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

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

Residential exposure to PM_2.5 components and risk of childhood non-hodgkin lymphoma in Denmark:A nationwide register-based case-control study

In a recent study, we observed an increased risk of childhood non-Hodgkin lymphoma (NHL) associated with exposure to fine atmospheric particulate matter (PM2.5) and black carbon (BC). In this nationwide register-based case-control study, we focus on specific components of PM2.5 in relation to childhood NHL in Denmark (1981–2013) by identifying all incidents of childhood NHL cases in the Danish Cancer Registry (n = 170) and four (cancer-free) randomly selected controls matched by date of birth and sex. We applied PM2.5 concentrations and the following sub-components: secondary organic aerosols (SOA), secondary inorganic aerosols (SIA; i.e., NO3−, NH4+ and SO42−), BC, organic carbon (OC) and sea salt. We calculated a time-weighted exposure average from birth to index-date at all addresses. Odds ratios (ORs) were adjusted for register-based socio-demographic variables. We observed adjusted ORs and 95% confidence intervals (95% CI) of 2.05 (1.10, 3.83) per interquartile range (IQR, 4.83 µg/m3) PM2.5 and 1.73 (0.68, 4.41) per IQR (3.71 µg/m3) SIA, 0.95 (0.71, 1.29) per IQR (0.05 µg/m3) SOA, 1.22 (1.02, 1.46) per IQR (0.39 µg/m3) BC, 1.02 (0.83, 1.26) per IQR (0.56 µg/m3) OC and 1.01 (0.79, 1.30) per IQR (0.87 µg/m3) sea salt, respectively. The estimates were attenuated after adjustment for PM2.5, whereas the OR for PM2.5 remained increased regardless of adjustment for specific components. The findings indicate that the previously observed relation between PM2.5 and childhood NHL may be related to BC (as reported in our previous study) but also partly to SIA, but the role of specific chemical components of PM2.5 remains ambiguous

Components of particulate matter air-pollution and brain tumors

Background Air pollution is an established carcinogen. Evidence for an association with brain tumors is, however, inconclusive. We investigated if individual particulate matter constituents were associated with brain tumor risk. Methods From comprehensive national registers, we identified all (n = 12 928) brain tumor cases, diagnosed in Denmark in the period 1989–2014, and selected 22 961 controls, matched on age, sex and year of birth. We established address histories and estimated 10-year mean residential outdoor concentrations of particulate matter ˂ 2.5 µm, primarily emitted black carbon (BC) and organic carbon (OC), and combined carbon (OC/BC), as well as secondary inorganic and organic PM air pollutants from a detailed dispersion model. We used conditional logistic regression to calculate odds ratios (OR) per inter quartile range (IQR) exposure. We adjusted for income, marital and employment status as well as area-level socio-demographic characteristics. Results Total tumors of the brain were associated with OC/BC (OR: 1.053, 95%CI: 1.005–1.103, per IQR). The data suggested strongest associations for malignant tumors with ORs per IQR for OC/BC, BC and OC of 1.063 (95% CI: 1.007–1.123), 1.036 (95% CI: 1.006–1.067) and 1.030 (95%CI: 0.979–1.085), respectively. The results did not indicate adverse effects of other PM components. Conclusions This large, population based study showed associations between primary emitted carbonaceous particles and risk for malignant brain tumors. As the first of its kind, this study needs replication.</p

Long-term residential exposure to PM2.5 constituents and mortality in a Danish cohort

Studies on health effects of long-term exposure to specific PM2.5 constituents are few. Previous studies have reported an association between black carbon (BC) exposure and cardiovascular diseases (CVD) and a few studies have found an association between sulfate exposure and mortality. These studies, however, relied mainly on exposure data from centrally located air-monitoring stations, which is a crude approximation of personal exposure. We focused on specific chemical constituents of PM2.5, i.e. elemental and primary organic carbonaceous particles (BC/OC), sea salt, secondary inorganic aerosols (SIA, i.e. NO3–, NH4+, and SO42-), and secondary organic aerosols (SOA), in relation to all-cause, CVD and respiratory disease mortality. We followed a Danish cohort of 49,564 individuals from enrollment in 1993–1997 through 2015. We combined residential address history from 1979 onwards with mean annual air pollution concentrations obtained by the AirGIS air pollution modelling system, lifestyle information from baseline questionnaires and socio-demography obtained by register linkage. During 895,897 person-years of follow-up, 10,193 deaths from all causes occurred – of which 2319 were CVD-related and 870 were related to respiratory disease. The 15-year time-weighted average concentrations of PM2.5, BC/OC, sea salt, SIA and SOA were 13.8, 2.8, 3.4, 4.9, and 0.3 µg/m3, respectively. For all-cause mortality, a higher risk was observed with higher exposure to PM2.5, BC/OC and SOA with adjusted hazard ratios of 1.03 (95% confidence intervals: 1.01, 1.05), 1.06 (1.03, 1.09), and 1.08 (1.03, 1.13) per interquartile range, respectively. The associations for BC/OC and SOA remained after adjustment for PM2.5 in two-pollutant models. For CVD mortality, we observed elevated risks with higher exposure to PM2.5, BC/OC and SIA. The results showed no clear relationship between sea salt and mortality. In this study, we observed a relationship between long-term exposure to PM2.5, BC/OC, and SOA and all-cause mortality and between PM2.5, BC/OC, and SIA and CVD mortality.</p