Socioeconomic differences in the risk of childhood central nervous system tumors in Denmark:a nationwide register-based case–control study

Purpose!#!Differences in the risk of childhood central nervous system (CNS) tumors by socioeconomic status (SES) may enhance etiologic insights. We conducted a nationwide register-based case-control study to evaluate socioeconomic differences in the risk of childhood CNS tumors in Denmark and examined whether associations varied by different SES measures, time points of assessment, specific tumor types, and age at diagnosis.!##!Methods!#!We identified all children born between 1981 and 2013 and diagnosed with a CNS tumor at ages 0-19 years (n = 1,273) from the Danish Cancer Registry and sampled four individually matched controls per case (n  = 5,086). We used conditional logistic regression models to estimate associations with individual-level and neighborhood-level socioeconomic measures.!##!Results!#!We observed elevated risks of ependymoma and embryonal CNS tumors in association with higher parental education (odds ratios (ORs) of 1.6-2.1 for maternal or paternal high education and ependymoma) and higher risk of all tumor types in association with higher maternal income, e.g., OR  1.93; 95% CI 1.05-3.52 for high versus low income for astrocytoma and other gliomas. Associations were often stronger in children diagnosed at ages 5-19 years. We found little evidence for an association with neighborhood SES.!##!Conclusion!#!This large nationwide register study with minimal risk of bias showed that having parents with higher educational level and a mother with higher income was associated with a higher risk of childhood CNS tumors. Bias or under-ascertainment of cases among families with low income or basic education is unlikely to explain our findings

Is the risk of childhood leukaemia associated with socioeconomic measures in Denmark? : A nationwide register-based case-control study

The aetiology of childhood leukaemia is poorly understood. Knowledge about differences in risk by socioeconomic status (SES) may enhance etiologic insights. We conducted a nationwide register-based case-control study to evaluate socioeconomic differences in the risk of childhood leukaemia in Denmark and to access whether associations varied by different measures of SES, time point of assessment, leukaemia type and age at diagnosis. We identified all cases of leukaemia in children aged 0 to 19 years, born and diagnosed between 1980 and 2013 from the Danish Cancer Registry (N = 1336) and sampled four individually matched controls per case (N = 5330). We used conditional logistic regression models for analysis. Medium and high level of parental education was associated with a higher risk of acute myeloid leukaemia (AML) in the offspring, mainly driven by children diagnosed at ages 0 to 4 years [odds ratio (OR) for high maternal education = 3.07; 95% confidence interval (CI): 1.44-6.55]. We also observed a modestly increased risk for lymphoid leukaemia (LL) in association with higher level of parental education, but only in children diagnosed at ages 5 to 19 years. Higher parental income was associated with an increased risk of LL but not AML among children aged 5 to 19 years at diagnosis (OR for high maternal income = 2.78; 95% CI: 1.32-5.89). Results for neighbourhood SES measures indicated null associations. Bias or under-ascertainment of cases among families with low income or basic education are unlikely to explain the observed socioeconomic differences. Future research addressing explicitly the underlying mechanisms of our results may help to enhance etiologic insights of the disease

Predictors of Urinary Arsenic Levels among Postmenopausal Danish Women

Arsenic is a risk factor for several noncommunicable diseases, even at low doses. Urinary arsenic (UAs) concentration is a good biomarker for internal dose, and demographic, dietary, and lifestyle factors are proposed predictors in nonoccupationally exposed populations. However, most predictor studies are limited in terms of size and number of predictors. We investigated demographic, dietary, and lifestyle determinants of UAs concentrations in 744 postmenopausal Danish women who had UAs measurements and questionnaire data on potential predictors. UAs concentrations were determined using mass spectrometry (ICP-MS), and determinants of the concentration were investigated using univariate and multivariate regression models. We used a forward selection procedure for model optimization. In all models, fish, alcohol, and poultry intake were associated with higher UAs concentration, and tap water, fruit, potato, and dairy intake with lower concentration. A forward regression model explained 35% (R2) of the variation in concentrations. Age, smoking, education, and area of residence did not predict concentration. The results were relatively robust across sensitivity analyses. The study suggested that UAs concentration in postmenopausal women was primarily determined by dietary factors, with fish consumption showing the strongest direct association. However, the majority of variation in UAs concentration in this study population is still unexplained

Long-term residential exposure to PM2.5, PM10, black carbon, NO2, and ozone and mortality in a Danish cohort

Air pollutants such as NO2 and PM2.5 have consistently been linked to mortality, but only few previous studies have addressed associations with long-term exposure to black carbon (BC) and ozone (O3). We investigated the association between PM2.5, PM10, BC, NO2, and O3 and mortality in a Danish cohort of 49,564 individuals who were followed up from enrollment in 1993–1997 through 2015. Residential address history from 1979 onwards was combined with air pollution exposure obtained by the state-of-the-art, validated, THOR/AirGIS air pollution modelling system, and information on residential traffic noise exposure, lifestyle and socio-demography. We observed higher risks of all-cause as well as cardiovascular disease (CVD) mortality with higher long-term exposure to PM2.5, PM10, BC, and NO2. For PM2.5 and CVD mortality, a hazard ratio (HR) of 1.29 (95% CI: 1.13–1.47) per 5 μg/m3 was observed, and correspondingly HRs of 1.16 (95% CI: 1.05–1.27) and 1.11 (95% CI: 1.04–1.17) were observed for BC (per 1 μg/m3) and NO2 (per 10 μg/m3), respectively. Adjustment for noise gave slightly lower estimates for the air pollutants and CVD mortality. Inverse relationships were observed for O3. None of the investigated air pollutants were related to risk of respiratory mortality. Stratified analyses suggested that the elevated risks of CVD and all-cause mortality in relation to long-term PM, NO2 and BC exposure were restricted to males. This study supports a role of PM, BC, and NO2 in all-cause and CVD mortality independent of road traffic noise exposure

Source-Specific Air Pollution Including Ultrafine Particles and Risk of Myocardial Infarction:A Nationwide Cohort Study from Denmark

BACKGROUND: Air pollution is negatively associated with cardiovascular health. Impediments to efficient regulation include lack of knowledge about which sources of air pollution contributes most to health burden and few studies on effects of the potentially more potent ultrafine particles (UFP). OBJECTIVE: The authors aimed to investigate myocardial infarction (MI) morbidity and specific types and sources of air pollution. METHODS: We identified all persons living in Denmark in the period 2005–2017, age &gt;50 y and never diagnosed with MI. We quantified 5-y running time-weighted mean concentrations of air pollution at residencies, both total and apportioned to traffic and nontraffic sources. We evaluated particulate matter (PM) with aerodynamic diameter ≤2:5 lm (PM 2:5), &lt;0:1 lm (UFP), elemental carbon (EC), and nitrogen dioxide (NO 2). We used Cox pro-portional hazards models, with adjustment for time-varying exposures, and personal and area-level demographic and socioeconomic covariates from high-quality administrative registers. RESULTS: In this nationwide cohort of 1,964,702 persons (with 18 million person-years of follow-up and 71,285 cases of MI), UFP and PM 2:5 were associated with increased risk of MI with hazard ratios (HRs) per interquartile range (IQR) of 1.040 [95% confidence interval (CI): 1.025, 1.055] and 1.053 (95% CI: 1.035, 1.071), respectively. HRs per IQR of UFP and PM 2:5 from nontraffic sources were similar to the total (1.034 and 1.051), whereas HRs for UFP and PM 2:5 from traffic sources were smaller (1.011 and 1.011). The HR for EC from traffic sources was 1.013 (95% CI: 1.003, 1.023). NO 2 from nontraffic sources was associated with MI (HR = 1:048; 95% CI: 1.034, 1.062) but not from traffic sources. In general, nontraffic sources contributed more to total air pollution levels than national traffic sources. CONCLUSIONS: PM 2:5 and UFP from traffic and nontraffic sources were associated with increased risk of MI, with nontraffic sources being the domi-nant source of exposure and morbidity. https://doi.org/10.1289/EHP10556.</p

Five year change in alcohol intake and risk of breast cancer and coronary heart disease among postmenopausal women:prospective cohort study

Objective To test the hypothesis that postmenopausal women who increase their alcohol intake over a five year period have a higher risk of breast cancer and a lower risk of coronary heart disease compared with stable alcohol intake. Design Prospective cohort study. Setting Denmark, 1993-2012. Participants 21 523 postmenopausal women who participated in the Diet, Cancer, and Health Study in two consecutive examinations in 1993-98 and 1999-2003. Information on alcohol intake was obtained from questionnaires completed by participants. Main outcome measures Incidence of breast cancer, coronary heart disease, and all cause mortality during 11 years of follow-up. Information was obtained from the Danish Cancer Register, Danish Hospital Discharge Register, Danish Register of Causes of Death, and National Central Person Register. We estimated hazard ratios according to five year change in alcohol intake using Cox proportional hazards models. Results During the study, 1054, 1750, and 2080 cases of breast cancer, coronary heart disease, and mortality occurred, respectively. Analyses modelling five year change in alcohol intake with cubic splines showed that women who increased their alcohol intake over the five year period had a higher risk of breast cancer and a lower risk of coronary heart disease than women with a stable alcohol intake. For instance, women who increased their alcohol intake by seven or 14 drinks per week (corresponding to one or two drinks more per day) had hazard ratios of breast cancer of 1.13 (95% confidence interval 1.03 to 1.23) and 1.29 (1.07 to 1.55), respectively, compared to women with stable intake, and adjusted for age, education, body mass index, smoking, Mediterranean diet score, parity, number of births, and hormone replacement therapy. For coronary heart disease, corresponding hazard ratios were 0.89 (0.81 to 0.97) and 0.78 (0.64 to 0.95), respectively, adjusted for age, education, body mass index, Mediterranean diet score, smoking, physical activity, hypertension, elevated cholesterol, and diabetes. Results among women who reduced their alcohol intake over the five year period were not significantly associated with risk of breast cancer or coronary heart disease. Analyses of all cause mortality showed that women who increased their alcohol intake from a high intake (≥14 drinks per week) to an even higher intake had a higher mortality risk that women with a stable high intake. Conclusion In this study of postmenopausal women over a five year period, results support the hypotheses that alcohol intake is associated with increased risk of breast cancer and decreased risk of coronary heart disease