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Background: The association between long-term exposure to air pollution and mortality from cardiorespiratory diseases is well established, yet the evidence for other diseases remains limited. Objectives: To examine the associations of long-term exposure to air pollution with mortality from diabetes, dementia, psychiatric disorders, chronic kidney disease (CKD), asthma, acute lower respiratory infection (ALRI), as well as mortality from all-natural and cardiorespiratory causes in the Danish nationwide administrative cohort. Methods: We followed all residents aged ≥ 30 years (3,083,227) in Denmark from 1 January 2000 until 31 December 2017. Annual mean concentrations of fine particulate matter (PM2.5), nitrogen dioxide (NO2), black carbon (BC), and ozone (warm season) were estimated using European-wide hybrid land-use regression models (100 m × 100 m) and assigned to baseline residential addresses. We used Cox proportional hazard models to evaluate the association between air pollution and mortality, accounting for demographic and socioeconomic factors. We additionally applied indirect adjustment for smoking and body mass index (BMI). Results: During 47,023,454 person-years of follow-up, 803,881 people died from natural causes. Long-term exposure to PM2.5 (mean: 12.4 µg/m3), NO2 (20.3 µg/m3), and/or BC (1.0 × 10-5/m) was statistically significantly associated with all studied mortality outcomes except CKD. A 5 µg/m3 increase in PM2.5 was associated with higher mortality from all-natural causes (hazard ratio 1.11; 95% confidence interval 1.09–1.13), cardiovascular disease (1.09; 1.07–1.12), respiratory disease (1.11; 1.07–1.15), lung cancer (1.19; 1.15–1.24), diabetes (1.10; 1.04–1.16), dementia (1.05; 1.00–1.10), psychiatric disorders (1.38; 1.27–1.50), asthma (1.13; 0.94–1.36), and ALRI (1.14; 1.09–1.20). Associations with long-term exposure to ozone (mean: 80.2 µg/m3) were generally negative but became significantly positive for several endpoints in two-pollutant models. Generally, associations were attenuated but remained significant after indirect adjustment for smoking and BMI. Conclusion: Long-term exposure to PM2.5, NO2, and/or BC in Denmark were associated with mortality beyond cardiorespiratory diseases, including diabetes, dementia, psychiatric disorders, asthma, and ALRI. © 2022 The Authors

Background: Recent epidemiological studies investigating the modifying effect of air temperature in ozone-mortality associations lack consensus as how to adjust for nonlinear and lagged temperature effect in addition to including an interaction term. Methods: We evaluated the influence of temperature confounding control on temperature-stratified ozone-mortality risks in a time series setting in eight European cities and 86 US cities, respectively. To investigate potential residual confounding, we additionally incorporated next day's ozone in models with differing temperature control. Results: Using only a categorical variable for temperature or only controlling nonlinear effect of low temperatures yielded highly significant ozone effects at high temperatures but also significant residual confounding in both regions. Adjustment for nonlinear effect of temperature, especially high temperatures, substantially reduced ozone effects at high temperatures and residual confounding. Conclusions: Inadequate control for confounding by air temperature leads to residual confounding and an overestimation of the temperature-modifying effect in studies of ozone-related mortality. © 2018 The Authors. Published by Wolters Kluwer Health

Background: Bulky DNA adducts are markers of exposure to genotoxic aromatic compounds, which reflect the ability of an individual to metabolically activate carcinogens and to repair DNA damage. Polycyclic aromatic hydrocarbons (PAHs) represent a major class of carcinogens that are capable of forming such adducts. Factors that have been reported to be related to DNA adduct levels include smoking, diet, body mass index (BMI), genetic polymorphisms, the season of collection of biologic material, and air pollutants. Methods: We pooled 11 studies (3,600 subjects) in which bulky DNA adducts were measured in human white blood cells with similar 32P-postlabeling techniques and for which a similar set of variables was available, including individual data on age, gender, ethnicity, batch, smoking habits, BMI, and season of blood collection, and a limited set of gene variants. Results: Lowest DNA adduct levels (P = 0.006) were observed in the spring (median = 0.50 adducts per 108 nucleotides), followed by summer (0.64), autumn (0.70), and winter (0.85). The same pattern emerged in multivariate analysis but only among never smokers (P = 0.02). Adduct levels were significantly lower (P = 0.001) in northern Europe (the Netherlands and Denmark; mean = 0.60, median = 0.40) than in southern Europe (Italy, Spain, France, and Greece; mean = 0.79, median = 0.60). Conclusions: In this large pooled analysis, we have found only weak associations between bulky DNA adducts and exposure variables. Seasonality (with higher adducts levels in winter) and air pollution may partly explain some of the interarea differences (north vs. south Europe), but most inter-area and interindividual variations in adduct levels still remain unexplained. Impact: Our study describes the largest pooled analysis of bulky DNA adducts so far, showing that interindividual variation is still largely unexplained, though seasonality seems to play a role. Cancer Epidemiol Biomarkers Prev; 19(12); 3174–81. ©2010 AACR.

This project (KoL 12-08) was performed for the Climate and Air Quality Group (KlimaogLuftgruppen, KoL), Nordic Council of Ministers by atmospheric emission, exposureand epidemiology experts from Denmark, Finland, Norway and Sweden. Emission inventory methods and exposure models were presented. A list of carcinogenic andco-carcinogenic pollutants (particles, heavy metals and organic compounds) emittedfrom energy production, industrial activities, road transport, navigation, agriculture, residential heating and product use was compiled. Pollutant emissions levels for 2010and trends for 1990 to 2010 were compiled and discussed, and modelled andmeasured atmospheric concentrations for 2010 were compiled on regional, urbanand local scales. Nordic maps of emissions and air concentrations of PM2.5, PM10, NOx,NMVOC, benzene, BaP, dioxin, cadmium and nickel were compiled for allaggregated main sources, traffic and residential wood combustion. An overview of local studies on exposure for cities or communities with emphasis on wood combustion and traffic and a discussion of existing epidemiological studies on cancer and environment were given

Bulky DNA adducts are biomarkers of exposure to aromatic compounds and of the ability of the individual to metabolically activate carcinogens and to repair DNA damage. Their ability to predict cancer onset is uncertain. We have performed a pooled analysis of three prospective studies on cancer risk in which bulky DNA adducts have been measured in blood samples collected from healthy subjects (N = 1947; average follow-up 51-137 months). In addition, we have performed a meta-analysis by identifying all articles on the same subject published up to the end of 2006, including case-control studies. In the pooled analysis, a weakly statistically significant increase in the risk of lung cancer was apparent (14% per unit standard deviation change in adduct levels, 95% confidence interval 1-28%; using the weighted mean difference method, 0.15 SD, units higher adducts in cases than in controls). The association was evident only in current smokers and was absent in former smokers. Also the meta-analysis, which included both lung and bladder cancers, showed a statistically significant association in current smokers, whereas the results in never smokers were equivocal; in former smokers, no association was detected. The results of our pooled and meta-analyses suggest that bulky DNA adducts are associated with lung cancer arising in current smokers after a follow-up of several years. European Union (FOOD-CT-2005-513943) (WP4-8) to Environmental Cancer Risk, nutrition and individual susceptibility Network of Excellence (EC CONTRACT Food-CT-2005-513943).