Long-term exposure to air pollution and incidence of gastric and the upper aerodigestive tract cancers in a pooled European cohort: The ELAPSE project.

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.

Long-term exposure to air pollution and chronic kidney disease-associated mortality-Results from the pooled cohort of the European multicentre ELAPSE-study.

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.

Long-term air pollution exposure and malignant intracranial tumours of the central nervous system: a pooled analysis of six European cohorts.

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.

Long-term exposure to transportation noise and risk of type 2 diabetes: A cohort study.

BACKGROUND: Some studies have found transportation noise to be associated with higher diabetes risk. This includes studies based on millions of participants, relying entirely on register-based confounder adjustment, which raises concern about residual lifestyle confounding. We aimed to investigate associations between noise and type 2 diabetes (T2D), including investigation of effects of increasing confounder adjustment for register-data and lifestyle. METHODS: In a cohort of 286,151 participants randomly selected across Denmark in 2010-2013 and followed up until 2017, we identified 7574 incident T2D cases. Based on residential address-history for all participants linked with exposure assessment of high spatial resolution, we calculated 10-year time-weighted mean road and railway noise at the most (LdenMax) and least (LdenMin) exposed façades and air pollution (PM2.5). We used Cox models to calculate hazard ratios (HR) with increasing adjustment for individual- and area-level register-based sociodemographic covariates, self-reported lifestyle and air pollution. RESULTS: We found that a 10 dB increase in 10-year mean road LdenMin was associated with HRs (95% CI) of 1.06 (1.02-1.10) after adjustment for age, sex and year, 1.08 (1.04-1.13) after further adjustment for register-based sociodemographic covariates, 1.07 (1.03-1.12) after further lifestyle adjustment (e.g. smoking, diet and alcohol) and 1.06 (1.02-1.11) after further PM2.5 adjustment. For road LdenMax, the corresponding HRs were 1.07 (1.04-1.10), 1.05 (1.02-1.08), 1.04 (1.01-1.07) and 1.03 (1.00-1.06). Railway noise was associated with HRs of 1.04 (0.98-1.11) for LdenMax and 1.02 (0.92-1.12) for LdenMin after adjustment for sociodemographic and lifestyle covariates and PM2.5. CONCLUSIONS: Long-term exposure to road traffic noise was associated with T2D, which together with previous literature indicates that T2D should be considered when calculating health impacts of noise. After sociodemographic adjustment, further lifestyle adjustment only changed HRs slightly, suggesting that large register-based studies with adjustment for key sociodemographic covariates can produce reliable results.

Air pollution with NO2, PM2.5, and elemental carbon in relation to risk of breast cancer- a nationwide case-control study from Denmark.

Air pollution with particulate matter is an established lung carcinogen. Studies have suggested an association with breast cancer, but the evidence is inconsistent. METHODS: From nationwide registers, we identified all breast cancer cases (n = 55 745) in Denmark between 2000 and 2014. We matched one control for each case on age and year of birth. We used a multi-scale dispersion model to estimate outdoor concentrations of particulate matter <2.5 µm (PM2.5), elemental carbon (EC) and nitrogen dioxide (NO2) as time-weighted average over all addresses up to 20 years prior to diagnosis. We calculated odds ratios (OR) and 95% confidence intervals (CI) by conditional logistic regression with adjustment for marital status, educational level, occupational status, personal income, region of origin, medication and area-level socio-economic indicators. RESULTS: A 10 µg/m3 higher PM2.5 was associated with an OR for breast cancer of 1.21 (95% CI: 1.11-1.33). The corresponding ORs for EC (per 1 µg/m3) and NO2 (per 10 µg/m3) were 1.03 (95% CI: 1.00-1.07) and 1.03 (95% CI: 1.01-1.06), respectively. In multi-pollutant models, the OR for PM2.5 changed only little, whereas ORs for EC or NO2 approached the null. In an analysis of persons below 55 years, PM2.5 was associated with an OR of 1.32 (95% CI: 1.09-1.60) per 10 µg/m3 increase. CONCLUSION: We found evidence of an association between the investigated air pollutants and breast cancer, especially PM2.5. There were indications that the association differed by age at diagnosis. We were not able to include all potential confounders and thus, results should be interpreted with caution.

Exposure to ambient air pollution and lipid levels and blood pressure in an adult, Danish cohort.

BACKGROUND: Air pollution is a well-recognized risk factor for cardiovascular disease. However, the mechanistic pathways underlying the association are not completely understood. Hence, further studies are required to shed light on potential mechanisms, through which air pollution may affect the development from subclinical to clinical cardiovascular disease. OBJECTIVES: To investigate associations between short-term exposure to air pollution and high-density lipoprotein (HDL), non-high density lipoprotein (non-HDL), systolic and diastolic blood pressure. METHODS: The study was conducted among 32,851 Danes from the Diet, Cancer and Health - Next Generations cohort, who had a blood sample taken and blood pressure measured. We measured HDL and non-HDL in the blood samples. We modelled exposure to fine particulate matter (PM2.5), ultrafine particles (UFP), elemental carbon (EC) and nitrogen dioxide (NO2) in time-windows from 24 h up to 90 days before blood sampling. Pollutants were modelled as total air pollution from all sources, and apportioned into contributions from non-traffic and traffic sources. We analyzed data using linear and logistic regression, with adjustment for socio-economic and lifestyle factors. RESULTS: Air pollution exposure over 24 h to 30 days was generally adversely associated with lipid profile and blood pressure, e.g. for 30-day UFP-exposure, adjusted ß-estimates were: -0.025 (-0.043; -0.006) for HDL, 0.086 (0.042; 0.130) for non-HDL, 2.45 (1.70; 3.11) for systolic and 1.56 (1.07; 20.4) for diastolic blood pressure, per 10,000 particles/cm3. The strongest associations were found for the non-traffic components of air pollution, and among those who were overweight/obese. DISCUSSION: In this large study of air pollution and lipid levels and blood pressure, we found that 24-h to 30-day PM2.5, UFP, EC and NO2 concentrations were generally adversely associated with lipid profile and blood pressure, two important cardiovascular risk factors. The study suggests potential pathways, through which air pollution could affect the development of cardiovascular disease.

Air pollution and myocardial infarction; effect modification by sociodemographic and environmental factors. A cohort study from Denmark.

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.

Multiple myeloma risk in relation to long-term air pollution exposure - A pooled analysis of four European cohorts.

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.

Long-term exposure to traffic noise and risk of incident colon cancer: A pooled study of eleven Nordic cohorts.

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.

Long-term Air Pollution Exposure and Pneumonia-related Mortality in a Large Pooled European Cohort.

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.

Underlying pathways of social inequality in tooth loss: the mediating role of sugary beverages and diabetes.

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.

Long-term exposure to ambient air pollution and bladder cancer incidence in a pooled European cohort: the ELAPSE project.

BACKGROUND: The evidence linking ambient air pollution to bladder cancer is limited and mixed. METHODS: We assessed the associations of bladder cancer incidence with residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight PM2.5 elemental components (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) in a pooled cohort (N = 302,493). Exposures were primarily assessed based on 2010 measurements and back-extrapolated to the baseline years. We applied Cox proportional hazard models adjusting for individual- and area-level potential confounders. RESULTS: During an average of 18.2 years follow-up, 967 bladder cancer cases occurred. We observed a positive though statistically non-significant association between PM2.5 and bladder cancer incidence. Hazard Ratios (HR) were 1.09 (95% confidence interval (CI): 0.93-1.27) per 5 µg/m3 for 2010 exposure and 1.06 (95% CI: 0.99-1.14) for baseline exposure. Effect estimates for NO2, BC and O3 were close to unity. A positive association was observed with PM2.5 zinc (HR 1.08; 95% CI: 1.00-1.16 per 10 ng/m3). CONCLUSIONS: We found suggestive evidence of an association between long-term PM2.5 mass exposure and bladder cancer, strengthening the evidence from the few previous studies. The association with zinc in PM2.5 suggests the importance of industrial emissions.

Long-Term Exposure to Source-Specific Fine Particles and Mortality─A Pooled Analysis of 14 European Cohorts within the ELAPSE Project.

We assessed mortality risks associated with source-specific fine particles (PM2.5) in a pooled European cohort of 323,782 participants. Cox proportional hazard models were applied to estimate mortality hazard ratios (HRs) for source-specific PM2.5 identified through a source apportionment analysis. Exposure to 2010 annual average concentrations of source-specific PM2.5 components was assessed at baseline residential addresses. The source apportionment resulted in the identification of five sources: traffic, residual oil combustion, soil, biomass and agriculture, and industry. In single-source analysis, all identified sources were significantly positively associated with increased natural mortality risks. In multisource analysis, associations with all sources attenuated but remained statistically significant with traffic, oil, and biomass and agriculture. The highest association per interquartile increase was observed for the traffic component (HR: 1.06; 95% CI: 1.04 and 1.08 per 2.86 µg/m3 increase) across five identified sources. On a 1 µg/m3 basis, the residual oil-related PM2.5 had the strongest association (HR: 1.13; 95% CI: 1.05 and 1.22), which was substantially higher than that for generic PM2.5 mass, suggesting that past estimates using the generic PM2.5 exposure response function have underestimated the potential clean air health benefits of reducing fossil-fuel combustion. Source-specific associations with cause-specific mortality were in general consistent with findings of natural mortality.

Occupational noise exposure and risk of incident stroke: a pooled study of five Scandinavian cohorts.

OBJECTIVES: To investigate the association between occupational noise exposure and stroke incidence in a pooled study of five Scandinavian cohorts (NordSOUND). METHODS: We pooled and harmonised data from five Scandinavian cohorts resulting in 78 389 participants. We obtained job data from national registries or questionnaires and recoded these to match a job-exposure matrix developed in Sweden, which specified the annual average daily noise exposure in five exposure classes (LAeq8h): <70, 70-74, 75-79, 80-84, ≥85 dB(A). We identified residential address history and estimated 1-year average road traffic noise at baseline. Using national patient and mortality registers, we identified 7777 stroke cases with a median follow-up of 20.2 years. Analyses were conducted using Cox proportional hazards models adjusting for individual and area-level potential confounders. RESULTS: Exposure to occupational noise at baseline was not associated with overall stroke in the fully adjusted models. For ischaemic stroke, occupational noise was associated with HRs (95% CI) of 1.08 (0.98 to 1.20), 1.09 (0.97 to 1.24) and 1.06 (0.92 to 1.21) in the 75-79, 80-84 and ≥85 dB(A) exposure groups, compared with <70 dB(A), respectively. In subanalyses using time-varying occupational noise exposure, we observed an indication of higher stroke risk among the most exposed (≥85 dB(A)), particularly when restricting analyses to people exposed to occupational noise within the last year (HR: 1.27; 95% CI: 0.99 to 1.63). CONCLUSIONS: We found no association between occupational noise and risk of overall stroke after adjustment for confounders. However, the non-significantly increased risk of ischaemic stroke warrants further investigation.

Residential road traffic and railway noise and risk of childhood cancer: A nationwide register-based case-control study in Denmark.

BACKGROUND: The aetiology of most childhood cancers remains poorly understood. We conducted a nationwide register-based case-control study to assess the association between residential road traffic and railway noise exposure and risk of childhood cancers. METHODS: We identified all cases of first cancers diagnosed in children aged 0-19 years in 1985-2013 from the Danish Cancer Registry (N = 3962) and sampled four individually matched (by sex and date of birth) controls per case (N = 14,790) using the Central Population Register. We estimated time-weighted exposure averages of residential road traffic and railway noise at the most (Lden max) and least (Lden min) exposed façades from birth to index-date (for additional analysis: in utero period) based on the individual address history for the respective time windows. We fitted conditional logistic regression models to estimate odds ratios (OR) and their 95% confidence intervals (CI). RESULTS: ORs varied by noise estimate and cancer type, with generally wide CIs mostly including 1.00. We found a tendency of higher ORs with increasing railway and road traffic noise for Hodgkin lymphoma (ORs for railway and road Lden min were 1.63 (95% CI 1.00; 2.66) and 1.14 (95% CI 0.87; 1.48) per 10 dB), as well as a tendency of higher ORs with increasing railway noise for non-Hodgkin lymphoma. For embryonal CNS tumours and astrocytoma and other glioma we observed also some weak suggestions of a positive association. Analysing exposure to traffic noise in utero revealed similar patterns to those of the main analyses. CONCLUSIONS: This nationwide study with minimal risk of bias suggests no strong associations between traffic noise and risk of most childhood cancers. We found however some suggestive evidence for a positive association with Hodgkin lymphoma, non-Hodgkin lymphoma and some CNS tumours. Further research is warranted to confirm these associations in other populations and elucidate the underlying biological mechanisms.

Air pollution at the residence of Danish adults, by socio-demographic characteristics, morbidity, and address level characteristics.

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.

Exposure to transportation noise and risk for cardiovascular disease in a nationwide cohort study from Denmark.

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.

The effect of adjustment to register-based and questionnaire-based covariates on the association between air pollution and cardiometabolic disease.

OBJECTIVE: Recent studies on air pollution and disease have been based on millions of participants within a region or country, relying entirely on register-based confounder adjustment. We aimed to investigate the effects of increasing adjustment for register- and questionnaire-based covariates on the association between air pollution and cardiometabolic diseases. METHODS: In a population-based cohort of 246,766 eligible participants randomly selected across Denmark in 2010 and 2013 and followed up until December 31, 2017, we identified 3,247 myocardial infarction (MI) cases, 4,166 stroke cases and 6,366 type 2 diabetes cases. Based on historical address-information, we calculated 5-year time-weighted exposure to PM2.5 and NO2 modelled using a validated air pollution model. We used Cox proportional hazards models to calculate hazard ratios (HR) with increasing adjustment for a number of individual- and area-level register-based covariates as well as lifestyle covariates assessed through questionnaires. RESULTS: We found that a 5 µg/m3 higher PM2.5 was associated with HRs (95% CI) for MI, stroke and diabetes, of respectively, 1.18 (0.91-1.52), 1.11 (0.88-1.40) and 1.24 (1.03-1.50) in the fully adjusted models. For all three diseases, adjustment for either individual-level, area-level or lifestyle covariates, or combinations of these resulted in higher HRs compared to HRs adjusted only for age, sex and calendar-year, most marked for MI and diabetes. Further adjustment for lifestyle in models with full register-based individual- and area-level adjustment resulted in only minor changes in HRs for all three diseases. CONCLUSIONS: Our findings suggest that in studies of air pollution and cardiometabolic disease, which use an adjustment strategy with a broad range of register-based socioeconomic variables, there is no effect on risk estimates from subsequent lifestyle adjustment.

Long-term exposure to transportation noise and risk for atrial fibrillation: A Danish nationwide cohort study.

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.

Long term exposure to air pollution and kidney parenchyma cancer - Effects of low-level air pollution: a Study in Europe (ELAPSE).

BACKGROUND: Particulate matter (PM) is classified as a group 1 human carcinogen. Previous experimental studies suggest that particles in diesel exhaust induce oxidative stress, inflammation and DNA damage in kidney cells, but the evidence from population studies linking air pollution to kidney cancer is limited. METHODS: We pooled six European cohorts (N = 302,493) to assess the association of residential exposure to fine particles (PM2.5), nitrogen dioxide (NO2), black carbon (BC), warm season ozone (O3) and eight elemental components of PM2.5 (copper, iron, potassium, nickel, sulfur, silicon, vanadium, and zinc) with cancer of the kidney parenchyma. The main exposure model was developed for year 2010. We defined kidney parenchyma cancer according to the International Classification of Diseases 9th and 10th Revision codes 189.0 and C64. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. RESULTS: The participants were followed from baseline (1985-2005) to 2011-2015. A total of 847 cases occurred during 5,497,514 person-years of follow-up (average 18.2 years). Median (5-95%) exposure levels of NO2, PM2.5, BC and O3 were 24.1 µg/m3 (12.8-39.2), 15.3 µg/m3 (8.6-19.2), 1.6 10-5 m-1 (0.7-2.1), and 87.0 µg/m3 (70.3-97.4), respectively. The results of the fully adjusted linear analyses showed a hazard ratio (HR) of 1.03 (95% confidence interval [CI]: 0.92, 1.15) per 10 µg/m³ NO2, 1.04 (95% CI: 0.88, 1.21) per 5 µg/m³ PM2.5, 0.99 (95% CI: 0.89, 1.11) per 0.5 10-5 m-1 BCE, and 0.88 (95% CI: 0.76, 1.02) per 10 µg/m³ O3. We did not find associations between any of the elemental components of PM2.5 and cancer of the kidney parenchyma. CONCLUSION: We did not observe an association between long-term ambient air pollution exposure and incidence of kidney parenchyma cancer.