Regression calibration of self-reported mobile phone use to optimize quantitative risk estimation in the COSMOS study.

The Cohort Study of Mobile Phone Use and Health (COSMOS) has repeatedly collected self-reported and operator-recorded data on mobile phone use. Assessing health effects using self-reported information is prone to measurement error, but operator data were available prospectively for only part of the study population and did not cover past mobile phone use. To optimize the available data and reduce bias, we evaluated different statistical approaches for constructing mobile phone exposure histories within COSMOS. We evaluated and compared the performance of four regression calibration (RC) methods (simple, direct, inverse, and generalized additive model for location, shape, and scale), complete-case (CC) analysis and multiple imputation (MI) in a simulation study with a binary health outcome. We used self-reported and operator-recorded mobile phone call data collected at baseline (2007-2012) from participants in Denmark, Finland, the Netherlands, Sweden, and the UK. Parameter estimates obtained using simple, direct, and inverse RC methods were associated with less bias and lower mean squared error than those obtained with CC analysis or MI. We showed that RC methods resulted in more accurate estimation of the relation between mobile phone use and health outcomes, by combining self-reported data with objective operator-recorded data available for a subset of participants.

Headache in the international cohort study of mobile phone use and health (COSMOS) in the Netherlands and the United Kingdom.

Headache is a common condition with a substantial burden of disease worldwide. Concerns have been raised over the potential impact of long-term mobile phone use on headache due to radiofrequency electromagnetic fields (RF-EMFs). We explored prospectively the association between mobile phone use at baseline (2009-2012) and headache at follow-up (2015-2018) by analysing pooled data consisting of the Dutch and UK cohorts of the Cohort Study of Mobile Phone Use and Health (COSMOS) (N = 78,437). Frequency of headache, migraine, and information on mobile phone use, including use of hands-free devices and frequency of texting, were self-reported. We collected objective operator data to obtain regression calibrated estimates of voice call duration. In the model mutually adjusted for call-time and text messaging, participants in the high category of call-time showed an adjusted odds ratio (OR) of 1.04 (95 % CI: 0.94-1.15), with no clear trend of reporting headache with increasing call-time. However, we found an increased risk of weekly headache (OR = 1.40, 95 % CI: 1.25-1.56) in the high category of text messaging, with a clear increase in reporting headache with increasing texting. Due to the negligible exposure to RF-EMFs from texting, our results suggest that mechanisms other than RF-EMFs are responsible for the increased risk of headache that we found among mobile phone users.

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.

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.

Urinary Cadmium and Incident Heart Failure: A Case-Cohort Analysis Among Never-Smokers in Denmark.

BACKGROUND: Epidemiologic studies suggest cadmium exposure is associated with cardiovascular disease risk, including heart failure. However, prior findings may be influenced by tobacco smoking, a dominant source of cadmium exposure and risk factor for heart failure. The present study leverages up to 20 years of follow-up in the Danish Diet, Cancer and Health cohort to examine the relationship between urinary cadmium and incident heart failure among people who never smoked. METHODS: Between 1993 and 1997, 19,394 never-smoking participants (ages 50-64 years) enrolled and provided a urine sample. From this sample, we randomly selected a subcohort of 600 men and 600 women and identified 958 incident heart failure cases occurring between baseline and 2015. Using a case-cohort approach, we estimated adjusted hazard ratios (aHR) for heart failure in Cox proportional hazards models with age as the time scale. RESULTS: Participants had relatively low concentrations of urinary cadmium, as expected for never smokers (median = 0.20; 25th, 75th = 0.13, 0.32 µg cadmium/g creatinine). In adjusted models, we found that higher urinary cadmium was associated with a higher rate of incident heart failure overall (aHR = 1.1 per interquartile range difference [95% CI = 1.0, 1.2). In sex-stratified analyses, the association seemed restricted to men (aHR = 1.5 [95% CI = 1.2, 1.9]). CONCLUSIONS: In this cohort of people who never smoked tobacco, environmental cadmium was positively associated with incident heart failure, especially among men.

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.

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 residential exposure to air pollution and Hodgkin lymphoma risk among adults in Denmark: a population-based case-control study.

PURPOSE: The etiology of Hodgkin lymphoma (HL) is obscure. Research on air pollution and risk of HL provides inconsistent results. We aimed to investigate the association between long-term residential exposure to air pollution and risk of adult Hodgkin lymphoma in Denmark. METHODS: We performed a nationwide register-based case-control study, including all (n = 2,681) Hodgkin lymphoma cases registered in the nationwide Danish Cancer Registry between 1989 and 2014. We randomly selected 8,853 age- and sex-matched controls from the entire Danish population using the Civil Registration System, and identified 20-year residential address history for all cases and controls. We modeled outdoor air pollution concentrations at all these addresses using the high-resolution multiscale air pollution model system DEHM/UBM/AirGIS. We used conditional logistic regression to estimate odds ratios adjusted for individual and neighborhood level sociodemographic variables. RESULTS: There was no association between 1, 5, 10, and 20 years' time-weighted average exposure to fine particles (PM2.5), O3, SO2, NO2, or the PM2.5 constituents OC, NH4, NO3, and SO4 and risk of Hodgkin lymphoma. CONCLUSION: Residential exposure to ambient air pollution does not seem to increase the risk of developing Hodgkin lymphoma.

Transportation noise and risk for colorectal cancer: a nationwide study covering Denmark.

PURPOSE: Few studies have suggested that traffic noise is a risk factor for cancer, but evidence is inconclusive. We aimed to investigate whether road traffic and railway noise are associated with risk of colorectal cancer. METHODS: We obtained address history for all 3.5 million people above 40 years of age and living in Denmark for the period 1990-2017 and estimated road traffic and railway noise (Lden) at the most and least exposed facades of all addresses as well as air pollution (PM2.5). During follow-up (2000-2017), 35,881 persons developed colon cancer and 19,755 developed rectal cancer. Information on individual and area-level demographic and socioeconomic variables was collected from Danish registries. We analyzed data using Cox proportional hazards models, including traffic noise as time-varying 10-year average exposure. RESULTS: Exposure to road traffic noise at the most exposed façade was associated with an incidence rate ratio and 95% confidence interval for proximal colon cancer of 1.018 (0.999-1.038) per 10 dB higher noise. We observed no associations for road traffic noise at the least exposed façade or for railway noise in relation to proximal colon cancer. Also, we found no association between road traffic or railway noise and risk for distal colon cancer or rectal cancer. CONCLUSION: Traffic noise did not seem associated with higher risk for colorectal cancer, although the suggestion of a slightly higher risk of proximal colon cancer following exposure to road traffic noise warrants further research.

Road and railway noise and risk for breast cancer: A nationwide study covering Denmark.

OBJECTIVE: Previous studies have suggested that transportation noise may increase risk for breast cancer, but existing literature is scarce and inconclusive. We aimed to investigate associations between road traffic and railway noise and risk for breast cancer across the entire Danish female population. METHODS: For all 2.8 million residential addresses across Denmark, we modelled road and railway noise at the most and least exposed façades for the period 1990-2017. We calculated 10-year time-weighted mean noise exposure for 1.8 million women aged >35 years, of whom 66,006 developed breast cancer during follow-up from 2000 to 2017. We analysed data using Cox proportional hazards models with noise exposure included as 10-year running means and adjusted for a number of individual and area-level socioeconomic co-variates and air pollution with fine particles estimated for all addresses. RESULTS: For exposures at the least exposed façade, we found that a 10 dB increase in 10-year time-weighted noise was associated with incidence rate ratios (IRRs) and 95% confidence intervals (CI) for breast cancer of 1.032 (1.019-1.046) for road noise and 1.023 (0.993-1.053) for railway noise. For exposures at the most exposed façade, the IRRs (95% CIs) were 1.012 (1.002-1.022) for road noise and 1.020 (1.001-1.039) for railway noise. Associations were strongest among women with human epidermal growth factor receptor 2 negative breast cancer. CONCLUSIONS: Road traffic and railway noise were associated with higher risk for breast cancer, especially noise at the least exposed façade, which is a proxy for noise exposure during sleep.

Urinary cadmium and stroke - a case-cohort study in Danish never-smokers.

BACKGROUND: and Purpose: Cadmium has been associated with risk of cardiovascular events, including stroke. Human cadmium exposure occurs primarily through diet and tobacco smoke. Recent cohort studies have found an association with stroke, but residual confounding from smoking, could not be ruled out. We therefore conducted a case-cohort study to evaluate whether cadmium is associated with stroke in never-smokers. METHODS: The Danish Diet Cancer and Health cohort consists of Danes 50-64 years old, recruited in 1993-1997. From never-smoking cohort members without previous cancer or stroke we sampled a sub-cohort of 1200 persons. We also identified all (n = 534) cases in the cohort with a validated stroke diagnosis between baseline and 2009. We quantified cadmium and creatinine concentrations from baseline urine samples and used cadmium per creatinine as our main exposure metric. We used Cox proportional hazards models to estimate hazard ratios (HRs) with age as time scale and adjusting for BMI, education and urinary cotinine with and without stratification by sex. RESULTS: The median urinary cadmium concentration was 0.21 µg cadmium/g creatinine in cases and 0.19 µg/g in the sub-cohort. The majority (83%) of stroke cases were diagnosed with ischemic stroke. The HR for stroke in the highest quartile of exposure (median 0.44 µg/g creatinine) was 1.11 (95% CI: 0.79-1.54) compared with the lowest quartile (median 0.10 µg/g creatinine). The HR per inter quartile range (IQR, 0.19 µg/g creatinine) was 1.02 (95% CI: 0.92-1.12). Among men, the HR per IQR higher levels of cadmium (0.16 µg/g creatinine) was 1.18 (95% CI: 0.92-1.52), and 1.00 (95% CI: 0.89-1.12) among women. Adjusting for creatinine or using osmolality instead of creatinine standardization generally attenuated observed relationships. CONCLUSIONS: Our results do not support that low levels of cadmium exposure among never-smokers are strongly associated with risk of stroke, although results varied somewhat by sex and method of accounting for urinary dilution.

Exposure to PM2.5 constituents and risk of adult leukemia in Denmark: A population-based case-control study.

BACKGROUND: Leukemia is one of the most common forms of hematologic malignancy, which can affect people of all ages. We previously showed an association between exposure to ambient particulate matter 2.5 µg (PM2.5) and risk for leukemia in adults. The aim of this study was to investigate which PM2.5 constituents were responsible for our previous observation. METHODS: This is a nationwide register-based case-control study. We identified 14,983 persons diagnosed with leukemia at age 20 or above, 1989-2014, in the Danish Cancer Registry. We selected up to four sex and age-matched controls per case at random from the entire Danish population (n = 51,613). We modelled concentrations of ambient PM2.5 and its constituents at the addresses of cases and controls for the 10-year period before index date with a state-of-the-art multiscale air pollution modeling system. We used conditional logistic regression to estimate odds ratios (ORs) adjusted for individual and neighborhood level socio-demographic variables. RESULT: The results showed higher risk for overall leukemia in association with interquartile range exposure to PM2.5 (OR = 1.09; 95% CI: 1.02, 1.17), black carbon (BC) (OR = 1.02; 95% CI: 1.00, 1.03), secondary inorganic aerosols (SIA) (OR = 1.15; 95% CI: 1.03, 1.29) and its components ammonium (NH4) (OR = 1.08; 95% CI: 1.00, 1.17) and nitrate (NO3) (OR = 1.08; 95% CI: 1.02, 1.14). In leukemia subtype analysis, statistically significant associations were found for AML with PM2.5 (OR = 1.14; 95% CI: 1.00, 1.29), BC (OR = 1.03; 95% CI: 1.00, 1.07), SIA (OR = 1.23; 95% CI: 1.01, 1.51), NH4 (OR = 1.16; 95% CI: 1.01, 1.34) and NO3 (OR = 1.12; 95% CI: 1.01, 1.24). The association between PM2.5 and leukemia persisted in two pollutants models including sum of primary emitted black and organic carbon (BC + OC), secondary organic aerosols (SOA), or sea-salt. The association between black carbon (BC) and leukemia persisted in two pollutants models including organic carbon (OC). The three pollutant model with sulfate (SO4), NH4 and NO3 showed an association with NO3 but not with SO4 or NH4. CONCLUSION: Ambient concentrations of the PM2.5 components BC, NH4 and NO3 at the residence showed associations with risk of incident leukemia in adults.

Relationship of leukaemias with long-term ambient air pollution exposures in the adult Danish population.

BACKGROUND: Few population-based epidemiological studies of adults have examined the relationship between air pollution and leukaemias. METHODS: Using Danish National Cancer Registry data and Danish DEHM-UBM-AirGIS system-modelled air pollution exposures, we examined whether particulate matter (PM2.5), black carbon (BC), nitrogen dioxide (NO2) and ozone (O3) averaged over 1, 5 or 10 years were associated with adult leukaemia in general or by subtype. In all, 14,986 adult cases diagnosed 1989-2014 and 51,624 age, sex and time-matched controls were included. Separate conditional logistic regression models, adjusted for socio-demographic factors, assessed exposure to each pollutant with leukaemias. RESULTS: Fully adjusted models showed a higher risk of leukaemia with higher 1-, 5- and 10-year-average exposures to PM2.5 prior to diagnosis (e.g. OR per 10 µg/m3 for 10-year average: 1.17, 95% CI: 1.03, 1.32), and a positive relationship with 1-year average BC. Results were driven by participants 70 years and older (OR per 10 µg/m3 for 10-year average: 1.35, 95% CI: 1.15-1.58). Null findings for younger participants. Higher 1-year average PM2.5 exposures were associated with higher risks for acute myeloid and chronic lymphoblastic leukaemia. CONCLUSION: Among older adults, higher risk for leukaemia was associated with higher residential PM2.5 concentrations averaged over 1, 5 and 10 years prior to diagnosis.

Long-term exposure to PM2.5 and its constituents and risk of Non-Hodgkin lymphoma in Denmark: A population-based case-control study.

BACKGROUND: Particulate matter (PM) air pollution is a complex mixture and the various PM constituents likely affect health differently. The literature on the relationships among specific PM constituents and the risk of cancer is sparse. In this study, we aimed to evaluate the association of PM2.5 and its constituents with the incidence of non-Hodgkin lymphoma (NHL) and the two main NHL subtypes. METHODS: We undertook a nationwide register-based case-control study including 20,847 cases registered in the Danish Cancer Registry with NHL between 1989 and 2014. Among the entire Danish population, we selected 41,749 age and sex-matched controls randomly from the Civil Registration System. We assessed modelled outdoor PM concentrations at addresses of cases and controls with a state-of-the-art multi scale air pollution modelling system and used conditional logistic regression to estimate odds ratios (ORs) adjusted for individual and neighborhood level socio-demographic variables. RESULTS: The 10-year time-weighted average concentrations of PM2.5, primary carbonaceous particles (BC/OC), secondary inorganic aerosols (SIA), secondary organic aerosols (SOA) and sea salt were 17.4, 2.3, 7.8, 0.3, and 4.1 µg/m3, respectively among controls. The results showed higher risk for NHL in association with exposure to BC/OC (OR = 1.03; 95% CI: 1.00, 1.07, per interquartile range (IQR)) and SOA (OR = 1.54; 95% CI: 1.13, 2.09, per IQR). The results indicated a higher risk for follicular lymphoma in association with several PM components. Including PM2.5 (OR = 1.16; 95% CI: 0.98-1.38), BC/OC (OR = 1.05; 95% CI: 0.97-1.14), SIA (OR = 1.44; 95% CI: 0.80-1.08), SOA (OR = 4.52; 95% CI: 0.86-23.83) per IQR. CONCLUSION: This is the first study on PM constituents and the risk of NHL. The results indicated an association with primary carbonaceous and secondary organic PM. The results need replication in other settings before any firm conclusion can be reached.

Intracranial tumors of the central nervous system and air pollution - a nationwide case-control study from Denmark.

BACKGROUND: Inconclusive evidence has suggested a possible link between air pollution and central nervous system (CNS) tumors. We investigated a range of air pollutants in relation to types of CNS tumors. METHODS: We identified all (n = 21,057) intracranial tumors in brain, meninges and cranial nerves diagnosed in Denmark between 1989 and 2014 and matched controls on age, sex and year of birth. We established personal 10-year mean residential outdoor exposure to particulate matter < 2.5 µm (PM2.5), nitrous oxides (NOX), primary emitted black carbon (BC) and ozone. We used conditional logistic regression to calculate odds ratios (OR) linearly (per interquartile range (IQR)) and categorically. We accounted for personal income, employment, marital status, use of medication as well as socio-demographic conditions at area level. RESULTS: Malignant tumors of the intracranial CNS was associated with BC (OR: 1.034, 95%CI: 1.005-1.065 per IQR. For NOx the OR per IQR was 1.026 (95%CI: 0.998-1.056). For malignant non-glioma tumors of the brain we found associations with PM2.5 (OR: 1.267, 95%CI: 1.053-1.524 per IQR), BC (OR: 1.049, 95%CI: 0.996-1.106) and NOx (OR: 1.051, 95% CI: 0.996-1.110). CONCLUSION: Our results suggest that air pollution is associated with malignant intracranial CNS tumors and malignant non-glioma of the brain. However, additional studies are needed.

Pregnancy exposure to wind turbine noise and adverse birth outcomes: a nationwide cohort study.

Noise from wind turbines (WTs) is reported as more annoying than traffic noise at similar levels, raising concerns as to whether WT noise (WTN) may negatively affect health, as reported for traffic noise. We aimed to investigate whether residential WTN is associated with adverse birth outcomes. Based on national registries, we identified all Danish dwellings situated within ≤ 20 wt heights radius and a random selection of 25% of dwellings situated within 20-40 wt heights radius of a WT. We identified 135,795 pregnant women living in the dwellings from 1982 to 2013, and collected information on gestational age and birth weight from a national birth registry. Using data on WT type and simulated hourly wind at each WT, we estimated hourly outdoor and low frequency (LF) indoor WTN at the dwellings of the pregnant women and aggregated as mean nighttime WTN during pregnancy. We used logistic regression with adjustment for individual and area-level covariates for the analyses. We did not find evidence suggesting that mean pregnancy or trimester-specific exposure to outdoor or indoor LF WTN were associated with any of the three adverse birth outcomes investigated: preterm birth (n = 13,003), term small for gestational age (n = 12,220) or term low birth weight (n = 1127). However, the number of cases in the highest exposure categories of ≥ 42 dB outdoor WTN or ≥ 15 dB indoor LF WTN were low for all outcomes (n between 0 and 31). The present study does not support an association between nighttime WTN and adverse birth outcomes. However, there were few cases in the high exposure groups and the results call for reproduction.

Long-term exposure to wind turbine noise at night and risk for diabetes: A nationwide cohort study.

Focus on renewable energy sources and reduced unit costs has led to increased number of wind turbines (WTs). WT noise (WTN) is reported to be highly annoying at levels from 30 to 35 dB and up, whereas for traffic noise people report to be highly annoyed from 40 to 45 dB and up. This has raised concerns as to whether WTN may increase risk for major diseases, as exposure to traffic noise has consistently been associated with increased risk of cardiovascular disease and diabetes. We identified all Danish dwellings within a radius of 20 WT heights and 25% of all dwellings within 20-40 WT heights from a WT. Using detailed data on WT type and hourly wind data at each WT position and height, we estimated hourly outdoor and low frequency indoor WTN for all dwellings, aggregated as nighttime 1- and 5-year running means. Using nationwide registries, we identified a study population of 614,731 persons living in these dwellings in the period from 1996 to 2012, of whom 25,148 developed diabetes. Data were analysed using Poisson regression with adjustment for individual and area-levels covariates. We found no associations between long-term exposure to WTN during night and diabetes risk, with incidence rate ratios (IRRs) of 0.90 (95% confidence intervals (CI): 0.79-1.02) and 0.92 (95% CI: 0.68-1.24) for 5-year mean nighttime outdoor WTN of 36-42 and ≥ 42 dB, respectively, compared to < 24 dB. For 5-year mean nighttime indoor low frequency WTN of 10-15 and ≥ 15 dB we found IRRs of 0.90 (0.78-1.04) and 0.74 (95% CI: 0.41-1.34), respectively, when compared to and < 5 dB. The lack of association was consistent across strata of sex, distance to major road, validity of noise estimate and WT height. The present study does not support an association between nighttime WTN and higher risk of diabetes. However, there were only few cases in the highest exposure groups and findings need reproduction.