Showing papers by "Ole Raaschou-Nielsen published in 2022"

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

Abstract: 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.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.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.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.

Exposure to source-specific air pollution and risk for type 2 diabetes: a nationwide study covering Denmark.

Abstract: 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 148 020 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.

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

Abstract: 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.

Geographical Distribution and Pattern of Pesticides in Danish Drinking Water 2002–2018: Reducing Data Complexity

Abstract: Pesticides are a large and heterogenous group of chemicals with a complex geographic distribution in the environment. The purpose of this study was to explore the geographic distribution of pesticides in Danish drinking water and identify potential patterns in the grouping of pesticides. Our data included 899,169 analyses of 167 pesticides and metabolites, of which 55 were identified above the detection limit. Pesticide patterns were defined by (1) pesticide groups based on chemical structure and pesticide–metabolite relations and (2) an exploratory factor analysis identifying underlying patterns of related pesticides within waterworks. The geographic distribution was evaluated by mapping the pesticide categories for groups and factor components, namely those detected, quantified, above quality standards, and not analysed. We identified five and seven factor components for the periods 2002–2011 and 2012–2018, respectively. In total, 16 pesticide groups were identified, of which six were representative in space and time with regards to the number of waterworks and analyses, namely benzothiazinone, benzonitriles, organophosphates, phenoxy herbicides, triazines, and triazinones. Pesticide mapping identified areas where multiple pesticides were detected, indicating areas with a higher pesticide burden. The results contribute to a better understanding of the pesticide pattern in Danish drinking water and may contribute to exposure assessments for future epidemiological studies.

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

Abstract: 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 'Effects of Low-Level Air Pollution: A Study in Europe' (ELAPSE), we pooled data from eight cohorts among six European countries. Annual mean residential concentrations in 2010 for fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (O3) 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 to normal weight, unemployed, or non-smoking 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.

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

Abstract: 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.

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

Abstract: 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.

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

Abstract: 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. 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). 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. 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.

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

Abstract: 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. 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. 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. 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.

Long-term residential exposure to air pollution and risk of testicular cancer in Denmark: A population-based case-control study.

Abstract: BACKGROUND The incidence rate risk of testicular cancer has increased over the last four decades, and most significant increase has been among Caucasian men in Nordic countries. Second-generation immigrant studies indicate a significant role of environmental exposure in testicular cancer. METHODS We conducted a nationwide register-based case-control study, including 6,390 testicular cancer cases registered in the Danish Cancer Registry between 1989 and 2014. Up to four age-matched controls for each case (n=18,997) were randomly selected from Civil Registration System. Ambient air pollution levels were estimated at addresses of cases and controls with a state-of-the-art air pollution modeling system. RESULTS We mostly found ORs close to 1.00 and with 95% confidence intervals (CI) spanning 1.00. Exposure during the year preceding birth was associated with ORs for NO2 of 0.87 (95%CI: 0.77-0.97) per 10 µg/m3 and for organic carbon of 0.84 (95%CI: 0.72-0.98) per 1 µg/m3. Exposure during the first 10 years of life was associated with ORs for organic carbon of 0.79 (95%CI: 0.67-0.93) per 1 µg/m3, for O3 of 1.20 (95%CI: 1.07-1.34) per 10 µg/m3 and for secondary inorganic aerosols of 1.07 (95%CI: 1.00-1.15) per 1 µg/m3. CONCLUSIONS Early-life exposure to NO2 and OC was associated with lower risk for testicular cancer whereas early-life exposure to O3 and SIA was associated with higher risk. IMPACT We report both positive and negative associations between ambient air pollutants and risk of testicular, dependent on pollutant, exposure time window and age at diagnosis. This is the first study to investigate such associations.

Long-term residential exposure to air pollution and risk of testicular cancer in Denmark: A population-based case-control study.

Abstract: BACKGROUND The incidence rate risk of testicular cancer has increased over the last four decades, and most significant increase has been among Caucasian men in Nordic countries. Second-generation immigrant studies indicate a significant role of environmental exposure in testicular cancer. METHODS We conducted a nationwide register-based case-control study, including 6,390 testicular cancer cases registered in the Danish Cancer Registry between 1989 and 2014. Up to four age-matched controls for each case (n=18,997) were randomly selected from Civil Registration System. Ambient air pollution levels were estimated at addresses of cases and controls with a state-of-the-art air pollution modeling system. RESULTS We mostly found ORs close to 1.00 and with 95% confidence intervals (CI) spanning 1.00. Exposure during the year preceding birth was associated with ORs for NO2 of 0.87 (95%CI: 0.77-0.97) per 10 µg/m3 and for organic carbon of 0.84 (95%CI: 0.72-0.98) per 1 µg/m3. Exposure during the first 10 years of life was associated with ORs for organic carbon of 0.79 (95%CI: 0.67-0.93) per 1 µg/m3, for O3 of 1.20 (95%CI: 1.07-1.34) per 10 µg/m3 and for secondary inorganic aerosols of 1.07 (95%CI: 1.00-1.15) per 1 µg/m3. CONCLUSIONS Early-life exposure to NO2 and OC was associated with lower risk for testicular cancer whereas early-life exposure to O3 and SIA was associated with higher risk. IMPACT We report both positive and negative associations between ambient air pollutants and risk of testicular, dependent on pollutant, exposure time window and age at diagnosis. This is the first study to investigate such associations.

Do nutrients modify the risk of cadmium on acute myocardial infarction among never smokers in the Danish Diet, Cancer and Health cohort?

Abstract: BACKGROUND/AIM: Urine cadmium (U-Cd) is an established biomarker of long-term Cd exposure. U-Cd may be associated with risk of acute myocardial infarction (AMI), but results are equivocal at low biomarker levels. Nutrients including calcium (Ca), magnesium (Mg), and potassium (K) may play an important role in slowing atherosclerosis progression, though research findings with AMI have been inconsistent, and studies are limited in examining whether Cd-AMI associations are modified by these nutrients. METHODS: We analyzed data from a never smoking subgroup of the Danish Diet, Cancer, and Health (DCH) cohort, a prospective study of 50–64-year-old participants recruited between 1993-1997. Using a case-cohort design, with complete case analysis, we identified 1135 members of the randomly selected subcohort and 776 AMI cases through 2015. We quantified Cd (&#x3bc;g/g) and Ca (mg/g) concentrations in baseline urine samples. We calculated combined nutrient dietary intake scores (3-12 points) from Ca, K, and Mg food frequency questionnaires. We estimated adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs) using Cox proportional hazard models, adjusted for sex, education, passive smoking, alcohol, waist circumference, exercise and healthy diet. We stratified by median cutpoints and defined as high and low urine Ca (U-Ca) concentrations (median: 117.5 &#x3bc;g/g) or dietary intake scores (median: 8 points). RESULTS: Results were not materially different when stratified. Among high and low U-Ca groups, HRs for AMI were 1.27 (95% CI: 0.81, 1.98) and 0.93 (95% CI: 0.62, 1.41), respectively, when comparing highest vs. lowest U-Cd quartiles. HRs among high and low dietary intake scores were 0.96 (95% CI: 0.62, 1.49) and 1.25 (95% CI: 0.80, 1.95), respectively, when comparing highest vs. lowest U-Cd quartiles. CONCLUSIONS: We did not find evidence that nutrient levels modified the association between low-level Cd and AMI among never smokers. KEYWORDS: metals, nutrients, cadmium, myocardial infarction, cardiovascular health

Long-term Traffic-related Air Pollutant Exposure and Amyotrophic Lateral Sclerosis Diagnosis in Denmark: A Bayesian Hierarchical Analysis

Abstract: Background: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease. Limited evidence suggests ALS diagnosis may be associated with air pollution exposure and specifically traffic-related pollutants. Methods: In this population-based case–control study, we used 3,937 ALS cases from the Danish National Patient Register diagnosed during 1989–2013 and matched on age, sex, year of birth, and vital status to 19,333 population-based controls free of ALS at index date. We used validated predictions of elemental carbon (EC), nitrogen oxides (NOx), carbon monoxide (CO), and fine particles (PM2.5) to assign 1-, 5-, and 10-year average exposures pre-ALS diagnosis at study participants’ present and historical residential addresses. We used an adjusted Bayesian hierarchical conditional logistic model to estimate individual pollutant associations and joint and average associations for traffic-related pollutants (EC, NOx, CO). Results: For a standard deviation (SD) increase in 5-year average concentrations, EC (SD = 0.42 µg/m3) had a high probability of individual association with increased odds of ALS (11.5%; 95% credible interval [CrI] = –1.0%, 25.6%; 96.3% posterior probability of positive association), with negative associations for NOx (SD = 20 µg/m3) (–4.6%; 95% CrI = 18.1%, 8.9%; 27.8% posterior probability of positive association), CO (SD = 106 µg/m3) (–3.2%; 95% CrI = 14.4%, 10.0%; 26.7% posterior probability of positive association), and a null association for nonelemental carbon fine particles (non-EC PM2.5) (SD = 2.37 µg/m3) (0.7%; 95% CrI = 9.2%, 12.4%). We found no association between ALS and joint or average traffic pollution concentrations. Conclusions: This study found high probability of a positive association between ALS diagnosis and EC concentration. Further work is needed to understand the role of traffic-related air pollution in ALS pathogenesis.

A nationwide study of air pollution on the NCD related morbidity in an unselected population

Abstract: Background and Aim: Very few studies of the effect of air pollution on national mortality exist. Even fewer studies have investigated the effect of air pollution on non-communicable disease (NCD) in the total population. Thus, this study aims to elucidate the burden of air pollution on the morbidity of the total unselected population. Methods: The study cohort consisted of all individuals age 50 years or older who were alive and resided in Denmark on their 50th birthday or 1st January 2004, whichever came later (entry date) (N=2,872,957). All hospital contacts for cancer, type 2 diabetes, asthma, Chronic Obstructive Pulmonary Disease (COPD), Alzheimer’s-, Parkinson’s-, ischemic heart -, and cerebrovascular-disease, between 1st January 2004 and 31st December 2016 were identified. We defined all NCD incident onsets as the date of first contact. For each case and 5 randomly selected controls, we modelled pollution (PM₂.₅, PM10, SIA, NO₂, O₃, BC, PPM₂.₅, Sea salt, and SOA) as personal average concentrations over the 20 years prior to the incident date. We estimated IRRs with 95% CIs for a fixed increase in air pollution assuming a linear exposure response relationship, adjusted for age, gender, calendar time, and individual as well as area-level socio-economic status. Results We found IRR (95% CI) per 5 µg/m³ increase in PM₂.₅ and per 10 µg/m³ increase in NO₂ to be highest for asthma, Alzheimer’s disease, type 2 diabetes, and COPD, table 1. IRR PM₂.₅ IRR NO₂ Type 2 Diabetes 1.47 (1.41 - 1.52)1.27 (1.24 - 1.30) Alzheimer&#x27;s Dis 1.76 (1.67 - 1.87) 1.30 (1.26 - 1.35) Asthma 1.88 (1.76 - 2.01) 1.47 (1.42 - 1.53) COPD 1.34 (1.30 - 1.39) 1.36 (1.33 - 1.39) In conclusion we find key NCDs are associated to PM₂.₅ and NO₂ even in a low exposure environment. Keywords: Air pollution, non-communicable diseases, Nationwide, Cohort.

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

Abstract: Air pollution with particulate matter is an established lung carcinogen. Studies have suggested an association with breast cancer, but the evidence is inconsistent.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.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.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.

Abstract: 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.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.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.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 β-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.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.

Exposure to air pollution, road noise and surrounding green space and risk for type 2 diabetes: a multi-exposure study covering Denmark

Abstract: BACKGROUND AND AIM Air pollution, road noise and lack of greenness coexist in urban environments and have all been associated with type 2 diabetes (T2D). We aimed to identify how air pollutants, road noise and greenness were associated with T2D risk in a multi-exposure perspective. METHODS We estimated 5-year time-weighted exposure to PM2.5, ultrafine particles (UFP), elemental carbon (EC), NO2 and road traffic noise for all persons living in Denmark in 2005–2017 (HERMES study). For each air pollutant, we estimated the total contribution together with the traffic and non-traffic contributions. We estimated road noise at the most and least exposed façade and address-specific greenness (150m and 1000m radius). In total, 1.9 million persons aged &#x3e;50 years were included, and 128,358 developed T2D during follow-up. Using Cox proportional hazards models, we conducted single-, two- and multi-pollutant analyses, with adjustment for individual and area-level sociodemographic co-variates. RESULTS In single-pollutant models, all air pollutants and road noise were associated with increased risk and green space with reduced risk of T2D. In two-pollutant models, HRs for NO2 total and UFP total were robust to further air pollution adjustment, besides when mutually adjusted, where HR for UFP total was markedly reduced. For air pollution originating from traffic, only UFP traffic was robust to adjustment for the other air pollutants. In models with mutual air pollution-noise adjustment, both air pollution and road noise were associated with higher T2D risk. HRs for green space remained virtually unchanged in all two-pollutant models. In a multi-pollutant analysis including both air pollution, noise and green space, HRs of all exposures but PM2.5 total and EC total remained associated with T2D. CONCLUSIONS Air pollution, road noise and green space were independently associated with risk for T2D in the Danish population. KEYWORDS Air pollution, road noise, greenness, type 2 diabetes, multi-pollutant

Breast cancer incidence in relation to long-term low-level exposure to air pollution in the ELAPSE pooled cohort.

Abstract: BACKGROUND Established risk factors for breast cancer include genetic disposition, reproductive factors, hormone therapy, and lifestyle-related factors such as alcohol consumption, physical inactivity, smoking, and obesity. More recently a role of environmental exposures, including air pollution, has also been suggested. The aim of this study, was to investigate the relationship between long-term air pollution exposure and breast cancer incidence. METHODS We conducted a pooled analysis among six European cohorts (n=199,719) on the association between long-term residential levels of ambient nitrogen dioxide (NO2), fine particles (PM2.5), black carbon (BC), and ozone in the warm season (O3) and breast cancer incidence in women. The selected cohorts represented the lower range of air pollutant concentrations in Europe. We applied Cox proportional hazards models adjusting for potential confounders at the individual and area-level. RESULTS During 3,592,885 person-years of follow-up, we observed a total of 9,659 incident breast cancer cases. The results of the fully adjusted linear analyses showed a hazard ratio (95% confidence interval) of 1.03 (1.00, 1.06) per 10 μg/m³ NO2, 1.06 (1.01, 1.11) per 5 μg/m³ PM2.5, 1.03 (0.99, 1.06) per 0.5 10-5m-1 BC, and 0.98 (0.94, 1.01) per 10 μg/m³ O3. The effect estimates were most pronounced in the group of middle-aged women (50-54 years) and among never smokers. CONCLUSIONS The results were in support of an association between especially PM2.5 and breast cancer. IMPACT The findings of this study suggest a role of exposure to NO2, PM2.5 and BC in development of breast cancer.