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Background Long-term air pollution is a risk factor for stroke. Which types and sources of air pollution contribute most to stroke in populations is unknown. We investigated whether risk of stroke differed by type and source of air pollution. Methods We selected all persons aged >50 years and living in Denmark in the period 2005–17. We estimated running 5-year mean residential air-pollution concentrations of particulate matter <2.5 µm (PM2.5), ultrafine particles (UFP), elemental carbon (EC) and nitrogen dioxide (NO2). Pollutants were modelled as total air pollution from all emission sources, as well as apportioned into contributions from non-traffic and traffic sources. Hazard ratios (HRs) and CIs were estimated by using Cox proportional hazards models, adjusting for area-level and personal demographic and socio-economic covariates. We identified all primary strokes from hospital and mortality registers. Results The cohort numbered 2 million people and 94 256 cases of stroke. Interquartile ranges (IQR) of air pollution were associated with risk of stroke with HRs of 1.077 (95% CI: 1.061–1.094, IQR: 1.85 µg/m3) for PM2.5, 1.039 (1.026–1.052, IQR: 4248 particles/cm3) for UFP, 1.009 (1.001–1.018, IQR: 0.28 µg/m3) for EC and 1.028 (1.017–1.040, IQR: 7.15 µg/m3) for NO2. Traffic sources contributed little to the total exposure. HRs associated with air pollution from traffic were close to the null, whereas non-traffic sources tended to be associated with HRs higher than those for total air pollution, e.g. for non-traffic PM2.5, the HR was 1.091 (1.074–1.108). Conclusions Air pollution, including UFP, was associated with risk of stroke. The risk appeared attributable mainly to air pollution from non-traffic sources. [ABSTRACT FROM AUTHOR]

Particulate matter air pollution and diesel engine exhaust have been classified as carcinogenic for lung cancer, yet few studies have explored associations with liver cancer. We used six European adult cohorts which were recruited between 1985 and 2005, pooled within the "Effects of low‐level air pollution: A study in Europe" (ELAPSE) project, and followed for the incidence of liver cancer until 2011 to 2015. The annual average exposure to nitrogen dioxide (NO2), particulate matter with diameter <2.5 μm (PM2.5), black carbon (BC), warm‐season ozone (O3), and eight elemental components of PM2.5 (copper, iron, zinc, sulfur, nickel, vanadium, silicon, and potassium) were estimated by European‐wide hybrid land‐use regression models at participants' residential addresses. We analyzed the association between air pollution and liver cancer incidence by Cox proportional hazards models adjusting for potential confounders. Of 330 064 cancer‐free adults at baseline, 512 developed liver cancer during a mean follow‐up of 18.1 years. We observed positive linear associations between NO2 (hazard ratio, 95% confidence interval: 1.17, 1.02‐1.35 per 10 μg/m3), PM2.5 (1.12, 0.92‐1.36 per 5 μg/m3), and BC (1.15, 1.00‐1.33 per 0.5 10−5/m) and liver cancer incidence. Associations with NO2 and BC persisted in two‐pollutant models with PM2.5. Most components of PM2.5 were associated with the risk of liver cancer, with the strongest associations for sulfur and vanadium, which were robust to adjustment for PM2.5 or NO2. Our study suggests that ambient air pollution may increase the risk of liver cancer, even at concentrations below current EU standards. What's new? Air pollution contains a number of known carcinogens. While air pollution is classified as carcinogenic and is a known risk factor for lung cancer, the evidence for cancers in other organs is limited. In this large European study, the authors detected associations between air pollution and liver cancer incidence, even at levels that are below current EU standards. These results corroborate findings from several earlier, substantially smaller studies, and suggest that ambient air pollution may increase the risk of liver cancer. [ABSTRACT FROM AUTHOR]

Objectives Exposure to traffic noise and air pollution is suspected to increase susceptibility to viral infections -- the main triggering factor for febrile seizures. No studies have examined these two exposures in relation to febrile seizures. We aimed to investigate whether exposure to road traffic noise and air pollution are associated with risk of febrile seizures in childhood. Methods From our study base of 51 465 singletons from a national birth cohort, we identified 2175 cases with febrile seizures using a nationwide registry. Residential address history from conception to six years of age were found in national registers, and road traffic noise (Lden) and air pollution (NO2) were modeled for all addresses. Analyses were done using Cox proportional hazard model with adjustment for potential confounders, including mutual exposure adjustment. Results An interquartile range (IQR) increase in childhood exposure to road traffic noise and air pollution was associated with an 11% [incidence rate ratio (IRR) 1.11, 95% confidence interval (CI) 1.04-1.19) and 5% (IRR 1.05, 95% CI 1.02-1.07) higher risk for febrile seizures, respectively, after adjustment for potential confounders. Weaker tendencies were seen for pregnancy exposure. In models with mutual exposure adjustment, the estimates were slightly lower, with IRR of 1.08 (95% CI 1.00-1.16) and 1.03 (95% CI 0.99-1.06) per IQR increase in childhood exposure to road traffic noise and air pollution, respectively. Conclusions This study suggests that residential exposure to road traffic noise and air pollution is associated with higher risk for febrile seizures. [ABSTRACT FROM AUTHOR]

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 (L den ) 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 10 dB 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 10 dB 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. [ABSTRACT FROM AUTHOR]

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 (L den ) and air pollution (NO 2 ) were modelled for all addresses. Analyses were performed using Cox proportional hazard models. Results Road traffic noise and NO 2 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 NO 2 , respectively. Mutual exposure adjustment reduced the association with 10-year NO 2 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 NO 2 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. [ABSTRACT FROM AUTHOR]

Background & Aims: Antioxidant intake has been reported to increase the risk of colorectal cancer (CRC) for smokers, yet reduce the risk for nonsmokers. We investigated the association between tobacco smoking and risk of colon or rectal cancer, and whether dietary and supplemental intake of the antioxidant vitamins A, C, E, β-carotene, selenium, zinc, and manganese affects the risk of CRC among smokers. Methods: Data on smoking habits and antioxidant intake were analyzed for 54,208 participants in the Danish Prospective Diet, Cancer and Health Study. Of these participants, 642 were diagnosed with colon cancer and 348 were diagnosed with rectal cancer. Hazard ratios and 95% confidence intervals were estimated using Cox proportional hazard models. Principal components were used to analyze intake of combinations of antioxidants. Results: Ever smoking increased the risk for CRC (hazard ratio, 1.19; 95% confidence interval, 1.03–1.37), especially for rectal cancer. Smoking for at least 20 years was associated with a 26% increase in risk of CRC, compared with never smokers, and smoking 20 g tobacco or more each day was associated with a 30% increase in risk. Smoking for more than 30 years, or more than 20 g tobacco each day, was associated with a 48% increase in risk of rectal cancer. We did not observe an interaction between smoking and antioxidant consumption on risk of CRC. Conclusions: Tobacco smoking increases the risk for CRC. We did not observe that consumption of antioxidant micronutrients modulates the effects of smoking on CRC risk. [ABSTRACT FROM AUTHOR]

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 10 dB 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. [ABSTRACT FROM AUTHOR]

• A major reason for organic food consumption is expected beneficial health effects. • Limited evidence exists regarding associations between organic food consumption and incidence of type 2 diabetes mellitus. • Is organic food consumption associated with the incidence of type 2 diabetes mellitus? • Organic food consumption was associated with a suggested lower incidence of type 2 diabetes mellitus. • Further studies are needed to support the findings. To investigate the association between organic food consumption and the incidence of type 2 diabetes mellitus. Among 41,286 cohort participants, aged 50–65 years, organic food consumption of vegetables, fruits, dairy products, eggs, meat, and cereal products, was summarized into an organic food score evaluated as never, low, medium and high consumption and as continuous intake. During follow-up, 4,843 cases were identified in the National Diabetes Register. Organic food consumption was associated to the disease incidence in Cox regression models. Organic food consumption was linearly associated with a lower incidence of type 2 diabetes mellitus (Women, HR: 0.94, 95% CI: 0.89–1.00, Men, HR: 0.95, 95% CI: 0.90–1.00). Organic food consumption frequency, compared to never consumption, showed HRs below 1.00 for both women (medium intake HR: 0.96, 95% CI: 0.84–1.10, high intake HR: 0.88, 95% CI: 0.74–1.05) and men (low intake, HR: 0.95, 95% CI: 0.85–1.05, medium intake, HR: 0.92, 95% CI: 0.83–1.03, high intake, HR: 0.89, 95% CI: 0.75–1.05) but were not statistically significant. Similar patterns were observed with consumption of the specific organic food groups for women, but not for men. Organic food consumption was associated with a suggested lower incidence of type 2 diabetes mellitus. [ABSTRACT FROM AUTHOR]

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 (PM 2.5), ultrafine particles (UFP, <0.1 μm), elemental carbon (EC) and nitrogen dioxide (NO 2). 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). PM 2.5 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 PM 2.5 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. • Air pollution is positively associated with risk of myocardial infarction. • People of low socioeconomic status or with comorbidities are more susceptible. • Effect modification appears to be most apparent with absolute risk estimates. [ABSTRACT FROM AUTHOR]

Background Epidemiological studies have shown that intake of drinking water with high levels of arsenic (>100 μg/L) is associated with risk for cardiovascular diseases, but studies on lower levels of arsenic show inconsistent results. Objective The aim of this study was to investigate the relationship between exposure to low level arsenic in drinking water and risk of myocardial infarction in Denmark. Methods From the Danish Diet, Cancer and Health cohort of 57,053 people aged 50–64 years at enrolment in 1993–1997, we identified 2707 cases of incident myocardial infarction from enrolment to end of follow-up in February 2012. Cohort participants were enrolled in the Copenhagen and Aarhus areas. We geocoded residential addresses of the cohort members and used a geographic information system to link addresses with water supply areas. Arsenic in tap water at each cohort members address from 1973 to 2012 was estimated for all cohort members. Poisson regression was used to estimate incidence rate ratios (IRRs) for myocardial infarction after adjustment for lifestyle factors and educational level. Results Arsenic levels in drinking water at baseline addresses ranged from 0.03 to 25.34 μg/L, with the highest concentrations in the Aarhus area. We found no overall association between 20-years average concentration of arsenic and risk of myocardial infarction. However, in the Aarhus area, fourth arsenic quartile (2.21–25.34 μg/L) was associated with an IRR of 1.48 (95% confidence interval (CI): 1.19–1.83) when compared with first quartile (0.05–1.83 μg/L). An IRR of 1.26 (95% CI: 0.89–1.79) was found for ever (versus never) having lived at an address with 10 μg/L or more arsenic in the drinking water. Conclusions This study provides some support for an association between low levels of arsenic in drinking water and the risk of myocardial infarction. [ABSTRACT FROM AUTHOR]

Air pollution increases the risk of stroke, but the literature on identifying susceptible subgroups of populations is scarce and inconsistent. The aim of this study was to investigate if the association between air pollution and risk of stroke differed by sociodemographic factors, financial stress, comorbid conditions, and residential road traffic noise, population density and green space. We assessed long-term exposure to air pollution with ultrafine particles, PM 2.5 , elemental carbon and NO 2 for a cohort of 1,971,246 Danes aged 50–85 years. During follow-up from 2005 to 2017, we identified 83,211 incident stroke cases. We used Cox proportional hazards model (relative risk) and Aalen additive hazards models (absolute risk) to estimate associations and confidence intervals (CI) between 5-year running means of air pollution at the residence and risk of stroke in population strata. All four pollutants were associated with higher risk of stroke. The association between air pollution and stroke was strongest among individuals with comorbidities, with shorter education, lower income and being retired. The results also indicated stronger associations among individuals living in less populated areas, and with low noise levels and more green space around the residence. Estimates of absolute risk seemed better suited to detect such interactions than estimates of relative risk. For example for PM 2.5 the hazard ratio for stroke was 1.28 (95%CI: 1.22–1.34) and 1.26 (95%CI: 1.16–1.37) among those with mandatory and medium/long education respectively. The corresponding rate difference estimates per 100,000 person years were 568 (95%CI: 543–594) and 423(95%CI: 390–456) The associations between air pollution and risk of stroke was stronger among individuals of lower socioeconomic status or with pre-existing comorbid conditions. Absolute risk estimates were better suited to identify such effect modification. [ABSTRACT FROM AUTHOR]

Abstract: Oxidative damage to guanine (8-oxoGua) is one of the most abundant lesions induced by oxidative stress and documented mutagenic. 8-Oxoguanine DNA glycosylase 1 (OGG1) removes 8-oxoGua from DNA by excision. The urinary excretion of 8-oxoGua is a biomarker of exposure, reflecting the rate of damage in the steady state. The aim of this study was to investigate urinary 8-oxoGua as a risk factor for lung cancer. In a nested case-cohort design we examined associations between urinary excretion of 8-oxoGua and risk of lung cancer as well as potential interaction with the OGG1 Ser326Cys polymorphism in a population-based cohort of 25,717 men and 27,972 women aged 50–64years with 3–7years follow-up. We included 260 cases with lung cancer and a subcohort of 263 individuals matched on sex, age, and smoking duration for comparison. Urine collected at entry was analysed for 8-oxoGua by HPLC with electrochemical detection. There was no significant effect of smoking or OGG1 genotype on the excretion of 8-oxoGua. Overall the incidence rate ratio (IRR) (95% confidence interval) of lung cancer was 1.06 (0.97–1.15) per doubling of 8-oxoGua excretion. The association between lung cancer risk and 8-oxoGua excretion was significant among men [IRR: 1.17 (1.03–1.31)], never-smokers [IRR: 9.94 (1.04–94.7)], and former smokers [IRR: 1.19 (1.07–1.33)]. There was no significant interaction with the OGG1 genotype, although the IRR was 1.14 (0.98–1.34) among subjects homozygous for Cys326. The association between urinary 8-oxoGua excretion and lung cancer risk among former and never-smokers suggests that oxidative stress with damage to DNA is important in this group. [Copyright &y& Elsevier]

Abstract: Background: Lymphoid neoplasms are a heterogeneous group of cancers that originate in the lymphatic cells of the immune system. Several risk factors have been identified or suggested, but they all account for only a small proportion of the lymphoid neoplasm incidence. It has been hypothesised that regular exercise may modulate the immune system and thereby reduce the risk of developing the disease. Design and methods: The European Investigation into Cancer and Nutrition (EPIC) cohort consists of 521,457 adults, recruited by 23 centres in 10 European countries. The analytical cohort included 343,756 participants, with 778 non-Hodgkin lymphoma (NHL) cases (376 men and 402 women) and 690 B-cell non-Hodgkin lymphoma (B-NHL) cases (326 men and 364 women). Multivariate Cox regression models were used to calculate hazard ratios (HR) for the association between total, recreational, occupational, and household physical activity and NHL and B-NHL risk, as well as the risk for several B-NHL subtypes. Models were stratified by study centre and age at recruitment and adjusted for various potential confounding factors. Results: We found no evidence of any effect of total physical activity on NHL (adjusted p-trend=0.76 and 0.30 for men and women, respectively) and B-NHL risk (adjusted p-trend=0.99 and 0.21 for men and women, respectively) for either men or women. Also no robust results were found for B-NHL subtype analyses among men or women. Conclusions: This study provided no consistent evidence for an association between various physical activity measures and the risk of lymphoid neoplasms or any of the B-NHL subtypes. [Copyright &y& Elsevier]

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. 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 PM 2.5 and NO 2 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. We found that a 5 μg/m3 higher PM 2.5 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. 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. • Results from strictly register-based studies may be biased by unmeasured confounders. • We investigated impact of different adjustment strategies in a cohort selected randomly across Denmark. • PM 2.5 and NO 2 seemed positively associated with risk of myocardial infarction, stroke and diabetes. • Crude adjustment models produced different results than more comprehensive register-based adjustment models. • With comprehensive register-based adjustment additional adjustment for lifestyle had limited effect on risk estimates. [ABSTRACT FROM AUTHOR]

Recent reports have raised the question, whether the previously observed protective effects of high intake of fruit and vegetables on the risk of lung cancer were due to insufficient adjustment for smoking leading to residual confounding. Association of intake of fruit and vegetables on lung cancer risk was examined, using the Danish prospective cohort study, “Diet, Cancer and Health”. Participants completed a food-frequency and lifestyle questionnaire, and age-standardized incidence rates and rate ratios were estimated for quartiles of dietary exposure. In 1993–2001, 247 out of the 54 158 participants were diagnosed with lung cancer. The incidence rate of lung cancer was highest in the lowest quartile of intake of plant food (fruit, vegetables, legumes and potatoes) and the age-standardized rate ratio of lung cancer decreased significantly with increasing intake of plant food to 0.35 (95% CI, 0.27–0.45) but after control for smoking it was attenuated to 0.65 (95% CI, 0.45–0.93). The incidence rate differences of current smokers with high (≥400 g per day) and low (<400 g per day) daily intake of plant food were independent of smoking intensity; assuming a true biological protective effect, 80–90 lung cancer cases per 100 000 current smokers could be prevented in our cohort if all smokers had a high intake of plant food. The observed inverse association between high intakes of plant food seems chiefly to be a real protective effect, and not solely due to residual confounding. [Copyright &y& Elsevier]