ABSTRACT
AIMS: The three correlated environmental exposures (air pollution, road traffic noise, and green space) have all been associated with the risk of myocardial infarction (MI). The present study aimed to analyse their independent and cumulative association with MI. METHODS AND RESULTS: In a cohort of all Danes aged 50 or older in the period 2005-17, 5-year time-weighted average exposure to fine particles (PM2.5), ultrafine particles, elemental carbon, nitrogen dioxide (NO2), and road traffic noise at the most and least exposed façades of residence was estimated. Green space around residences was estimated from land use maps. Cox proportional hazard models were used to estimate hazard ratios (HRs) and 95% confidence interval (CI), and cumulative risk indices (CRIs) were calculated. All expressed per interquartile range. Models were adjusted for both individual and neighbourhood-level socio-demographic covariates. The cohort included 1 964 702 persons. During follow-up, 71 285 developed MI. In single-exposure models, all exposures were associated with an increased risk of MI. In multi-pollutant analyses, an independent association with risk of MI was observed for PM2.5 (HR: 1.026; 95% CI: 1.002-1.050), noise at most exposed façade (HR: 1.024; 95% CI: 1.012-1.035), and lack of green space within 150 m of residence (HR: 1.018; 95% CI: 1.010-1.027). All three factors contributed significantly to the CRI (1.089; 95% CI: 1.076-1.101). CONCLUSION: In a nationwide cohort study, air pollution, noise, and lack of green space were all independently associated with an increased risk of MI. The air pollutant PM2.5 was closest associated with MI risk.
The present study aimed to analyse their independent and cumulative association of the three correlated environmental exposures: air pollution, road traffic noise, and green space with MI. Air pollution, noise, and lack of green space were all independently associated with MI.Risk estimates for air pollution, noise, and lack of green space were similar, indicating that all may be equally relevant targets for regulatory measures.
Subject(s)
Air Pollutants , Air Pollution , Myocardial Infarction , Humans , Noise/adverse effects , Cohort Studies , Parks, Recreational , Air Pollution/adverse effects , Air Pollutants/adverse effects , Myocardial Infarction/diagnosis , Myocardial Infarction/epidemiology , Myocardial Infarction/etiology , Particulate Matter/adverse effects , Environmental Exposure/adverse effects , Denmark/epidemiologyABSTRACT
Aryl-hydrocarbon receptor repressor (AHRR) hypomethylation in peripheral blood is tightly linked with tobacco smoking and lung cancer. Here, we investigated AHRR methylation in non-Hodgkin lymphoma (NHL), a non-smoking-associated cancer. In a case-cohort study within the population-based Danish Diet, Cancer and Health cohort, we measured AHRR (cg23576855) methylation in prediagnostic blood from 161 participants who developed NHL within 13.4 years of follow-up (median: 8.5 years), with a comparison group of 164 randomly chosen participants. We measured DNA-methylation levels using bisulfite pyrosequencing and estimated incidence rate ratios (IRR) using Cox proportional hazards models with adjustment for baseline age, sex, educational level, smoking status, body mass index, alcohol intake, physical activity, and diet score. Global DNA-methylation levels were assessed by long interspersed nucleotide element 1 (LINE-1) analysis. Overall, the IRR for AHRR hypomethylation (lowest vs. other quartiles) was 2.52 [95% confidence interval (CI), 1.24-5.15]. When stratified according to time between blood draw and diagnosis, low AHRR methylation levels were associated with a future diagnosis of NHL [IRR: 4.50 (95% CI, 1.62-12.50) at 0-<5 years, 7.04 (95% CI, 2.36-21.02) at 5-<10 years, and 0.56 (95% CI, 0.21-1.45) at ≥10 years]. There was no association between global DNA-methylation levels and risk of NHL. Our results show that AHRR hypomethylation in blood leukocytes is associated with a higher risk of NHL in a time-dependent manner, suggesting that it occurs as a response to tumor development. Significance: Our population-based study demonstrated that lower AHRR methylation levels in peripheral blood leukocytes were associated with an increased risk of NHL. This association was independent of tobacco smoking, sex, and lifestyle characteristics, but was highly dependent on time to diagnosis. These findings highlight the potential of AHRR methylation as a biomarker for NHL risk, effective up to 10 years after blood draw.
Subject(s)
Basic Helix-Loop-Helix Transcription Factors , Lymphoma, Non-Hodgkin , Repressor Proteins , Humans , Basic Helix-Loop-Helix Transcription Factors/genetics , Cohort Studies , DNA , DNA Methylation/genetics , Leukocytes , Lymphoma, Non-Hodgkin/epidemiology , Repressor Proteins/geneticsABSTRACT
Background: Air pollution, road traffic noise, and green space are correlated factors, associated with risk of stroke. We investigated their independent relationship with stroke in multi-exposure analyses and estimated their cumulative stroke burden. Methods: For all persons, ≥50 years of age and living in Denmark from 2005 to 2017, we established complete address histories and estimated running 5-year mean exposure to fine particles (PM2.5), ultrafine particles, elemental carbon, nitrogen dioxide (NO2), and road traffic noise at the most, and least exposed façade. For air pollutants, we estimated total, and non-traffic contributions. Green space around the residence was estimated from land use maps. Hazard ratios (HR) and 95% confidence limits (CL) were estimated with Cox proportional hazards models and used to calculate cumulative risk indices (CRI). We adjusted for the individual and sociodemographic covariates available in our dataset (which did not include information about individual life styles and medical conditions). Findings: The cohort accumulated 18,344,976 years of follow-up and 94,256 cases of stroke. All exposures were associated with risk of stroke in single pollutant models. In multi-pollutant analyses, only PM2.5 (HR: 1.058, 95% CI: 1.040-1.075) and noise at most exposed façade (HR: 1.033, 95% CI: 1.024-1.042) were independently associated with a higher risk of stroke. Both noise and air pollution contributed substantially to the CRI (1.103, 95% CI: 1.092-1.114) in the model with noise, green space, and total PM2.5 concentrations. Interpretation: Environmental exposure to air pollution and noise were both independently associated with risk of stroke. Funding: Health Effects Institute (HEI) (Assistance Award No. R-82811201).
ABSTRACT
BACKGROUND: Previous studies show social inequality in tooth loss, but the underlying pathways are not well understood. The aim was to investigate the mediated proportion of sugary beverages (SBs) and diabetes and the association between educational level and tooth loss, and to investigate whether the indirect effect of SBs and diabetes varied between educational groups in relation to tooth loss. METHODS: Data from 47,109 Danish men and women aged 50 years or older included in the Danish Diet, Cancer and Health Study was combined with data from Danish registers. Using natural effect models, SBs and diabetes were considered as mediators, and tooth loss was defined as having <15 teeth present. RESULTS: In total, 10,648 participants had tooth loss. The analyses showed that 3% (95% confidence interval 2-4%) of the social inequality in tooth loss was mediated through SBs and diabetes. The mediated proportion was mainly due to differential exposure to SBs and diabetes among lower educational groups. CONCLUSIONS: The findings show that SBs and diabetes to a minor degree contribute to tooth-loss inequalities. The explanation indicates that individuals in lower educational groups have higher consumption of SBs and more often suffer from diabetes than higher educational groups.
ABSTRACT
Air pollution is associated with increased risk of myocardial infarction (MI), but it is unresolved to what extent the association is modified by factors such as socioeconomic status, comorbidities, financial stress, residential green space, or road traffic noise. We formed a cohort of all (n = 1,964,702) Danes, aged 50-85 years, with 65,311 cases of MI during the followed-up period 2005-2017. For all participants we established residential five-year running average exposure to particulate matter <2.5 µm (PM2.5), ultrafine particles (UFP, <0.1 µm), elemental carbon (EC) and nitrogen dioxide (NO2). We evaluated risk in population strata, using Aalen additive hazards models to estimate absolute risk and Cox proportional hazards models to estimate relative risk of MI with 95% confidence intervals (CI). PM2.5 and the other pollutant were associated with MI. Lower education and lower income were associated with higher absolute risks of MI from air pollution, whereas no clear effect modification was apparent for relative risk estimates. For example, 5 µg/m3 higher PM2.5 was associated with HR for MI of 1.16 (95% CI: 1.10-1.22) among those with only mandatory education and 1.13 (95% CI: 1.03-1.24) among those with long education. The corresponding rate differences per 100,000 person years were 243 (95% CI: 216-271) and 358 (95% CI: 338-379), respectively. Higher level of comorbidity was consistently across all four pollutants associated with both higher absolute and relative risk of MI. In conclusion, people with comorbid conditions or of lower SES appeared more vulnerable to long-term exposure to air pollution and more cases of MI may be prevented by focused interventions in these groups.
Subject(s)
Air Pollutants , Air Pollution , Environmental Pollutants , Myocardial Infarction , Humans , Cohort Studies , Air Pollutants/analysis , Environmental Exposure/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Particulate Matter/analysis , Myocardial Infarction/chemically induced , Myocardial Infarction/epidemiologyABSTRACT
Background Colon cancer incidence is rising globally, and factors pertaining to urbanization have been proposed involved in this development. Traffic noise may increase colon cancer risk by causing sleep disturbance and stress, thereby inducing known colon cancer risk-factors, e.g. obesity, diabetes, physical inactivity, and alcohol consumption, but few studies have examined this. Objectives The objective of this study was to investigate the association between traffic noise and colon cancer (all, proximal, distal) in a pooled population of 11 Nordic cohorts, totaling 155,203 persons. Methods We identified residential address history and estimated road, railway, and aircraft noise, as well as air pollution, for all addresses, using similar exposure models across cohorts. Colon cancer cases were identified through national registries. We analyzed data using Cox Proportional Hazards Models, adjusting main models for harmonized sociodemographic and lifestyle data. Results During follow-up (median 18.8 years), 2757 colon cancer cases developed. We found a hazard ratio (HR) of 1.05 (95% confidence interval (CI): 0.99-1.10) per 10-dB higher 5-year mean time-weighted road traffic noise. In sub-type analyses, the association seemed confined to distal colon cancer: HR 1.06 (95% CI: 0.98-1.14). Railway and aircraft noise was not associated with colon cancer, albeit there was some indication in sub-type analyses that railway noise may also be associated with distal colon cancer. In interaction-analyses, the association between road traffic noise and colon cancer was strongest among obese persons and those with high NO2-exposure. Discussion A prominent study strength is the large population with harmonized data across eleven cohorts, and the complete address-history during follow-up. However, each cohort estimated noise independently, and only at the most exposed façade, which may introduce exposure misclassification. Despite this, the results of this pooled study suggest that traffic noise may be a risk factor for colon cancer, especially of distal origin.
Subject(s)
Air Pollution , Colonic Neoplasms , Noise, Transportation , Humans , Cohort Studies , Risk Factors , Environmental Exposure/analysis , Denmark/epidemiologyABSTRACT
BACKGROUND: The link between exposure to ambient air pollution and mortality from cardiorespiratory diseases is well established, while evidence on neurodegenerative disorders including Parkinson's Disease (PD) remains limited. OBJECTIVE: We examined the association between long-term exposure to ambient air pollution and PD mortality in seven European cohorts. METHODS: Within the project 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from seven cohorts among six European countries. Annual mean residential concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (O3), as well as 8 PM2.5 components (copper, iron, potassium, nickel, sulphur, silicon, vanadium, zinc), for 2010 were estimated using Europe-wide hybrid land use regression models. PD mortality was defined as underlying cause of death being either PD, secondary Parkinsonism, or dementia in PD. We applied Cox proportional hazard models to investigate the associations between air pollution and PD mortality, adjusting for potential confounders. RESULTS: Of 271,720 cohort participants, 381 died from PD during 19.7 years of follow-up. In single-pollutant analyses, we observed positive associations between PD mortality and PM2.5 (hazard ratio per 5 µg/m3: 1.25; 95% confidence interval: 1.01-1.55), NO2 (1.13; 0.95-1.34 per 10 µg/m3), and BC (1.12; 0.94-1.34 per 0.5 × 10-5m-1), and a negative association with O3 (0.74; 0.58-0.94 per 10 µg/m3). Associations of PM2.5, NO2, and BC with PD mortality were linear without apparent lower thresholds. In two-pollutant models, associations with PM2.5 remained robust when adjusted for NO2 (1.24; 0.95-1.62) or BC (1.28; 0.96-1.71), whereas associations with NO2 or BC attenuated to null. O3 associations remained negative, but no longer statistically significant in models with PM2.5. We detected suggestive positive associations with the potassium component of PM2.5. CONCLUSION: Long-term exposure to PM2.5, at levels well below current EU air pollution limit values, may contribute to PD mortality.
Subject(s)
Air Pollutants , Air Pollution , Environmental Pollutants , Parkinson Disease , Humans , Air Pollutants/adverse effects , Air Pollutants/analysis , Nitrogen Dioxide/analysis , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Particulate Matter/adverse effects , Particulate Matter/analysis , Environmental Pollutants/analysis , Soot/analysisABSTRACT
BACKGROUND: Ambient fine particulate matter (PM2.5) causes millions of deaths every year worldwide. Identification of the most harmful types of PM2.5 would facilitate efficient prevention strategies. OBJECTIVES: The aim of this study was to investigate associations between components of PM2.5 and mortality in a nation-wide Danish population. METHODS: Our study base was Danes born 1921-1985 and aged 30-85 years, who were followed up for mortality from 1991 to 2015. We included 678,465 natural cause mortality cases and selected five age, sex and calendar time matched controls to each case from the study base. We retrieved the address history of the study population from Danish registries and assessed five-year average concentrations of eight PM2.5 components using deterministic Chemistry-Transport Models air pollution models. We estimated mortality rate ratios (MRRs) by conditional logistic regression and adjusted for socio-demographical factors at individual and neighborhood level. RESULTS: Single pollutant models showed the strongest associations between natural cause mortality and an interquartile increase in sulfate particles (SO4--) (MRR: 1.123; 95 % CI: 1.100-1.147 per 1.5 µg/m3) and secondary organic aerosol (SOA) (MRR: 1.054; 95 % CI: 1.048-1.061 per 0.050 µg/m3). Two-pollutant models showed robust associations between SO4-- and SOA and natural cause mortality. Elemental carbon and mineral dust showed robust associations with higher respiratory and lung cancer mortality. CONCLUSION: This nation-wide study found robust associations between natural cause mortality and SO4-- particles and SOA, which is in line with the results of previous studies. Elemental carbon and mineral dust showed robust associations with higher respiratory and lung cancer mortality.
Subject(s)
Air Pollutants , Air Pollution , Lung Neoplasms , Humans , Air Pollutants/adverse effects , Air Pollutants/analysis , Respiratory Aerosols and Droplets , Air Pollution/adverse effects , Air Pollution/analysis , Particulate Matter/adverse effects , Particulate Matter/analysis , Dust , Environmental Exposure/adverse effectsABSTRACT
OBJECTIVE: Air pollution, road traffic noise and lack of greenness coexist in urban environments and have all been associated with type 2 diabetes. We aimed to investigate how these co-exposures were associated with type 2 diabetes in a multi-exposure perspective. METHODS: We estimated 5-year residential mean exposure to fine particles (PM2.5), ultrafine particles (UFP), elemental carbon (EC), nitrogen dioxide (NO2) and road traffic noise at the most (LdenMax) and least (LdenMin) exposed facade for all persons aged > 50 years living in Denmark in 2005 to 2017. For each air pollutant, we estimated total concentrations and traffic contributions. Based on land use maps, we estimated proportion of green and non-green space within 150 and 1000 m of all residences. In total, 1.9 million persons were included and 128,358 developed type 2 diabetes during follow-up. We performed analyses using Cox proportional hazards models, with adjustment for individual and neighborhood-level sociodemographic co-variates. RESULTS: In single-pollutant models, all air pollutants, noise and lack of green space were associated with higher risk of diabetes. In two-, three- and four-pollutant analyses of the air pollutants, only UFP and NO2 remained associated with higher diabetes risk in all models. LdenMax, LdenMin and the two proxies of green space remained associated with diabetes in two-pollutant models of, respectively, noise and green space. In a multi-pollutant analysis, we found hazard ratios (95 % confidence intervals) per interquartile range of 1.021 (1.005; 1.038) for UFP, 1.012 (0.996; 1.028) for NO2, 1.022 (1.012; 1.033) for LdenMin, 1.013 (1.004; 1.022) for LdenMax, and 1.038 (1.031; 1.044) and 1.018 (1.010; 1.025) for lack of green space within, respectively, 150 m and 1000 m, and a cumulative risk index of 1.131 (1.113; 1.149). CONCLUSIONS: Air pollution, road traffic noise and lack of green space were independently associated with higher risk of type 2 diabetes.
Subject(s)
Air Pollutants , Air Pollution , Diabetes Mellitus, Type 2 , Humans , Prospective Studies , Diabetes Mellitus, Type 2/epidemiology , Air Pollution/adverse effects , Air Pollutants/adverse effectsABSTRACT
Ambient air pollution is an established risk factor for premature mortality from chronic cardiovascular, respiratory and metabolic diseases, while evidence on neurodegenerative diseases and psychiatric disorders remains limited. We examined the association between long-term exposure to air pollution and mortality from dementia, psychiatric disorders, and suicide in seven European cohorts. Within the multicenter project 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from seven European cohorts from six countries. Based on the residential addresses, annual mean levels of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), ozone (O3), and 8 PM2.5 components were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and mortality from dementia, psychiatric disorders, and suicide. Of 271,720 participants, 900 died from dementia, 241 from psychiatric disorders, and 164 from suicide, during a mean follow-up of 19.7 years. In fully adjusted models, we observed positive associations of NO2 (hazard ratio [HR] = 1.38; 95 % confidence interval [CI]: 1.13, 1.70 per 10 µg/m3), PM2.5 (HR = 1.29; 95 % CI: 0.98, 1.71 per 5 µg/m3), and BC (HR = 1.37; 95 % CI: 1.11, 1.69 per 0.5 × 10-5/m) with psychiatric disorders mortality, as well as with suicide (NO2: HR = 1.13 [95 % CI: 0.92, 1.38]; PM2.5: HR = 1.19 [95 % CI: 0.76, 1.87]; BC: HR = 1.08 [95 % CI: 0.87, 1.35]), and no association with dementia mortality. We did not detect any positive associations of O3 and 8 PM2.5 components with any of the three mortality outcomes. Long-term exposure to NO2, PM2.5, and BC may lead to premature mortality from psychiatric disorders and suicide.
Subject(s)
Air Pollution , Dementia , Suicide , Humans , Europe/epidemiology , Air Pollution/adverse effectsABSTRACT
BACKGROUND: Transportation noise increases the risk of ischemic heart disease (IHD), but few studies have investigated subtypes of IHD, such as myocardial infarction (MI), angina pectoris, or heart failure. We aimed to study whether exposure to road, railway and aircraft noise increased risk for ischemic heart disease (IHD), IHD subtypes, and heart failure in the entire adult Danish population, investigating exposures at both maximum exposed and silent façades of each residence. METHODS: We modelled road, railway, and aircraft noise at the most and least exposed façades for the period 1995-2017 for all addresses in Denmark and calculated 10-year time-weighted running means for 2.5 million individuals age ≥50 years, of whom 122,523 developed IHD and 79,358 developed heart failure during follow-up (2005-2017). Data were analyzed using Cox proportional hazards models, adjusted for individual and area-level sociodemographic covariates and air pollution. RESULTS: We found road traffic noise at the most exposed façade (Lden) to be associated with higher risk of IHD, myocardial infarction (MI), angina pectoris, and heart failure, with hazard ratios (HRs) (95% confidence intervals (CI)) of 1.052 (1.044-1.059), 1.041 (1.032-1.051), 1.095 (1.071-1.119), and 1.039 (1.033-1.045) per 10 dB higher 10-year mean exposure, respectively. These associations followed a near-linear exposure-response relationship and were robust to adjustment for air pollution with PM2.5. Railway noise at the least exposed façade was associated with heart failure (HR 1.28; 95% CI: 1.004-1.053), but not the other outcomes. Exposure to aircraft noise (>45 dB) seemed associated with increased risk for MI and heart failure. CONCLUSIONS: We found road traffic noise and potentially railway and aircraft noise to increase risk of various major cardiovascular outcomes, highlighting the importance of preventive actions towards transportation noise.
Subject(s)
Cardiovascular Diseases , Heart Failure , Myocardial Infarction , Myocardial Ischemia , Noise, Transportation , Adult , Angina Pectoris , Cardiovascular Diseases/epidemiology , Cardiovascular Diseases/etiology , Cohort Studies , Denmark/epidemiology , Environmental Exposure , Humans , Middle Aged , Myocardial Infarction/epidemiology , Myocardial Infarction/etiology , Noise, Transportation/adverse effectsABSTRACT
Rationale: Ambient air pollution exposure has been linked to mortality from chronic cardiorespiratory diseases, while evidence on respiratory infections remains more limited. Objectives: We examined the association between long-term exposure to air pollution and pneumonia-related mortality in adults in a pool of eight European cohorts. Methods: Within the multicenter project ELAPSE (Effects of Low-Level Air Pollution: A Study in Europe), we pooled data from eight cohorts among six European countries. Annual mean residential concentrations in 2010 for fine particulate matter, nitrogen dioxide (NO2), black carbon (BC), and ozone were estimated using Europe-wide hybrid land-use regression models. We applied stratified Cox proportional hazard models to investigate the associations between air pollution and pneumonia, influenza, and acute lower respiratory infections (ALRI) mortality. Measurements and Main Results: Of 325,367 participants, 712 died from pneumonia and influenza combined, 682 from pneumonia, and 695 from ALRI during a mean follow-up of 19.5 years. NO2 and BC were associated with 10-12% increases in pneumonia and influenza combined mortality, but 95% confidence intervals included unity (hazard ratios, 1.12 [0.99-1.26] per 10 µg/m3 for NO2; 1.10 [0.97-1.24] per 0.5 10-5m-1 for BC). Associations with pneumonia and ALRI mortality were almost identical. We detected effect modification suggesting stronger associations with NO2 or BC in overweight, employed, or currently smoking participants compared with normal weight, unemployed, or nonsmoking participants. Conclusions: Long-term exposure to combustion-related air pollutants NO2 and BC may be associated with mortality from lower respiratory infections, but larger studies are needed to estimate these associations more precisely.
Subject(s)
Air Pollutants , Air Pollution , Influenza, Human , Pneumonia , Adult , Air Pollutants/adverse effects , Air Pollutants/analysis , Air Pollution/adverse effects , Air Pollution/analysis , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Humans , Nitrogen Dioxide/adverse effects , Particulate Matter/adverse effects , Particulate Matter/analysisABSTRACT
BACKGROUND: Only few epidemiological studies have investigated whether chronic exposure to air pollution from different sources have different impacts on risk of diabetes. We aimed to investigate associations between air pollution from traffic versus non-traffic sources and risk of type 2 diabetes in the Danish population. METHODS: We estimated long-term exposure to traffic and non-traffic contributions of particulate matter with a diameter <2.5 µg (PM2.5), elemental carbon (EC), ultrafine particles (UFP) and nitrogen dioxide (NO2) for all persons living in Denmark for the period 2005-17. In total, 2.6 million persons aged >35 years were included, of whom 148â020 developed type 2 diabetes during follow-up. We applied Cox proportional hazards models for analyses, using 5-year time-weighted running means of air pollution and adjustment for individual- and area-level demographic and socioeconomic covariates. RESULTS: We found that 5-year exposure to all particle measures (PM2.5, UFP and EC) and NO2 were associated with higher type 2 diabetes risk. We observed that for UFP, EC and potentially PM2.5, the pollution originating from traffic was associated with higher risks than the non-traffic contributions, whereas for NO2 similar hazard ratios (HR) were observed. For example, in two-source models, hazard ratios (HRs) per interquartile change in traffic UFP, EC and PM2.5 were 1.025, 1.045 and 1.036, respectively, whereas for non-traffic UFP, EC and PM2.5, the HRs were 1.013, 1.018 and 1.001, respectively. CONCLUSIONS: Our finding of stronger associations with particulate matter from traffic compared with non-traffic sources implies that prevention strategies should focus on limiting traffic-related particulate matter air pollution.
Subject(s)
Air Pollutants , Air Pollution , Diabetes Mellitus, Type 2 , Air Pollutants/adverse effects , Air Pollutants/analysis , Air Pollution/adverse effects , Denmark/epidemiology , Diabetes Mellitus, Type 2/epidemiology , Environmental Exposure/adverse effects , Humans , Nitrogen Dioxide/adverse effects , Particulate Matter/adverse effects , Particulate Matter/analysisABSTRACT
BACKGROUND: Exposure to outdoor air pollution is associated with adverse health effects. Previous studies have indicated higher levels of air pollution in socially deprived areas. AIM: To investigate associations between air pollution and socio-demographic variables, comorbidity, stress, and green space at the residence in Denmark. METHODS: We included 2,237,346 persons living in Denmark, aged 35 years or older in 2017. We used the high resolution, multi-scale DEHM/UBM/AirGIS air pollution modelling system to calculate mean concentrations of air pollution with PM2.5, elemental carbon, ultrafine particles and NO2 at residences held the preceding five years. We used nationwide registries to retrieve information about socio-demographic indicators at the individual and neighborhood levels. We used general linear regression models to analyze associations between socio-demographic indicators and air pollution at the residence. RESULTS: Individuals with high SES (income, higher white-collar worker and high educational level) and of non-Danish origin were exposed to higher levels of air pollution than individuals of low SES and of Danish origin, respectively. We found comparable levels of air pollution according to sex, stress events and morbidity. For neighborhood level SES indicators, we found high air pollution levels in neighborhoods with low SES measured as proportion of social housing, sole providers, low income and unemployment. In contrast, we found higher air pollution levels in neighborhoods with higher educational level and a low proportion of manual labor. People living in an apartment and/or with little green space had higher air pollution levels. CONCLUSION: In Denmark, high levels of residential air pollution were associated with higher individual SES and non-Danish origin. For neighborhood-level indicators of SES, no consistent pattern was observed. These results highlight the need for analyzing many different socio-demographic indicators to understand the complex associations between SES and exposure to air pollution.
Subject(s)
Air Pollutants , Air Pollution , Adult , Air Pollutants/analysis , Air Pollution/analysis , Denmark/epidemiology , Environmental Exposure/analysis , Housing , Humans , Morbidity , Particulate Matter/analysis , Residence CharacteristicsABSTRACT
BACKGROUND: Long-term exposure to ambient air pollution has been associated with premature mortality, but associations at concentrations lower than current annual limit values are uncertain. We analysed associations between low-level air pollution and mortality within the multicentre study Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE). METHODS: In this multicentre longitudinal study, we analysed seven population-based cohorts of adults (age ≥30 years) within ELAPSE, from Belgium, Denmark, England, the Netherlands, Norway, Rome (Italy), and Switzerland (enrolled in 2000-11; follow-up until 2011-17). Mortality registries were used to extract the underlying cause of death for deceased individuals. Annual average concentrations of fine particulate matter (PM2·5), nitrogen dioxide (NO2), black carbon, and tropospheric warm-season ozone (O3) from Europe-wide land use regression models at 100 m spatial resolution were assigned to baseline residential addresses. We applied cohort-specific Cox proportional hazard models with adjustment for area-level and individual-level covariates to evaluate associations with non-accidental mortality, as the main outcome, and with cardiovascular, non-malignant respiratory, and lung cancer mortality. Subset analyses of participants living at low pollutant concentrations (as per predefined values) and natural splines were used to investigate the concentration-response function. Cohort-specific effect estimates were pooled in a random-effects meta-analysis. FINDINGS: We analysed 28â153â138 participants contributing 257â859â621 person-years of observation, during which 3â593â741 deaths from non-accidental causes occurred. We found significant positive associations between non-accidental mortality and PM2·5, NO2, and black carbon, with a hazard ratio (HR) of 1·053 (95% CI 1·021-1·085) per 5 µg/m3 increment in PM2·5, 1·044 (1·019-1·069) per 10 µg/m3 NO2, and 1·039 (1·018-1·059) per 0·5â×â10-5/m black carbon. Associations with PM2·5, NO2, and black carbon were slightly weaker for cardiovascular mortality, similar for non-malignant respiratory mortality, and stronger for lung cancer mortality. Warm-season O3 was negatively associated with both non-accidental and cause-specific mortality. Associations were stronger at low concentrations: HRs for non-accidental mortality at concentrations lower than the WHO 2005 air quality guideline values for PM2·5 (10 µg/m3) and NO2 (40 µg/m3) were 1·078 (1·046-1·111) per 5 µg/m3 PM2·5 and 1·049 (1·024-1·075) per 10 µg/m3 NO2. Similarly, the association between black carbon and non-accidental mortality was highest at low concentrations, with a HR of 1·061 (1·032-1·092) for exposure lower than 1·5×â10-5/m, and 1·081 (0·966-1·210) for exposure lower than 1·0×â10-5/m. INTERPRETATION: Long-term exposure to concentrations of PM2·5 and NO2 lower than current annual limit values was associated with non-accidental, cardiovascular, non-malignant respiratory, and lung cancer mortality in seven large European cohorts. Continuing research on the effects of low concentrations of air pollutants is expected to further inform the process of setting air quality standards in Europe and other global regions. FUNDING: Health Effects Institute.
Subject(s)
Air Pollution , Environmental Exposure , Mortality, Premature , Adult , Air Pollution/adverse effects , Air Pollution/analysis , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Europe/epidemiology , Humans , Longitudinal Studies , Multicenter Studies as Topic , Particulate Matter/adverse effects , Particulate Matter/analysisABSTRACT
BACKGROUND: Epidemiological studies have linked transportation noise and cardiovascular diseases, however, atrial fibrillation (AF) has received limited attention. We aimed to investigate the association between transportation noise and AF risk. METHODS: Over the period 1990-2017 we estimated road and railway noise (Lden) at the most and least exposed façades for all residential addresses across Denmark. We estimated time-weighted mean noise exposure for 3.6 million individuals age ≥35 years. Of these, 269,756 incident cases of AF were identified with a mean follow-up of 13.0 years. Analyses were conducted using Cox proportional hazards models with adjustment for individual and area-level sociodemographic covariates and long-term residential air pollution. RESULTS: A 10 dB higher 10-year mean road traffic noise at the most and least exposed façades were associated with incidence rate ratios (IRR) and 95% confidence intervals (CI) for AF of 1.006 (1.001-1.011) and 1.013 (1.007-1.019), respectively. After further adjustment for PM2.5, the IRRs (CIs) were 1.000 (0.995-1.005) and 1.007 (1.000-1.013), respectively. For railway noise, the IRRs per 10 dB increase in 10-year mean exposure were 1.017 (1.007-1.026) and 1.035 (1.021-1.050) for the most and least exposed façades, respectively, and were slightly attenuated when adjusted for PM2.5. Aircraft noise between 55 and 60 dB and ≥60 dB were associated with IRRs of 1.055 (0.996-1.116) and 1.036 (0.931-1.154), respectively, when compared to <45 dB. CONCLUSION: Transportation noise seems to be associated with a small increase in AF risk, especially for exposure at the least exposed façade.
Subject(s)
Atrial Fibrillation , Noise, Transportation , Adult , Atrial Fibrillation/epidemiology , Atrial Fibrillation/etiology , Cohort Studies , Denmark/epidemiology , Environmental Exposure/analysis , Humans , Noise, Transportation/adverse effectsABSTRACT
BACKGROUND: Epidemiologic studies have linked transportation noise to increased morbidity and mortality, particularly for cardiovascular outcomes. However, studies investigating metabolic outcomes such as diabetes are limited and have focused only on noise exposures estimated for the loudest residential façade. OBJECTIVES: We aimed to examine the influence of long-term residential exposure to transportation noise at the loudest and quietest residential façades and the risk for type 2 diabetes. METHODS: Road traffic and railway noise exposures (Lden) at the most and least exposed façades were estimated for all dwellings in Denmark during 1990-2017. Aircraft noise was estimated in 5-dB categories. Ten-year time-weighted mean noise exposures were estimated for 3.56 million individuals ≥35 years of age. From 2000 to 2017, 233,912 incident cases of type 2 diabetes were identified using hospital and prescription registries, with a mean follow-up of 12.9 y. We used Cox proportional hazards models adjusting for individual- and area-level covariates and long-term residential air pollution. The population-attributable fraction (PAF) was also computed. RESULTS: Hazard ratios (HRs) and 95% confidence intervals (CIs) for type 2 diabetes in association with 10-dB increases in 10-y mean road traffic noise at the most and least exposed façades, respectively, were 1.05 (95% CI: 1.04, 1.05) and 1.09 (95% CI: 1.08, 1.10). Following subsequent adjustment for fine particulate matter [particulate matter ≤2.5µm in aerodynamic diameter] (10-y mean), the HRs (CIs) were 1.03 (95% CI: 1.03, 1.04) and 1.08 (95% CI: 1.07, 1.09), respectively. For railway noise, the HRs per 10-dB increase in 10-y mean exposure were 1.03 (95% CI: 1.02, 1.04) and 1.02 (95% CI: 1.01, 1.04) for the most and least exposed façades, respectively. Categorical models supported a linear exposure-outcome relationship for road traffic noise and, to a lesser extent, for railway noise. Aircraft noise >45 dB was associated with a 1-4% higher likelihood of type 2 diabetes compared with those who were unexposed. We found road traffic and railway noise associated with a PAF of 8.5% and 1.4%, respectively, of the diabetes cases. DISCUSSION: Long-term exposure to road, railway, and possibly aircraft traffic noise was associated with an increased risk of type 2 diabetes in a nationwide cohort of Danish adults. Our findings suggest that diabetes should be included when estimating the burden of disease due to transportation noise. https://doi.org/10.1289/EHP9146.
Subject(s)
Diabetes Mellitus, Type 2 , Noise, Transportation , Adult , Cohort Studies , Denmark/epidemiology , Diabetes Mellitus, Type 2/epidemiology , Environmental Exposure , Humans , Noise, Transportation/adverse effectsABSTRACT
This study aims to estimate the mortality risk associated with air pollution in a Swedish cohort with relatively low exposure. Air pollution models were used to estimate annual mean concentrations of particulate matter with aerodynamic diameter ≤ 2.5 µm (PM2.5), primary emitted carbonaceous particles (BC/pOC), sea salt, chemically formed particles grouped as secondary inorganic and organic aerosols (SIA and SOA) as well as ozone (O3) and nitrogen dioxide (NO2). The exposure, as a moving average was calculated based on home address for the time windows 1 year (lag 1), 1-5 years (lag 1-5) and 1-10 years (lag 1-10) preceding the death. During the study period, 1151 cases of natural mortality, 253 cases of cardiovascular disease (CVD) mortality and 113 cases of respiratory and lung cancer mortality were observed during 369,394 person-years of follow-up. Increased natural mortality was observed in association with NO2 (3% [95% CI -8-14%] per IQR) and PM2.5 (2% [95% CI -5-9%] for an IQR increase) and its components, except for SOA where a decreased risk was observed. Higher risk increases were observed for CVD mortality (e.g., 18% [95% CI 1-39%] per IQR for NO2). These findings at low exposure levels are relevant for future decisions concerning air quality policies.
Subject(s)
Air Pollutants , Air Pollution , Ozone , Air Pollutants/analysis , Air Pollutants/toxicity , Air Pollution/adverse effects , Air Pollution/analysis , Cohort Studies , Environmental Exposure/adverse effects , Environmental Exposure/analysis , Humans , Nitrogen Dioxide/analysis , Nitrogen Dioxide/toxicity , Ozone/analysis , Ozone/toxicity , Particulate Matter/analysis , Particulate Matter/toxicity , Sweden/epidemiologyABSTRACT
Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the "Effects of low-level air pollution: A study in Europe" (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO2 ), particulate matter with diameter <2.5 µm (PM2.5 ), black carbon (BC), warm-season ozone (O3 ), and eight elemental components of PM2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European-wide hybrid land-use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer-free adults at baseline, 512 developed liver cancer during a mean follow-up of 18.1 years. We observed positive linear associations between NO2 (hazard ratio, 95% confidence interval: 1.17, 1.02-1.35 per 10 µg/m3 ), PM2.5 (1.12, 0.92-1.36 per 5 µg/m3 ), and BC (1.15, 1.00-1.33 per 0.5 10-5 /m) and liver cancer incidence. Associations with NO2 and BC persisted in two-pollutant models with PM2.5 . Most components of PM2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM2.5 or NO2 . Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards.
Subject(s)
Air Pollution/adverse effects , Environmental Exposure/adverse effects , Liver Neoplasms/etiology , Adult , Air Pollutants/toxicity , Air Pollution/statistics & numerical data , Environmental Exposure/statistics & numerical data , Europe/epidemiology , Female , Humans , Incidence , Liver Neoplasms/epidemiology , Male , Middle Aged , Particle Size , Particulate Matter/toxicity , Proportional Hazards ModelsABSTRACT
BACKGROUND: Long-term exposure to ambient air pollution has been linked to childhood-onset asthma, although evidence is still insufficient. Within the multicentre project Effects of Low-Level Air Pollution: A Study in Europe (ELAPSE), we examined the associations of long-term exposures to particulate matter with a diameter <2.5â µm (PM2.5), nitrogen dioxide (NO2) and black carbon (BC) with asthma incidence in adults. METHODS: We pooled data from three cohorts in Denmark and Sweden with information on asthma hospital diagnoses. The average concentrations of air pollutants in 2010 were modelled by hybrid land-use regression models at participants' baseline residential addresses. Associations of air pollution exposures with asthma incidence were explored with Cox proportional hazard models, adjusting for potential confounders. RESULTS: Of 98â326 participants, 1965 developed asthma during a mean follow-up of 16.6â years. We observed associations in fully adjusted models with hazard ratios of 1.22 (95% CI 1.04-1.43) per 5â µg·m-3 for PM2.5, 1.17 (95% CI 1.10-1.25) per 10â µg·m-3 for NO2 and 1.15 (95% CI 1.08-1.23) per 0.5×10-5â m-1 for BC. Hazard ratios were larger in cohort subsets with exposure levels below the European Union and US limit values and possibly World Health Organization guidelines for PM2.5 and NO2. NO2 and BC estimates remained unchanged in two-pollutant models with PM2.5, whereas PM2.5 estimates were attenuated to unity. The concentration-response curves showed no evidence of a threshold. CONCLUSIONS: Long-term exposure to air pollution, especially from fossil fuel combustion sources such as motorised traffic, was associated with adult-onset asthma, even at levels below the current limit values.