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.

Burden of disease due to transportation noise in the Nordic countries.

BACKGROUND: Environmental noise is of increasing concern for public health. Quantification of associated health impacts is important for regulation and preventive strategies. AIM: To estimate the burden of disease (BoD) due to road traffic and railway noise in four Nordic countries and their capitals, in terms of DALYs (Disability-Adjusted Life Years), using comparable input data across countries. METHOD: Road traffic and railway noise exposure was obtained from the noise mapping conducted according to the Environmental Noise Directive (END) as well as nationwide noise exposure assessments for Denmark and Norway. Noise annoyance, sleep disturbance and ischaemic heart disease were included as the main health outcomes, using exposure-response functions from the WHO, 2018 systematic reviews. Additional analyses included stroke and type 2 diabetes. Country-specific DALY rates from the Global Burden of Disease (GBD) study were used as health input data. RESULTS: Comparable exposure data were not available on a national level for the Nordic countries, only for capital cities. The DALY rates for the capitals ranged from 329 to 485 DALYs/100,000 for road traffic noise and 44 to 146 DALY/100,000 for railway noise. Moreover, the DALY estimates for road traffic noise increased with up to 17% upon inclusion of stroke and diabetes. DALY estimates based on nationwide noise data were 51 and 133% higher than the END-based estimates, for Norway and Denmark, respectively. CONCLUSION: Further harmonization of noise exposure data is required for between-country comparisons. Moreover, nationwide noise models indicate that DALY estimates based on END considerably underestimate national BoD due to transportation noise. The health-related burden of traffic noise was comparable to that of air pollution, an established risk factor for disease in the GBD framework. Inclusion of environmental noise as a risk factor in the GBD is strongly encouraged.

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.

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.

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.

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.

High-resolution assessment of road traffic noise exposure in Denmark.

Recent studies show associations between transportation noise and various diseases. However, selection bias remains an inherent limitation in many cohort studies. In this study, we aimed to model road traffic noise exposure across the entire Danish population and investigate its distribution in relation to area-level socioeconomic indicators and green space. Based on the Nordic prediction method, we estimated road traffic noise for all Danish residential addresses, in total 2,761,739 addresses, for the years 1995, 2000, 2005, 2010, and 2015 at the most and least exposed façades. Area-level sociodemographic variables encompassing education, income, and unemployment were collected and residential green within a 150 m radius buffer at the address level was estimated using high-resolution national land use classification data. Median levels of noise at both the most and least exposed facades across Denmark increased slightly from 1995 to 2015. Correlations between most and least exposed façades varied based on population density and building type, with the highest correlations between the most and least exposed façades found for semidetached homes and lowest for multistory buildings. Increasing median noise levels were observed across increasing levels of higher education, lower income, and higher unemployment. A decreasing trend in median noise levels with increasing levels of green space was observed. In conclusion, we showed that it is feasible to estimate nationwide, address-specific exposure over a long time-period. Furthermore, the low correlations found between most and least exposed façade for multistory buildings, which characterize metropolitan centers, suggests that the most exposed façade estimation used in most previous studies and predicts exposure at the silent façade relatively poorly.

One-carbon metabolism biomarkers and risk of urothelial cell carcinoma in the European prospective investigation into cancer and nutrition.

Published associations between dietary folate and bladder cancer risk are inconsistent. Biomarkers may provide more accurate measures of nutrient status. This nested case-control analysis within the European Prospective Investigation into Cancer and Nutrition (EPIC) investigated associations between pre-diagnostic serum folate, homocysteine, vitamins B6 and B12 and the risk of urothelial cell carcinomas of the bladder (UCC). A total of 824 patients with newly diagnosed UCC were matched with 824 cohort members. Serum folate, homocysteine, and vitamins B6 and B12 were measured. Odds ratios (OR) and 95% confidence intervals (CI) for total, aggressive, and non-aggressive UCC were estimated using conditional logistic regression with adjustment for smoking status, smoking duration and intensity, and other potential confounders. Additionally, statistical interaction with smoking status was assessed. A halving in serum folate concentrations was moderately associated with risk of UCC (OR: 1.18; 95% CI: 0.98-1.43), in particular aggressive UCC (OR: 1.34; 95% CI: 1.02-1.75; p-heterogeneity = 0.19). Compared to never smokers in the highest quartile of folate concentrations, this association seemed only apparent among current smokers in the lowest quartile of folate concentrations (OR: 6.26; 95% CI: 3.62-10.81, p-interaction = 0.07). Dietary folate was not associated with aggressive UCC (OR: 1.26; 95% CI: 0.81-1.95; p-heterogeneity = 0.14). No association was observed between serum homocysteine, vitamins B6 and B12 and risk of UCC. This study suggests that lower serum folate concentrations are associated with increased UCC risk, in particular aggressive UCC. Residual confounding by smoking cannot be ruled out and these findings require confirmation in future studies with multiple measurements.

Ambient benzene at the residence and risk for subtypes of childhood leukemia, lymphoma and CNS tumor.

Exposure to benzene increases the risk for acute myeloid leukemia and possibly other types of cancer in adults. For children, only limited evidence about benzene and cancer exists. A few studies have indicated that benzene may increase risk for some subtypes of childhood cancer but not for others. We aimed to investigate if outdoor levels of benzene at the residence increase the risk for subtypes of leukemia, lymphoma and CNS tumor in children. We identified 1,989 children diagnosed with leukemia, lymphoma or CNS tumor during 1968-1991 in the Danish Cancer Registry and randomly selected 5,506 control children from the Danish population, matched on sex, age and calendar time. We traced residential history of all children from 9 months before birth to time of diagnosis, calculated outdoor benzene concentration at all addresses and summarized cumulative exposure over fetal and childhood periods separately. We used conditional logistic regression for the statistical analyses. Benzene exposure during childhood above the 90th percentile was associated with relative risks for acute lymphocytic leukemia (ALL) and acute myeloid leukemia (AML) of 1.0 (95% confidence intervals (CI): 0.6-1.7) and 1.9 (95% CI: 0.3-11.1), respectively, when compared with exposure levels below the median. For CNS tumors, there was a tendency of lower risk for ependymoma and higher risk for medulloblastoma in association with higher exposure. In conclusion, benzene was associated with higher risk for childhood AML, but not ALL, which is consistent with the few previous studies.

Pre-diagnostic circulating insulin-like growth factor-I and bladder cancer risk in the European Prospective Investigation into Cancer and Nutrition.

Previous in vitro and case-control studies have found an association between the insulin-like growth factor (IGF)-axis and bladder cancer risk. Circulating concentrations of IGF-I have also been found to be associated with an increased risk of several cancer types; however, the relationship between pre-diagnostic circulating IGF-I concentrations and bladder cancer has never been studied prospectively. We investigated the association of pre-diagnostic plasma concentrations of IGF-I with risk of overall bladder cancer and urothelial cell carcinoma (UCC) in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 843 men and women diagnosed with bladder cancer between 1992 and 2005 were matched with 843 controls by recruitment centre, sex, age at recruitment, date of blood collection, duration of follow-up, time of day and fasting status at blood collection using an incidence density sampling protocol. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression with adjustment for smoking status. No association was found between pre-diagnostic circulating IGF-I concentration and overall bladder cancer risk (adjusted OR for highest versus lowest fourth: 0.91, 95% CI: 0.66-1.24, ptrend = 0.40) or UCC (n of cases = 776; 0.91, 0.65-1.26, ptrend = 0.40). There was no significant evidence of heterogeneity in the association of IGF-I with bladder cancer risk by tumour aggressiveness, sex, smoking status, or by time between blood collection and diagnosis (pheterogeneity > 0.05 for all). This first prospective study indicates no evidence of an association between plasma IGF-I concentrations and bladder cancer risk.

Residential traffic noise and mammographic breast density in the Diet, Cancer, and Health cohort.

OBJECTIVES: Traffic is the most important source of community noise, and it has been proposed to be associated with a range of disease outcomes, including breast cancer. As mammographic breast density (MD) is one of the strongest risk factors for developing breast cancer, the present study investigated whether there is an association between residential exposure to traffic noise and MD in a Danish cohort. METHODS: We included women with reproductive and lifestyle information available from the Diet, Cancer, and Health cohort, who also participated in the Copenhagen Mammography Screening Programme (n = 5,260). Present and historical addresses from 1987 to 2011 were found in national registries, and traffic noise was modeled 5 years before mammogram. Analyses between residential traffic noise and MD were performed using logistic regression. RESULTS: We found no association between residential road and railway noise exposure 5 years before mammogram, and having a mixed/dense versus a fatty mammogram, and no interaction with menopausal status, BMI, HRT use, and railway noise exposure, for analyses on road traffic noise. CONCLUSION: The present study does not suggest an association between residential traffic noise exposure and subsequent MD in a cohort of middle-aged Danish women.

Organochlorine concentrations in adipose tissue and survival in postmenopausal, Danish breast cancer patients.

BACKGROUND: Several studies have investigated an association between organochlorine-concentrations and breast cancer incidence, whereas few have investigated an association with breast cancer mortality. METHODS: We used Cox Proportional Hazards Models to estimate the association between adipose organochlorine-concentrations and mortality after breast cancer in a survivor-cohort of 399 postmenopausal women. During a median follow-up of 16.1 years, 177 women died; 119 from breast cancer. RESULTS: There was a general inverse association with PCB-concentration (e.g. ΣPCBs: Mortality Rate Ratio (MRR) 0.79, 95% confidence interval (CI) (0.64-0.98) per inter-quartile range (IQR)), and for all pesticides, except ß-Hexachlorocyclohexane, which was not associated with mortality (MRR 1.02(0.87-1.18) per IQR), and dieldrin, which was associated with a significantly increased risk of death (MRR 1.22(1.05-1.41) per IQR). We found an interaction with prognostic factors for all PCBs, confining the inverse association to those with adverse prognostic factors. Results for pesticides suggested a similar, but mostly non-significant interaction. Dieldrin diverged from the general picture by being associated with increased mortality across all strata. CONCLUSION: A higher concentration of PCBs and several organochlorine pesticides may be inversely associated with breast cancer mortality among women with adverse prognostic factors. Further studies are required to investigate if this is a causal association. Dieldrin was associated with a higher mortality, regardless of prognostic factors. IMPACT: This is the first study to investigate an association between organochlorine concentrations in adipose tissue and breast cancer mortality. A prominent finding is a strong interaction with prognostic factors. The unexpected direction of association for most organochlorines encourages further studies of the role of individual metabolism of the organochlorines and a potentially stronger effect of the metabolites on mortality.

Long-term exposure to residential railway and road traffic noise and risk for diabetes in a Danish cohort.

BACKGROUND: Road traffic noise exposure has been found associated with diabetes incidence. Evidence for an association between railway noise exposure is less clear, as large studies with detailed railway noise modelling are lacking. PURPOSE: To investigate the association between residential railway noise and diabetes incidence, and to repeat previous analyses on road traffic noise and diabetes with longer follow-up time. METHODS: Among 50,534 middle-aged Danes enrolled into the Diet, Cancer and Health cohort from 1993 to 97, we identified 5062 cases of incident diabetes during a median follow-up of 15.5 years. Present and historical residential addresses from 1987 to 2012 were found in national registries, and railway and road traffic noise (Lden) were modelled for all addresses, using the Nordic prediction method. We used Cox proportional hazard models to investigate the association between residential traffic noise over 1 and 5 years before diagnosis, and diabetes incidence. Hazard ratios (HRs) were calculated as crude and adjusted for potential confounders. RESULTS: We found no association between railway noise exposure and diabetes incidence among the 9527 persons exposed, regardless of exposure time-window: HR 0.99 (0.94-1.04) per 10dB for 5-year exposure in fully adjusted models. There was no effect modification by sex, road traffic noise, and education. We confirmed the previously found association between road traffic noise exposure and diabetes including 6 additional years of follow-up: HR 1.08 (1.04-1.13) per 10dB for 5-year exposure in fully adjusted models. CONCLUSION: The study does not suggest an association between residential railway noise exposure and diabetes incidence, but supports the finding of a direct association with residential road traffic noise.

Modeled traffic noise at the residence and colorectal cancer incidence: a cohort study.

PURPOSE: Traffic noise has become an increasing public health concern, associated with pervasive negative health effects, most likely through pathways of sleep disruption and stress. Both sleep disruption and stress have been associated with colorectal cancer. The purpose of this study was to investigate the association between residential traffic noise and colorectal cancer incidence. METHODS: Traffic noise was calculated for all residential addresses from 1987 to 2012 for 51,283 Danes in the Diet, Cancer and Health Cohort. We used Cox proportional hazard models to investigate the association between residential traffic noise 5 and 10 years before diagnosis, and overall colorectal cancer incidence, as well as subtypes (rectal, proximal, and distal colon). Hazard ratios (HRs) were calculated as crude and adjusted for potential confounders. RESULTS: During follow-up, 1,134 colorectal cancers developed (737 colon, 397 rectal). We found no association between residential road traffic noise and rectal cancer. We observed an association with distal colon cancer: HR 1.18, 95% CI 1.00-1.40, but not for proximal colon cancer: 0.99 (0.83-1.18), per 10 dB, 10 years preceding diagnosis. There was no association between railway noise and colorectal cancer, or any subtype. CONCLUSION: The present study suggested that long-term exposure to residential road traffic noise might increase the risk for colon cancer, especially distal colon cancer.

Residential traffic noise exposure and vestibular schwannoma - a Danish case-control study.

BACKGROUND: Few risk factors for sporadic vestibular schwannoma (VS) are known. Several studies have proposed an increased risk with occupational noise exposure, whereas no studies have investigated residential traffic noise exposure as a risk factor. The present study investigated if residential traffic noise was associated with vestibular schwannoma in a large, population-based Danish case-control study. MATERIAL AND METHODS: We identified 1454 VS cases, age above 30 years at diagnosis, between 1990 and 2007. For each case, we selected two random population controls, matched on sex and year of birth. Road and railway traffic noise at the residence was calculated for all present and historical addresses between 1987 and index date. Associations between traffic noise and risk for VS were estimated using conditional logistic regression, adjusted for education, disposable personal income, cohabitation status, railway noise exposure, municipal population density, and municipal income. RESULTS: A two-year time-weighted mean road traffic noise exposure was associated with an adjusted odds ratio of 0.92 (0.82-1.03) for developing VS, per 10 dB increment. There was no clear trend in categorical analyses. Similarly, linear and categorical analyses of residential railway noise did not suggest an association. We found no interaction with demographics, year of diagnosis, individual and municipal socioeconomic variables, and railway noise exposure. The results did not differ by tumor side, spread or size. CONCLUSIONS: The present study does not suggest an association between residential traffic noise and VS.

Long-term residential road traffic noise and NO2 exposure in relation to risk of incident myocardial infarction - A Danish cohort study.

BACKGROUND: Road traffic is a source of both air pollution and noise; two environmental hazards both found to increase the risk of ischemic heart disease. Given the high correlation between these pollutants, it is important to investigate combined effects, in relation to myocardial infarction (MI). METHODS: Among 50,744 middle-aged Danes enrolled into the Diet, Cancer and Health cohort from 1993 to 97, we identified 2403 cases of incident MI during a median follow-up of 14.5 years. Present and historical residential addresses from 1987 to 2011 were found in national registries, and traffic noise (Lden) and air pollution (NO2) were modelled for all addresses. Analyses were performed using Cox proportional hazard models. RESULTS: Road traffic noise and NO2 were both individually associated with a higher risk of MI, with hazard ratios of 1.14 (1.07-1.21) and 1.08 (1.03-1.12) per inter-quartile range higher 10-year mean of road traffic noise and NO2, respectively. Mutual exposure adjustment reduced the association with 10-year NO2 exposure (1.02 (0.96-1.08)), whereas the association with road traffic noise remained: 1.12 (1.03-1.21). For fatal incident MI, the pattern was similar, but the associations for both pollutants were stronger. In analyses of tertiles across both pollutants, the strongest effects were seen for combined medium/high exposure, especially for fatal MI's. CONCLUSION: Both road traffic noise and NO2 were associated with a higher risk of MI in single-pollutant models. In two-pollutant models, mainly noise was associated with MI. Combined exposure to both pollutants was associated with the highest risk.

Intake of Total and Subgroups of Fat Minimally Affect the Associations between Selected Single Nucleotide Polymorphisms in the PPARγ Pathway and Changes in Anthropometry among European Adults from Cohorts of the DiOGenes Study.

BACKGROUND: Although the peroxisome proliferator-activated receptor γ (PPARγ) pathway is central in adipogenesis, it remains unknown whether it influences change in body weight (BW) and whether dietary fat has a modifying effect on the association. OBJECTIVES: We examined whether 27 single nucleotide polymorphisms (SNPs) within 4 genes in the PPARγ pathway are associated with the OR of being a BW gainer or with annual changes in anthropometry and whether intake of total fat, monounsaturated fat, polyunsaturated fat, or saturated fat has a modifying effect on these associations. METHODS: A case-noncase study included 11,048 men and women from cohorts in the European Diet, Obesity and Genes study; 5552 were cases, defined as individuals with the greatest BW gain during follow-up, and 6548 were randomly selected, including 5496 noncases. We selected 4 genes [CCAAT/enhancer binding protein ß (CEBPB), phosphoenolpyruvate carboxykinase 2, PPARγ gene (PPARG), and sterol regulatory element binding transcription factor 1] according to evidence about biologic plausibility for interactions with dietary fat in weight regulation. Diet was assessed at baseline, and anthropometry was followed for 7 y. RESULTS: The ORs for being a BW gainer for the 27 genetic variants ranged from 0.87 (95% CI: 0.79, 1.03) to 1.12 (95% CI: 0.96, 1.22) per additional minor allele. Uncorrected, CEBPB rs4253449 had a significant interaction with the intake of total fat and subgroups of fat. The OR for being a BW gainer for each additional rs4253449 minor allele per 100 kcal higher total fat intake was 1.07 (95% CI: 1.02, 1.12; P = 0.008), and similar associations were found for subgroups of fat. CONCLUSIONS: Among European men and women, the influence of dietary fat on associations between SNPs in the PPARγ pathway and anthropometry is likely to be absent or marginal. The observed interaction between rs4253449 and dietary fat needs confirmation.

Residential road traffic noise exposure and survival after breast cancer - A cohort study.

BACKGROUND: It is generally acknowledged that patients with already existing clinical conditions are especially vulnerable to the effects of traffic noise exposure. The aim of the present study was to investigate the association between residential road traffic noise and breast cancer survival. METHODS: Road traffic noise was calculated for all residential addresses from 1987 to February 2012 for incident breast cancer cases (n=1,759) in a cohort of 57,053 Danes. We used Cox Proportional Hazard Models to investigate the association between residential road traffic noise at different time-windows, and overall and breast cancer-specific mortality. Furthermore, we investigated interaction with prognostic and socioeconomic factors. Mortality Rate Ratios (MRR) were calculated in both unadjusted models, and adjusted for residential railway noise, lifestyle factors and socioeconomic variables. RESULTS: During a median of 7.3 years of follow-up, 402 patients died; 274 from breast cancer. We found no association between time-weighted averages of residential road traffic noise 1-, 3- or 5-years before death, or over the entire follow-up period, and overall or breast cancer-specific mortality. A 10dB higher road traffic noise from diagnosis until censoring was associated with an adjusted MRR of 0.94 (0.81-1.08) for all-cause mortality. The association was modified by lymph node involvement, with a MRR of 1.20 (0.97-1.48) for those with tumor-positive lymph nodes and 0.76 (0.59-0.98) for those without. CONCLUSION: The present study suggests no association between residential road traffic noise and concurrent mortality. As it is the first study of its kind, with relatively limited power, further studies are warranted.