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BACKGROUND: Short-term exposure to low and high air temperatures can cause serious harmful effects on human health. Existing literature has mostly focused on associations of ambient air temperature with mortality and the need for health care in population-level studies. Studies that have considered self-perceived health status as an outcome when examining the effects of air temperature on health are scarce. In this study, we explored the short-term association of daily mean air temperature with various measures of self-perceived health status. METHODS: This cross-sectional analysis is based on the Cooperative Health Research in the Region of Augsburg (KORA) FIT study conducted in 2018/2019 and included participants from the Augsburg region of Southern Germany. Health-related quality of life (HRQOL) was evaluated by using the 5-level EuroQol Five Dimension (EQ-5D-5L) questionnaire, including the EuroQol visual analog scale (EQ-VAS). Self-rated health (SRH) and comparative self-rated health (CSRH) were each assessed using a single question. Daily mean air temperature data was estimated using a spatiotemporal model and assigned to participants' home addresses at a resolution of 1 × 1 km. Regression models with a Distributed Lag Non-linear Modeling (DLNM) approach were used to investigate the associations between daily mean air temperature and self-perceived health measures. RESULTS: We found no association of heat or cold with the HRQOL, SRH or CSRH. Nevertheless, there was a significant protective association of low air temperature with the EQ-5D-5L dimension "usual activities." CONCLUSION: There was no evidence of daily mean air temperature adversely affecting participants' self-perceived health status.
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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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Promising evidence suggests a link between environmental factors, particularly air pollution, and diabetes and obesity. However, it is still unclear whether men and women are equally susceptible to environmental exposures. Therefore, we aimed to assess sex-specific long-term effects of environmental exposures on metabolic diseases. We analyzed cross-sectional data from 3,034 participants (53.7% female, aged 53-74 years) from the KORA Fit study (2018/19), a German population-based cohort. Environmental exposures, including annual averages of air pollutants [nitrogen oxides (NO2, NOx), ozone, particulate matter of different diameters (PM10, PMcoarse, PM2.5), PM2.5abs, particle number concentration], air temperature and surrounding greenness, were assessed at participants' residences. We evaluated sex-specific associations of environmental exposures with prevalent diabetes, obesity, body-mass-index (BMI) and waist circumference using logistic or linear regression models with an interaction term for sex, adjusted for age, lifestyle factors and education. Further effect modification, in particular by urbanization, was assessed in sex-stratified analyses. Higher annual averages of air pollution, air temperature and greenness at residence were associated with diabetes prevalence in men (NO2: Odds Ratio (OR) per interquartile range increase in exposure: 1.49 [95% confidence interval (CI): 1.13, 1.95], air temperature: OR: 1.48 [95%-CI: 1.15, 1.90]; greenness: OR: 0.78 [95%-CI: 0.59, 1.01]) but not in women. Conversely, higher levels of air pollution, temperature and lack of greenness were associated with lower obesity prevalence and BMI in women. After including an interaction term for urbanization, only higher greenness was associated with higher BMI in rural women, whereas higher air pollution was associated with higher BMI in urban men. To conclude, we observed sex-specific associations of environmental exposures with metabolic diseases. An additional interaction between environmental exposures and urbanization on obesity suggests a higher susceptibility to air pollution among urban men, and higher susceptibility to greenness among rural women, which needs corroboration in future studies.
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Poluentes Atmosféricos , Diabetes Mellitus , Exposição Ambiental , Obesidade , Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Idoso , Obesidade/epidemiologia , Alemanha/epidemiologia , Exposição Ambiental/efeitos adversos , Diabetes Mellitus/epidemiologia , Estudos Transversais , Poluentes Atmosféricos/análise , Prevalência , Fatores Sexuais , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Material Particulado/análiseRESUMO
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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Poluentes Atmosféricos , Poluição do Ar , Exposição Ambiental , Insuficiência Renal Crônica , Humanos , Insuficiência Renal Crônica/mortalidade , Insuficiência Renal Crônica/epidemiologia , Insuficiência Renal Crônica/induzido quimicamente , Masculino , Feminino , Europa (Continente)/epidemiologia , Pessoa de Meia-Idade , Idoso , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/efeitos adversos , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Material Particulado/análise , Material Particulado/efeitos adversos , AdultoRESUMO
Introduction: Type 2 diabetes (T2D) is a major public health concern, and various environmental factors have been associated with the development of this disease. This study aimed to investigate the longitudinal effects of multiple environmental exposures on the risk of incident T2D in a German population-based cohort. Methods: We used data from the KORA cohort study (Augsburg, Germany) and assessed exposure to air pollutants, traffic noise, greenness, and temperature at the participants' residencies. Cox proportional hazard models were used to analyze the associations with incident T2D, adjusting for potential confounders. Results: Of 7736 participants included in the analyses, 10.5% developed T2D during follow-up (mean: 15.0 years). We found weak or no association between environmental factors and the risk of T2D, with sex and education level significantly modifying the effects of air pollutants. Conclusion: Our study contributes to the growing body of literature investigating the impact of environmental factors on T2D risks and suggests that the impact of environmental factors may be small.
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Air pollution has been shown to significantly impact human health including cancer. Gastric and upper aerodigestive tract (UADT) cancers are common and increased risk has been associated with smoking and occupational exposures. However, the association with air pollution remains unclear. We pooled European subcohorts (N = 287,576 participants for gastric and N = 297,406 for UADT analyses) and investigated the association between residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC) and ozone in the warm season (O3w) with gastric and UADT cancer. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. During 5,305,133 and 5,434,843 person-years, 872 gastric and 1139 UADT incident cancer cases were observed, respectively. For gastric cancer, we found no association with PM2.5, NO2 and BC while for UADT the hazard ratios (95% confidence interval) were 1.15 (95% CI: 1.00-1.33) per 5 µg/m3 increase in PM2.5, 1.19 (1.08-1.30) per 10 µg/m3 increase in NO2, 1.14 (1.04-1.26) per 0.5 × 10-5 m-1 increase in BC and 0.81 (0.72-0.92) per 10 µg/m3 increase in O3w. We found no association between long-term ambient air pollution exposure and incidence of gastric cancer, while for long-term exposure to PM2.5, NO2 and BC increased incidence of UADT cancer was observed.
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Poluentes Atmosféricos , Poluição do Ar , Neoplasias Gástricas , Humanos , Material Particulado/efeitos adversos , Material Particulado/análise , Dióxido de Nitrogênio/efeitos adversos , Neoplasias Gástricas/epidemiologia , Neoplasias Gástricas/etiologia , Incidência , Exposição Ambiental/efeitos adversos , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Poluentes Atmosféricos/efeitos adversos , Poluentes Atmosféricos/análiseRESUMO
It is unclear whether cancers of the upper aerodigestive tract (UADT) and gastric cancer are related to air pollution, due to few studies with inconsistent results. The effects of particulate matter (PM) may vary across locations due to different source contributions and related PM compositions, and it is not clear which PM constituents/sources are most relevant from a consideration of overall mass concentration alone. We therefore investigated the association of UADT and gastric cancers with PM2.5 elemental constituents and sources components indicative of different sources within a large multicentre population based epidemiological study. Cohorts with at least 10 cases per cohort led to ten and eight cohorts from five countries contributing to UADT- and gastric cancer analysis, respectively. Outcome ascertainment was based on cancer registry data or data of comparable quality. We assigned home address exposure to eight elemental constituents (Cu, Fe, K, Ni, S, Si, V and Zn) estimated from Europe-wide exposure models, and five source components identified by absolute principal component analysis (APCA). Cox regression models were run with age as time scale, stratified for sex and cohort and adjusted for relevant individual and neighbourhood level confounders. We observed 1139 UADT and 872 gastric cancer cases during a mean follow-up of 18.3 and 18.5 years, respectively. UADT cancer incidence was associated with all constituents except K in single element analyses. After adjustment for NO2, only Ni and V remained associated with UADT. Residual oil combustion and traffic source components were associated with UADT cancer persisting in the multiple source model. No associations were found for any of the elements or source components and gastric cancer incidence. Our results indicate an association of several PM constituents indicative of different sources with UADT but not gastric cancer incidence with the most robust evidence for traffic and residual oil combustion.
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Poluentes Atmosféricos , Poluição do Ar , Neoplasias Gástricas , Humanos , Material Particulado/análise , Neoplasias Gástricas/induzido quimicamente , Neoplasias Gástricas/epidemiologia , Incidência , Exposição Ambiental/análise , Poluição do Ar/análise , Poluentes Atmosféricos/análiseRESUMO
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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Poluentes Atmosféricos , Poluição do Ar , Poluentes Ambientais , Leucemia , Linfoma , Adulto , Feminino , Humanos , Masculino , Dióxido de Nitrogênio/análise , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Material Particulado/análise , Poluentes Ambientais/análise , Leucemia/induzido quimicamente , Leucemia/epidemiologia , Linfoma/induzido quimicamente , Linfoma/epidemiologia , Potássio/análise , Poluentes Atmosféricos/análiseRESUMO
Previous studies consistently showed an association between fine atmospheric particulate matter (PM2.5) and cardiovascular diseases. Concerns about adverse health effects of ultrafine particles (UFP) are growing but long-term studies are still scarce. In this study, we examined the association between long-term exposure to ambient air pollutants and blood biomarkers of inflammation and coagulation, including fibrinogen, high-sensitivity C-reactive protein (hs-CRP), serum amyloid A (SAA) adiponectin and interleukin-6 (IL-6), measured in the German KORA-S4 cohort study (1999-2001). IL-6 was available for older participants only, who were therefore considered as a subsample. Annual mean concentrations of UFP (as particle number concentration), particulate matter in different particles sizes (PM10, PMcoarse, PM2.5, PM2.5 absorbance), ozone (O3), and nitrogen oxides (NO2, NOX) were estimated by land-use regression models and assigned to participants' home addresses. We performed a multiple linear regression between each pollutant and each biomarker with adjustment for confounders. Per 1 interquartile range (IQR, 1945 particles/cm3) increase of UFP, fibrinogen increased by 0.70 % (0.04; 1.37) and hs-CRP increased by 3.16 % (-0.52; 6.98). Adiponectin decreased by -2.53 % (-4.78; -0.24) per 1 IQR (1.4 µg/m3) increase of PM2.5. Besides, PM2.5 was associated with increased IL-6 in the subsample. In conclusion, we observed that long-term exposure to air pollutants, including both fine and ultrafine particles, was associated with higher concentrations of pro-inflammatory and lower concentrations of an anti-inflammatory blood biomarkers, which is consistent with an increased risk for cardiovascular disease observed for long-term exposure to air pollutants.
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Poluentes Atmosféricos , Poluição do Ar , Doenças Cardiovasculares , Poluentes Ambientais , Humanos , Proteína C-Reativa/metabolismo , Estudos de Coortes , Adiponectina , Interleucina-6 , Exposição Ambiental/análise , Poluição do Ar/análise , Poluentes Atmosféricos/análise , Material Particulado/análise , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/induzido quimicamente , Biomarcadores , Fibrinogênio , Dióxido de NitrogênioRESUMO
BACKGROUND: Studies across the globe generally reported increased mortality risks associated with particulate matter with aerodynamic diameter ≤2.5µm (PM2.5) exposure with large heterogeneity in the magnitude of reported associations and the shape of concentration-response functions (CRFs). We aimed to evaluate the impact of key study design factors (including confounders, applied exposure model, population age, and outcome definition) on PM2.5 effect estimates by harmonizing analyses on three previously published large studies in Canada [Mortality-Air Pollution Associations in Low Exposure Environments (MAPLE), 1991-2016], the United States (Medicare, 2000-2016), and Europe [Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), 2000-2016] as much as possible. METHODS: We harmonized the study populations to individuals 65+ years of age, applied the same satellite-derived PM2.5 exposure estimates, and selected the same sets of potential confounders and the same outcome. We evaluated whether differences in previously published effect estimates across cohorts were reduced after harmonization among these factors. Additional analyses were conducted to assess the influence of key design features on estimated risks, including adjusted covariates and exposure assessment method. A combined CRF was assessed with meta-analysis based on the extended shape-constrained health impact function (eSCHIF). RESULTS: More than 81 million participants were included, contributing 692 million person-years of follow-up. Hazard ratios and 95% confidence intervals (CIs) for all-cause mortality associated with a 5-µg/m3 increase in PM2.5 were 1.039 (1.032, 1.046) in MAPLE, 1.025 (1.021, 1.029) in Medicare, and 1.041 (1.014, 1.069) in ELAPSE. Applying a harmonized analytical approach marginally reduced difference in the observed associations across the three studies. Magnitude of the association was affected by the adjusted covariates, exposure assessment methodology, age of the population, and marginally by outcome definition. Shape of the CRFs differed across cohorts but generally showed associations down to the lowest observed PM2.5 levels. A common CRF suggested a monotonically increased risk down to the lowest exposure level. https://doi.org/10.1289/EHP12141.
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Poluentes Atmosféricos , Poluição do Ar , Humanos , Idoso , Poluentes Atmosféricos/análise , Exposição Ambiental/análise , Programas Nacionais de Saúde , Poluição do Ar/análise , Material Particulado/análise , Europa (Continente)/epidemiologia , Estudos de Coortes , Canadá/epidemiologiaRESUMO
BACKGROUND: Air pollution is a growing concern worldwide, with significant impacts on human health. Multiple myeloma is a type of blood cancer with increasing incidence. Studies have linked air pollution exposure to various types of cancer, including leukemia and lymphoma, however, the relationship with multiple myeloma incidence has not been extensively investigated. METHODS: We pooled four European cohorts (N = 234,803) and assessed the association between residential exposure to nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone (O3) and multiple myeloma. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. RESULTS: During 4,415,817 person-years of follow-up (average 18.8 years), we observed 404 cases of multiple myeloma. The results of the fully adjusted linear analyses showed hazard ratios (95% confidence interval) of 0.99 (0.84, 1.16) per 10 µg/m³ NO2, 1.04 (0.82, 1.33) per 5 µg/m³ PM2.5, 0.99 (0.84, 1.18) per 0.5 10-5 m-1 BCE, and 1.11 (0.87, 1.41) per 10 µg/m³ O3. CONCLUSIONS: We did not observe an association between long-term ambient air pollution exposure and incidence of multiple myeloma.
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Poluentes Atmosféricos , Poluição do Ar , Mieloma Múltiplo , Humanos , Poluentes Atmosféricos/toxicidade , Poluentes Atmosféricos/análise , Poluição do Ar/efeitos adversos , Poluição do Ar/análise , Estudos de Coortes , Exposição Ambiental/efeitos adversos , Exposição Ambiental/análise , Mieloma Múltiplo/induzido quimicamente , Mieloma Múltiplo/epidemiologia , Dióxido de Nitrogênio/toxicidade , Dióxido de Nitrogênio/análise , Material Particulado/análiseRESUMO
The lack of readily available methods for estimating high-resolution near-surface relative humidity (RH) and the incapability of weather stations to fully capture the spatiotemporal variability can lead to exposure misclassification in studies of environmental epidemiology. We therefore aimed to predict German-wide 1 × 1 km daily mean RH during 2000-2021. RH observations, longitude and latitude, modelled air temperature, precipitation and wind speed as well as remote sensing information on topographic elevation, vegetation, and the true color band composite were incorporated in a Random Forest (RF) model, in addition to date for capturing the temporal variations of the response-explanatory variables relationship. The model achieved high accuracy (R2 = 0.83) and low errors (Root Mean Square Error (RMSE) of 5.07%, Mean Absolute Percentage Error (MAPE) of 5.19% and Mean Percentage Error (MPE) of - 0.53%), calculated via ten-fold cross-validation. A comparison of our RH predictions with measurements from a dense monitoring network in the city of Augsburg, South Germany confirmed the good performance (R2 ≥ 0.86, RMSE ≤ 5.45%, MAPE ≤ 5.59%, MPE ≤ 3.11%). The model displayed high German-wide RH (22y-average of 79.00%) and high spatial variability across the country, exceeding 12% on yearly averages. Our findings indicate that the proposed RF model is suitable for estimating RH for a whole country in high-resolution and provide a reliable RH dataset for epidemiological analyses and other environmental research purposes.
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Poluentes Atmosféricos , Monitoramento Ambiental , Monitoramento Ambiental/métodos , Umidade , Algoritmo Florestas Aleatórias , Tempo (Meteorologia) , Temperatura , Poluentes Atmosféricos/análiseRESUMO
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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Poluição do Ar , Acidente Vascular Cerebral , Adulto , Humanos , Poluição do Ar/efeitos adversos , Ambiente Construído , Europa (Continente)/epidemiologia , Incidência , Dióxido de Nitrogênio/efeitos adversos , Acidente Vascular Cerebral/epidemiologia , TemperaturaRESUMO
Increasing evidence has revealed that exposure to low temperatures is linked to a higher risk of chronic diseases and death; however, the mechanisms underlying the observed associations are still poorly understood. We performed a cross-sectional analysis with 1115 participants from the population-based KORA F4 study, which was conducted in Augsburg, Germany, from 2006 to 2008. Seventy-one inflammation-related protein biomarkers were analyzed in serum using proximity extension assay technology. We employed generalized additive models to explore short- and medium-term effects of air temperature on biomarkers of subclinical inflammation at cumulative lags of 0-1 days, 2-6 days, 0-13 days, 0-27 days, and 0-55 days. We found that short- and medium-term exposures to lower air temperature were associated with higher levels in 64 biomarkers of subclinical inflammation, such as Protein S100-A12 (EN-RAGE), Interleukin-6 (IL-6), Interleukin-10 (IL-10), C-C motif chemokine 28 (CCL28), and Neurotrophin-3 (NT-3). More pronounced associations between lower air temperature and higher biomarker of subclinical inflammation were observed among older participants, people with cardiovascular disease or prediabetes/diabetes, and people exposed to higher levels of air pollution (PM2.5, NO2, and O3). Our findings provide intriguing insight into how low air temperature may cause adverse health effects by activating inflammatory pathways.
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Poluentes Atmosféricos , Poluição do Ar , Humanos , Temperatura , Material Particulado/análise , Estudos Transversais , Poluição do Ar/análise , Inflamação/induzido quimicamente , Inflamação/metabolismo , Biomarcadores/análise , Poluentes Atmosféricos/análise , Exposição Ambiental/análiseRESUMO
Climate change poses a serious threat to human health worldwide, while aging populations increase. However, no study has ever investigated the effects of air temperature on epigenetic age acceleration. This study involved 1,725 and 1,877 participants from the population-based KORA F4 (2006-2008) and follow-up FF4 (2013-2014) studies, respectively, conducted in Augsburg, Germany. The difference between epigenetic age and chronological age was referred to as epigenetic age acceleration and reflected by Horvath's epigenetic age acceleration (HorvathAA), Hannum's epigenetic age acceleration (HannumAA), PhenoAge acceleration (PhenoAA), GrimAge acceleration (GrimAA), and Epigenetic Skin and Blood Age acceleration (SkinBloodAA). Daily air temperature was estimated using hybrid spatiotemporal regression-based models. To explore the medium- and long-term effects of air temperature modeled in time and space on epigenetic age acceleration, we applied generalized estimating equations (GEE) with distributed lag non-linear models, and GEE, respectively. We found that high temperature exposure based on the 8-week moving average air temperature (97.5th percentile of temperature compared to median temperature) was associated with increased HorvathAA, HannumAA, GrimAA, and SkinBloodAA: 1.83 (95% CI: 0.29-3.37), 11.71 (95% CI: 8.91-14.50), 2.26 (95% CI: 1.03-3.50), and 5.02 (95% CI: 3.42-6.63) years, respectively. Additionally, we found consistent results with high temperature exposure based on the 4-week moving average air temperature was associated with increased HannumAA, GrimAA, and SkinBloodAA: 9.18 (95% CI: 6.60-11.76), 1.78 (95% CI: 0.66-2.90), and 4.07 (95% CI: 2.56-5.57) years, respectively. For the spatial variation in annual average temperature, a 1 °C increase was associated with an increase in all five measures of epigenetic age acceleration (HorvathAA: 0.41 [95% CI: 0.24-0.57], HannumAA: 2.24 [95% CI: 1.95-2.53], PhenoAA: 0.32 [95% CI: 0.05-0.60], GrimAA: 0.24 [95%: 0.11-0.37], and SkinBloodAA: 1.17 [95% CI: 1.00-1.35] years). In conclusion, our results provide first evidence that medium- and long-term exposures to high air temperature affect increases in epigenetic age acceleration.
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Poluição do Ar , Humanos , Lactente , Poluição do Ar/análise , Temperatura , Material Particulado/análise , Envelhecimento/genética , Epigênese Genética , Metilação de DNARESUMO
BACKGROUND: Short-term exposure to air pollution has been reported to be associated with cardiopulmonary diseases, but the underlying mechanisms remain unclear. This study aimed to investigate changes in serum metabolites associated with immediate, short- and medium-term exposures to ambient air pollution. METHODS: We used data from the German population-based Cooperative Health Research in the Region of Augsburg (KORA) S4 survey (1999-2001) and two follow-up examinations (F4: 2006-08 and FF4: 2013-14). Mass-spectrometry-based targeted metabolomics was used to quantify metabolites among serum samples. Only participants with repeated metabolites measurements were included in this analysis. We collected daily averages of fine particles (PM2.5), coarse particles (PMcoarse), nitrogen dioxide (NO2), and ozone (O3) at urban background monitors located in Augsburg, Germany. Covariate-adjusted generalized additive mixed-effects models were used to examine the associations between immediate (2-day average of same day and previous day as individual's blood withdrawal), short- (2-week moving average), and medium-term exposures (8-week moving average) to air pollution and metabolites. We further performed pathway analysis for the metabolites significantly associated with air pollutants in each exposure window. RESULTS: Of 9,620 observations from 4,261 study participants, we included 5,772 (60.0%) observations from 2,583 (60.6%) participants in this analysis. Out of 108 metabolites that passed quality control, multiple significant associations between metabolites and air pollutants with several exposure windows were identified at a Bonferroni corrected p-value threshold (p < 3.9 × 10-5). We found the highest number of associations for NO2, particularly at the medium-term exposure windows. Among the identified metabolic pathways based on the metabolites significantly associated with air pollutants, the glycerophospholipid metabolism was the most robust pathway in different air pollutants exposures. CONCLUSIONS: Our study suggested that short- and medium-term exposure to air pollution might induce alterations of serum metabolites, particularly in metabolites involved in metabolic pathways related to inflammatory response and oxidative stress.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Ozônio , Humanos , Estudos de Coortes , Dióxido de Nitrogênio/análise , Poluentes Atmosféricos/análise , Ozônio/análise , Material Particulado/análise , Exposição Ambiental/análiseRESUMO
BACKGROUND: Risk factors for malignant tumours of the central nervous system (CNS) are largely unknown. METHODS: We pooled six European cohorts (N = 302,493) and assessed the association between residential exposure to nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), ozone (O3) and eight elemental components of PM2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) and malignant intracranial CNS tumours defined according to the International Classification of Diseases ICD-9/ICD-10 codes 192.1/C70.0, 191.0-191.9/C71.0-C71.9, 192.0/C72.2-C72.5. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. RESULTS: During 5,497,514 person-years of follow-up (average 18.2 years), we observed 623 malignant CNS tumours. The results of the fully adjusted linear analyses showed a hazard ratio (95% confidence interval) of 1.07 (0.95, 1.21) per 10 µg/m³ NO2, 1.17 (0.96, 1.41) per 5 µg/m³ PM2.5, 1.10 (0.97, 1.25) per 0.5 10-5m-1 BC, and 0.99 (0.84, 1.17) per 10 µg/m³ O3. CONCLUSIONS: We observed indications of an association between exposure to NO2, PM2.5, and BC and tumours of the CNS. The PM elements were not consistently associated with CNS tumour incidence.
Assuntos
Poluentes Atmosféricos , Poluição do Ar , Neoplasias Encefálicas , Ozônio , Humanos , Material Particulado/efeitos adversos , Dióxido de Nitrogênio , Exposição Ambiental/efeitos adversos , Poluição do Ar/efeitos adversos , Neoplasias Encefálicas/epidemiologia , Neoplasias Encefálicas/etiologia , Poluentes Atmosféricos/efeitos adversosRESUMO
BACKGROUND: Emerging evidence supports an association between light at night (LAN) exposure with obesity or overweight in adults. However, effects of LAN exposure during childhood have yet to be further investigated. OBJECTIVE: In this study, we aimed to determine whether LAN exposure is associated with body mass in young children. RESEARCH DESIGN AND METHOD: We used data from the Fr1da cohort study which screened children for early-stage islet autoimmunity in Bavaria, Germany from February 2015 to March 2019. A total of 62,212 children aged <11 years with complete residential information was included in the analysis. Self-reported weight and height were used to calculate age- and sex-specific body mass index (BMI) z-scores. LAN exposure was based on remotely sensed images from Visible Infrared Imaging Radiometer Suite and assigned to the children's residencies. We used generalized additive models to estimate the associations between LAN exposure and BMI adjusting for potential confounders. RESULTS: We observed an increase in BMI z-scores of 34.0% (95% confidence interval (CI): 25.4-42.6) per 10 nW/cm2/sr increment in LAN exposure at baseline (2015) and of 32.6% (24.3-41.0) for LAN exposure one year prior to screening, both adjusted for age and sex. Similar associations were observed after adjustment for socioeconomic status and urbanization degree. CONCLUSION: Our findings suggest that outdoor light exposure may be a risk factor for weight gain during childhood.