1.08) and for central obesity 1.03 (95% CI = 1.01, 1.05) per 10 dB Lden. Thresholds were observed at around 50-55 and 55-60 dB Lden, respectively, above which there was an approximate 10% risk increase per 10 dB Lden increment for both outcomes. However, linear associations only occurred in participants with measured obesity markers and were strongly influenced by the largest cohort. Similar risk estimates as for road traffic noise were found for railway noise, with no clear thresholds. For aircraft noise, results were uncertain due to the low number of exposed participants. Conclusion: Our results support an association between road traffic and railway noise and obesity.
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BACKGROUND: The evidence for acute effects of air pollution on mortality in India is scarce, despite the extreme concentrations of air pollution observed. This is the first multi-city study in India that examines the association between short-term exposure to PM2·5 and daily mortality using causal methods that highlight the importance of locally generated air pollution. METHODS: We applied a time-series analysis to ten cities in India between 2008 and 2019. We assessed city-wide daily PM2·5 concentrations using a novel hybrid nationwide spatiotemporal model and estimated city-specific effects of PM2·5 using a generalised additive Poisson regression model. City-specific results were then meta-analysed. We applied an instrumental variable causal approach (including planetary boundary layer height, wind speed, and atmospheric pressure) to evaluate the causal effect of locally generated air pollution on mortality. We obtained an integrated exposure-response curve through a multivariate meta-regression of the city-specific exposure-response curve and calculated the fraction of deaths attributable to air pollution concentrations exceeding the current WHO 24 h ambient PM2·5 guideline of 15 µg/m3. To explore the shape of the exposure-response curve at lower exposures, we further limited the analyses to days with concentrations lower than the current Indian standard (60 µg/m3). FINDINGS: We observed that a 10 µg/m3 increase in 2-day moving average of PM2·5 was associated with 1·4% (95% CI 0·7-2·2) higher daily mortality. In our causal instrumental variable analyses representing the effect of locally generated air pollution, we observed a stronger association with daily mortality (3·6% [2·1-5·0]) than our overall estimate. Our integrated exposure-response curve suggested steeper slopes at lower levels of exposure and an attenuation of the slope at high exposure levels. We observed two times higher risk of death per 10 µg/m3 increase when restricting our analyses to observations below the Indian air quality standard (2·7% [1·7-3·6]). Using the integrated exposure-response curve, we observed that 7·2% (4·2%-10·1%) of all daily deaths were attributed to PM2·5 concentrations higher than the WHO guidelines. INTERPRETATION: Short-term PM2·5 exposure was associated with a high risk of death in India, even at concentrations well below the current Indian PM2·5 standard. These associations were stronger for locally generated air pollutants quantified through causal modelling methods than conventional time-series analysis, further supporting a plausible causal link. FUNDING: Swedish Research Council for Sustainable Development.
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Contaminantes Atmosféricos , Contaminación del Aire , Ciudades , Exposición a Riesgos Ambientales , Mortalidad , Material Particulado , India/epidemiología , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Humanos , Material Particulado/efectos adversos , Material Particulado/análisis , Contaminantes Atmosféricos/efectos adversos , Contaminantes Atmosféricos/análisis , Exposición a Riesgos Ambientales/efectos adversos , Modelos TeóricosRESUMEN
Rationale: The benefits of improved air quality on asthma remain understudied. Objectives: Our aim was to investigate associations of changes in ambient air pollution with incident asthma from school age until young adulthood in an area with mostly low air pollution levels. Methods: Participants in the BAMSE (Swedish abbreviation for Children, Allergy, Environment, Stockholm, Epidemiology) birth cohort from Stockholm without asthma before the 8-year follow-up were included (N = 2,371). We estimated the association of change in individual-level air pollutant exposure (particulate matter with an aerodynamic diameter ≤ 2.5 µm [PM2.5] and ≤ 10 µm [PM10], black carbon [BC], and nitrogen oxides [NOx]) from the first year of life to the 8-year follow-up with asthma incidence from the 8-year until the 24-year follow-up. Multipollutant trajectories were identified using the group-based multivariate trajectory model. We also used parametric G-computation to quantify the asthma incidence under different hypothetical interventions regarding air pollution levels. Results: Air pollution levels at residency decreased during the period, with median reductions of 5.6% for PM2.5, 3.1% for PM10, 5.9% for BC, and 26.8% for NOx. A total of 395 incident asthma cases were identified from the 8-year until the 24-year follow-up. The odds ratio for asthma was 0.89 (95% confidence interval [CI], 0.80-0.99) for each interquartile range reduction in PM2.5 (equal to 8.1% reduction). Associations appeared less clear for PM10, BC, and NOx. Five multipollutant trajectories were identified; the largest reduction trajectory displayed the lowest odds of asthma (odds ratio, 0.55; 95% CI, 0.31-0.98) compared with the lowest reduction trajectory. If the PM2.5 exposure had not declined up to the 8-year follow-up, the hypothetical asthma incidence was estimated to have been 10.9% higher (95% CI, 0.8-20.8%). Conclusions: A decrease in PM2.5 levels during childhood was associated with a lower risk of incident asthma from school age to young adulthood in an area with relatively low air pollution levels, suggesting broad respiratory health benefits from improved air quality.
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Contaminantes Atmosféricos , Contaminación del Aire , Asma , Exposición a Riesgos Ambientales , Material Particulado , Humanos , Asma/epidemiología , Masculino , Incidencia , Femenino , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Estudios Prospectivos , Niño , Suecia/epidemiología , Adolescente , Adulto Joven , Material Particulado/análisis , Material Particulado/efectos adversos , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Preescolar , Adulto , Estudios de Seguimiento , Análisis MultivarianteRESUMEN
Background: Many studies reported associations between long-term exposure to environmental factors and mortality; however, little is known on the combined effects of these factors and health. We aimed to evaluate the association between external exposome and all-cause mortality in large administrative and traditional adult cohorts in Europe. Methods: Data from six administrative cohorts (Catalonia, Greece, Rome, Sweden, Switzerland and the Netherlands, totaling 27,913,545 subjects) and three traditional adult cohorts (CEANS-Sweden, EPIC-NL-the Netherlands, KORA-Germany, totaling 57,653 participants) were included. Multiple exposures were assigned at the residential addresses, and were divided into three a priori defined domains: (1) air pollution [fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and warm-season Ozone (warm-O3)]; (2) land/built environment (Normalized Difference Vegetation Index-NDVI, impervious surfaces, and distance to water); (3) air temperature (cold- and warm-season mean and standard deviation). Each domain was synthesized through Principal Component Analysis (PCA), with the aim of explaining at least 80% of its variability. Cox proportional-hazards regression models were applied and the total risk of the external exposome was estimated through the Cumulative Risk Index (CRI). The estimates were adjusted for individual- and area-level covariates. Results: More than 205 million person-years at risk and more than 3.2 million deaths were analyzed. In single-component models, IQR increases of the first principal component of the air pollution domain were associated with higher mortality [HRs ranging from 1.011 (95% CI: 1.005-1.018) for the Rome cohort to 1.076 (1.071-1.081) for the Swedish cohort]. In contrast, lower levels of the first principal component of the land/built environment domain, pointing to reduced vegetation and higher percentage of impervious surfaces, were associated with higher risks. Finally, the CRI of external exposome increased mortality for almost all cohorts. The associations found in the traditional adult cohorts were generally consistent with the results from the administrative ones, albeit without reaching statistical significance. Discussion: Various components of the external exposome, analyzed individually or in combination, were associated with increased mortality across European cohorts. This sets the stage for future research on the connections between various exposure patterns and human health, aiding in the planning of healthier cities.
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BACKGROUND AND AIMS: Despite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis. METHODS: We performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 µm (PM2.5), <10 µm (PM10), and nitrogen oxides (NOx) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders. RESULTS: Median 10-year average PM2.5 exposure was 6.2 µg/m3 (range 3.5-13.4 µg/m3). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 µg/m3). Associations with significant stenoses were inconsistent. CONCLUSIONS: In this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease.
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Contaminación del Aire , Enfermedad de la Arteria Coronaria , Material Particulado , Humanos , Femenino , Masculino , Suecia/epidemiología , Enfermedad de la Arteria Coronaria/epidemiología , Enfermedad de la Arteria Coronaria/etiología , Enfermedad de la Arteria Coronaria/diagnóstico por imagen , Material Particulado/efectos adversos , Persona de Mediana Edad , Estudios Transversales , Anciano , Factores de Tiempo , Contaminación del Aire/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Exposición a Riesgos Ambientales/efectos adversos , Factores de Riesgo , Calcificación Vascular/epidemiología , Calcificación Vascular/diagnóstico por imagen , Óxidos de Nitrógeno/efectos adversos , Óxidos de Nitrógeno/análisis , Placa Aterosclerótica/epidemiología , Estenosis Coronaria/epidemiología , Estenosis Coronaria/diagnóstico por imagen , Medición de Riesgo , Adulto , PrevalenciaRESUMEN
Despite the known link between air pollution and cause-specific mortality, its relation to chronic kidney disease (CKD)-associated mortality is understudied. Therefore, we investigated the association between long-term exposure to air pollution and CKD-related mortality in a large multicentre population-based European cohort. Cohort data were linked to local mortality registry data. CKD-death was defined as ICD10 codes N18-N19 or corresponding ICD9 codes. Mean annual exposure at participant's home address was determined with fine spatial resolution exposure models for nitrogen dioxide (NO2), black carbon (BC), ozone (O3), particulate matter ≤2.5 µm (PM2.5) and several elemental constituents of PM2.5. Cox regression models were adjusted for age, sex, cohort, calendar year of recruitment, smoking status, marital status, employment status and neighbourhood mean income. Over a mean follow-up time of 20.4 years, 313 of 289,564 persons died from CKD. Associations were positive for PM2.5 (hazard ratio (HR) with 95% confidence interval (CI) of 1.31 (1.03-1.66) per 5 µg/m3, BC (1.26 (1.03-1.53) per 0.5 × 10- 5/m), NO2 (1.13 (0.93-1.38) per 10 µg/m3) and inverse for O3 (0.71 (0.54-0.93) per 10 µg/m3). Results were robust to further covariate adjustment. Exclusion of the largest sub-cohort contributing 226 cases, led to null associations. Among the elemental constituents, Cu, Fe, K, Ni, S and Zn, representing different sources including traffic, biomass and oil burning and secondary pollutants, were associated with CKD-related mortality. In conclusion, our results suggest an association between air pollution from different sources and CKD-related mortality.
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Contaminantes Atmosféricos , Contaminación del Aire , Exposición a Riesgos Ambientales , Insuficiencia Renal Crónica , Humanos , Insuficiencia Renal Crónica/mortalidad , Insuficiencia Renal Crónica/epidemiología , Insuficiencia Renal Crónica/inducido químicamente , Masculino , Femenino , Europa (Continente)/epidemiología , Persona de Mediana Edad , Anciano , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Contaminantes Atmosféricos/análisis , Contaminantes Atmosféricos/efectos adversos , Estudios de Cohortes , Exposición a Riesgos Ambientales/efectos adversos , Material Particulado/análisis , Material Particulado/efectos adversos , AdultoRESUMEN
High-resolution assessment of historical levels is essential for assessing the health effects of ambient air pollution in the large Indian population. The diversity of geography, weather patterns, and progressive urbanization, combined with a sparse ground monitoring network makes it challenging to accurately capture the spatiotemporal patterns of ambient fine particulate matter (PM2.5) pollution in India. We developed a model for daily average ambient PM2.5 between 2008 and 2020 based on monitoring data, meteorology, land use, satellite observations, and emissions inventories. Daily average predictions at each 1â km × 1â km grid from each learner were ensembled using a Gaussian process regression with anisotropic smoothing over spatial coordinates, and regression calibration was used to account for exposure error. Cross-validating by leaving monitors out, the ensemble model had an R2 of 0.86 at the daily level in the validation data and outperformed each component learner (by 5-18%). Annual average levels in different zones ranged between 39.7â µg/m3 (interquartile range: 29.8-46.8) in 2008 and 30.4â µg/m3 (interquartile range: 22.7-37.2) in 2020, with a cross-validated (CV)-R2 of 0.94 at the annual level. Overall mean absolute daily errors (MAE) across the 13 years were between 14.4 and 25.4â µg/m3. We obtained high spatial accuracy with spatial R2 greater than 90% and spatial MAE ranging between 7.3-16.5â µg/m3 with relatively better performance in urban areas at low and moderate elevation. We have developed an important validated resource for studying PM2.5 at a very fine spatiotemporal resolution, which allows us to study the health effects of PM2.5 across India and to identify areas with exceedingly high levels.
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BACKGROUND: Heatwaves are expected to increase with climate change, posing a significant threat to population health. In India, with the world's largest population, heatwaves occur annually but have not been comprehensively studied. Accordingly, we evaluated the association between heatwaves and all-cause mortality and quantifying the attributable mortality fraction in India. METHODS: We obtained all-cause mortality counts for ten cities in India (2008-2019) and estimated daily mean temperatures from satellite data. Our main extreme heatwave was defined as two-consecutive days with an intensity above the 97th annual percentile. We estimated city-specific heatwave associations through generalised additive Poisson regression models, and meta-analysed the associations. We reported effects as the percentage change in daily mortality, with 95% confidence intervals (CI), comparing heatwave vs non-heatwave days. We further evaluated heatwaves using different percentiles (95th, 97th, 99th) for one, two, three and five-consecutive days. We also evaluated the influence of heatwave duration, intensity and timing in the summer season on heatwave mortality, and estimated the number of heatwave-related deaths. FINDINGS: Among â¼ 3.6 million deaths, we observed that temperatures above 97th percentile for 2-consecutive days was associated with a 14.7 % (95 %CI, 10.3; 19.3) increase in daily mortality. Alternative heatwave definitions with higher percentiles and longer duration resulted in stronger relative risks. Furthermore, we observed stronger associations between heatwaves and mortality with higher heatwave intensity. We estimated that around 1116 deaths annually (95 %CI, 861; 1361) were attributed to heatwaves. Shorter and less intense definitions of heatwaves resulted in a higher estimated burden of heatwave-related deaths. CONCLUSIONS: We found strong evidence of heatwave impacts on daily mortality. Longer and more intense heatwaves were linked to an increased mortality risk, however, resulted in a lower burden of heatwave-related deaths. Both definitions and the burden associated with each heatwave definition should be incorporated into planning and decision-making processes for policymakers.
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Calor , Mortalidad , Ciudades , Riesgo , Temperatura , India/epidemiologíaRESUMEN
Leukemia and lymphoma are the two most common forms of hematologic malignancy, and their etiology is largely unknown. Pathophysiological mechanisms suggest a possible association with air pollution, but little empirical evidence is available. We aimed to investigate the association between long-term residential exposure to outdoor air pollution and risk of leukemia and lymphoma. We pooled data from four cohorts from three European countries as part of the "Effects of Low-level Air Pollution: a Study in Europe" (ELAPSE) collaboration. We used Europe-wide land use regression models to assess annual mean concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone (O3) at residences. We also estimated concentrations of PM2.5 elemental components: copper (Cu), iron (Fe), zinc (Zn); sulfur (S); nickel (Ni), vanadium (V), silicon (Si) and potassium (K). We applied Cox proportional hazards models to investigate the associations. Among the study population of 247,436 individuals, 760 leukemia and 1122 lymphoma cases were diagnosed during 4,656,140 person-years of follow-up. The results showed a leukemia hazard ratio (HR) of 1.13 (95% confidence intervals [CI]: 1.01-1.26) per 10 µg/m3 NO2, which was robust in two-pollutant models and consistent across the four cohorts and according to smoking status. Sex-specific analyses suggested that this association was confined to the male population. Further, the results showed increased lymphoma HRs for PM2.5 (HR = 1.16; 95% CI: 1.02-1.34) and potassium content of PM2.5, which were consistent in two-pollutant models and according to sex. Our results suggest that air pollution at the residence may be associated with adult leukemia and lymphoma.
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Contaminantes Atmosféricos , Contaminación del Aire , Contaminantes Ambientales , Leucemia , Linfoma , Adulto , Femenino , Humanos , Masculino , Dióxido de Nitrógeno/análisis , Exposición a Riesgos Ambientales/efectos adversos , Exposición a Riesgos Ambientales/análisis , Contaminación del Aire/efectos adversos , Contaminación del Aire/análisis , Material Particulado/análisis , Contaminantes Ambientales/análisis , Leucemia/inducido químicamente , Leucemia/epidemiología , Linfoma/inducido químicamente , Linfoma/epidemiología , Potasio/análisis , Contaminantes Atmosféricos/análisisRESUMEN
Background Air pollution is one of the main risk factors for cardiovascular disease globally, but its association with out-of-hospital cardiac arrest at low air pollution levels is unclear. This nationwide study in Sweden aims to investigate if air pollution is associated with a higher risk of out-of-hospital cardiac arrest in an area with relatively low air pollution levels. Methods and Results This study was a nationwide time-stratified case-crossover study investigating the association between short-term air pollution exposures and out-of-hospital cardiac arrest using data from the SRCR (Swedish Registry for Cardiopulmonary Resuscitation) between 2009 and 2019. Daily air pollution levels were estimated in 1×1-km grids for all of Sweden using a satellite-based machine learning model. The association between daily air pollutant levels and out-of-hospital cardiac arrest was quantified using conditional logistic regression adjusted for daily air temperature. Particulate matter <2.5 µm exposure was associated with a higher risk of out-of-hospital cardiac arrest among a total of 29 604 cases. In a multipollutant model, the association was most pronounced for intermediate daily lags, with an increased relative risk of 6.2% (95% CI, 1.0-11.8) per 10 µg/m3 increase of particulate matter <2.5 µm 4 days before the event. A similar pattern of association was observed for particulate matter <10 µm. No clear association was observed for O3 and NO2. Conclusions Short-term exposure to air pollution was associated with higher risk of out-of-hospital cardiac arrest. The findings add to the evidence of an adverse effect of particulate matter on out-of-hospital cardiac arrest, even at very low levels below current regulatory standards.
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Contaminantes Atmosféricos , Contaminación del Aire , Paro Cardíaco Extrahospitalario , Humanos , Estudios Cruzados , Suecia , Contaminación del Aire/efectos adversos , Contaminantes Atmosféricos/efectos adversos , Material Particulado/efectos adversos , Factores de Riesgo , Exposición a Riesgos Ambientales/efectos adversosRESUMEN
INTRODUCTION: The complex interplay of multiple environmental factors and cardiovascular has scarcely been studied. Within the EXPANSE project, we evaluated the association between long-term exposure to multiple environmental indices and stroke incidence across Europe. METHODS: Participants from three traditional adult cohorts (Germany, Netherlands and Sweden) and four administrative cohorts (Catalonia [region Spain], Rome [city-wide], Greece and Sweden [nationwide]) were followed until incident stroke, death, migration, loss of follow-up or study end. We estimated exposures at residential addresses from different exposure domains: air pollution (nitrogen dioxide (NO2), particulate matter < 2.5 µm (PM2.5), black carbon (BC), ozone), built environment (green/blue spaces, impervious surfaces) and meteorology (seasonal mean and standard deviation of temperatures). Associations between environmental exposures and stroke were estimated in single and multiple-exposure Cox proportional hazard models, and Principal Component (PC) Analyses derived prototypes for specific exposures domains. We carried out random effects meta-analyses by cohort type. RESULTS: In over 15 million participants, increased levels of NO2 and BC were associated with increased higher stroke incidence in both cohort types. Increased Normalized Difference Vegetation Index (NDVI) was associated with a lower stroke incidence in both cohort types, whereas an increase in impervious surface was associated with an increase in stroke incidence. The first PC of the air pollution domain (PM2.5, NO2 and BC) was associated with an increase in stroke incidence. For the built environment, higher levels of NDVI and lower levels of impervious surfaces were associated with a protective effect [%change in HR per 1 unit = -2.0 (95 %CI, -5.9;2.0) and -1.1(95 %CI, -2.0; -0.3) for traditional adult and administrative cohorts, respectively]. No clear patterns were observed for distance to blue spaces or temperature parameters. CONCLUSIONS: We observed increased HRs for stroke with exposure to PM2.5, NO2 and BC, lower levels of greenness and higher impervious surface in single and combined exposure models.
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Contaminación del Aire , Accidente Cerebrovascular , Adulto , Humanos , Contaminación del Aire/efectos adversos , Entorno Construido , Europa (Continente)/epidemiología , Incidencia , Dióxido de Nitrógeno/efectos adversos , Accidente Cerebrovascular/epidemiología , TemperaturaRESUMEN
Although emerging research has investigated the relationship between outdoor air pollution and depression risk in older adults, the results remain inconclusive. We aimed to determine the relationship between long-term exposure to ambient air pollution and depression among older adults and explore whether active social engagement may modify this association. At baseline (2001-2004), 2812 depression-free older adults from Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) were included. SNAC-K is a longitudinal population-based cohort in Stockholm, Sweden. Incident depression cases occurred during 2004-2013 were ascertained using the Diagnostic and Statistical Manual of Mental Disorders 4th Edition. Air pollution [particulate matter (PM) and nitrogen oxides (NOx)] at the residency were estimated using dispersion models. Social engagement was measured as active participation in social activities (at least twice/week) or inactive (less than twice/week) in the last 12 months. The hazard ratios (HR) and 95% confidence intervals of depression from air pollution exposure of 3-year moving average before diagnosis (1-µg/m3 difference in PM2.5 and PM10, and 10-µg/m3 difference in NOx) were obtained from Cox models considering greenspace and noise. A product term of air pollutant and social activity was added to test the multiplicative interaction and attributable proportion due to interaction was calculated for assessing additive interaction. We identified 137 (4.9%) incident depression cases. Participants exposed to higher concentrations of PM2.5, NOx, and PM10 had 53% (HR:1.53 [1.22, 1.93]), 26% (HR:1.26 [1.01, 1.58]), and 7% (HR:1.07 [0.98, 1.18]) increased hazard of depression, respectively. These associations were largely attenuated in people with active social engagement (HR for PM2.5: 1.04 [0.70, 1.55]; HR for PM10: 0.98 [0.81, 1.18]; and HR for NOx: 1.09 [0.71, 1.66]). Our findings suggest long-term exposure to air pollution may be a risk factor for depression among older adults. An active social engagement might however decrease this risk.