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Background: Prolonged exposure to air pollution has been linked to adverse respiratory health, yet the evidence concerning its association with chronic obstructive pulmonary disease (COPD) is inconsistent. The evidence of a greenness effect on chronic respiratory diseases is limited., Objective: This study aimed to investigate the association between long-term exposure to particulate matter (PM 2.5 and PM 10 ), black carbon (BC), nitrogen dioxide (NO 2 ), ozone (O 3 ) and greenness (as measured by the normalized difference vegetation index - NDVI) and incidence of self-reported chronic bronchitis or COPD (CB/COPD)., Methods: We analyzed data from 5355 adults from 7 centers participating in the Respiratory Health in Northern Europe (RHINE) study. Mean exposures to air pollution and greenness were assessed at available residential addresses in 1990, 2000 and 2010 using air dispersion models and satellite data, respectively. Poisson regression with log person-time as an offset was employed to analyze the association between air pollution, greenness, and CB/COPD incidence, adjusting for confounders., Results: Overall, there were 328 incident cases of CB/COPD during 2010-2023. Despite wide statistical uncertainty, we found a trend for a positive association between NO 2 exposure and CB/COPD incidence, with incidence rate ratios (IRRs) per 10 μg/m³ difference ranging between 1.13 (95% CI: 0.90-1.41) in 1990 and 1.18 (95% CI: 0.96-1.45) in 2000. O 3 showed a tendency for inverse association with CB/COPD incidence (IRR from 0.84 (95% CI: 0.66-1.07) in 2000 to 0.88 (95% CI: 0.69-1.14) in 2010. No consistent association was found between PM, BC and greenness with CB/COPD incidence across different exposure time windows., Conclusion: Consistent with prior research, our study suggests that individuals exposed to higher concentrations of NO 2 may face an elevated risk of developing COPD, although evidence remains inconclusive. Greenness was not associated with CB/COPD incidence, while O 3 showed a tendency for an inverse association with the outcome., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Objectives: The association between air pollution and risk of respiratory tract infection (RTI) in adults needs to be clarified in settings with low to moderate levels of air pollution. We investigated this in the Danish population between 2004 and 2016., Methods: We included 3 653 490 persons aged 18-64 years in a nested case-control study. Exposure was defined as the average daily concentration at the individual's residential address of CO, NO X , NO 2 , O 3 , SO 2 , NH 3 , PPM 2.5 , black carbon, organic carbon, mineral dust, sea salt, secondary inorganic aerosols, SO 4 2- , NO 3 - , NH 4 + , secondary organic aerosols, PM 2.5 , and PM 10 during a 3-month exposure window. RTIs were defined by hospitalization for RTIs. Incidence rate ratios (IRRs) and 95% CIs were estimated comparing highest with lowest decile of exposure using conditional logistic regression models., Results: In total, 188 439 incident cases of RTI were identified. Exposure to most air pollutants was positively associated with risk of RTI. For example, NO 2 showed an IRR of 1.52 (CI: 1.48-1.55), and PM 2.5 showed an IRR of 1.45 (CI: 1.40-1.50). In contrast, exposure to sea salt, PM 10 , NH 3 , and O 3 was negatively associated with a risk of RTIs., Discussion: In this nationwide study comprising adults, exposure to air pollution was associated with risk of RTIs and subgroups hereof. Sea salt, PM 10 , NH 3 , and O 3 may be proxies for rural areas, as the levels of these species in Denmark are higher near the western coastlines and/or in rural areas with fewer combustion sources., (Copyright © 2023 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Air pollution has been linked to mortality, but there are few studies examining the association with different exposure time windows spanning across several decades. The evidence for the effects of green space and mortality is contradictory., Objective: We investigated all-cause mortality in relation to exposure to particulate matter (PM 2.5 and PM 10 ), black carbon (BC), nitrogen dioxide (NO 2 ), ozone (O 3 ) and greenness (normalized difference vegetation index - NDVI) across different exposure time windows., Methods: The exposure assessment was based on a combination of the Danish Eulerian Hemispheric Model and the Urban Background Model for the years 1990, 2000 and 2010. The analysis included a complete case dataset with 9,135 participants from the third Respiratory Health in Northern Europe study (RHINE III), aged 40-65 years in 2010, with mortality follow-up to 2021. We performed Cox proportional hazard models, adjusting for potential confounders., Results: Altogether, 327 (3.6 %) persons died in the period 2010-2021. Increased exposures in 1990 of PM 2.5 , PM 10 , BC and NO 2 were associated with increased all-cause mortality hazard ratios of 1.40 (95 % CI1.04-1.87 per 5 μg/m 3 ), 1.33 (95 % CI: 1.02-1.74 per 10 μg/m 3 ), 1.16 (95 % CI: 0.98-1.38 per 0.4 μg/m 3 ) and 1.17 (95 % CI: 0.92-1.50 per 10 μg/m 3 ), respectively. No statistically significant associations were observed between air pollution and mortality in other time windows. O 3 showed an inverse association with mortality, while no association was observed between greenness and mortality. Adjusting for NDVI increased the hazard ratios for PM 2.5 , PM 10 , BC and NO 2 exposures in 1990. We did not find significant interactions between greenness and air pollution metrics., Conclusion: Long term exposure to even low levels of air pollution is associated with mortality. Opening up for a long latency period, our findings indicate that air pollution exposures over time may be even more harmful than anticipated., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Air pollution is a significant contributor to the global burden of disease with a plethora of associated health effects such as pulmonary and systemic inflammation. C-reactive protein (CRP) is associated with a wide range of diseases and is associated with several exposures. Studies on the effect of air pollution exposure on CRP levels in low to moderate pollution settings have shown inconsistent results. In this cross-sectional study high sensitivity CRP measurements on 18,463 Danish blood donors were linked to modelled air pollution data for NO x , NO 2 , O 3 , CO, SO 2 , NH 3 , mineral dust, black carbon, organic carbon, sea salt, secondary inorganic aerosols and its components, primary PM 2.5 , secondary organic aerosols, total PM 2.5 , and total PM 10 at their residential address over the previous month. Associations were analysed using ordered logistic regression with CRP quartile as individuals outcome and air pollution exposure as scaled deciles. Analyses were adjusted for health related and socioeconomic covariates using health questionnaires and Danish register data. Exposure to different air pollution components was generally associated with higher CRP (odds ratio estimates ranging from 1.11 to 1.67), while exposure to a few air pollution components was associated with lower CRP. For example, exposure to NO 2 increased the odds of high CRP 1.32-fold (95%CI 1.16-1.49), while exposure to NH3 decreased the odds of high CRP 0.81-fold (95%CI 0.73-0.89). This large study among healthy individuals found air pollution exposure to be associated with increased levels of CRP even in a setting with low to moderate air pollution levels., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests:Co-author is chairman of Zealand Regional Committee on Health Research Ethics - Ole Birger Pedersen., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Air pollution with particulate matter is an established lung carcinogen. Studies have suggested an association with breast cancer, but the evidence is inconsistent., Methods: From nationwide registers, we identified all breast cancer cases (n = 55 745) in Denmark between 2000 and 2014. We matched one control for each case on age and year of birth. We used a multi-scale dispersion model to estimate outdoor concentrations of particulate matter <2.5 μm (PM 2.5 ), elemental carbon (EC) and nitrogen dioxide (NO 2 ) as time-weighted average over all addresses up to 20 years prior to diagnosis. We calculated odds ratios (OR) and 95% confidence intervals (CI) by conditional logistic regression with adjustment for marital status, educational level, occupational status, personal income, region of origin, medication and area-level socio-economic indicators., Results: A 10 μg/m 3 higher PM 2.5 was associated with an OR for breast cancer of 1.21 (95% CI: 1.11-1.33). The corresponding ORs for EC (per 1 μg/m 3 ) and NO 2 (per 10 μg/m 3 ) were 1.03 (95% CI: 1.00-1.07) and 1.03 (95% CI: 1.01-1.06), respectively. In multi-pollutant models, the OR for PM 2.5 changed only little, whereas ORs for EC or NO 2 approached the null. In an analysis of persons below 55 years, PM 2.5 was associated with an OR of 1.32 (95% CI: 1.09-1.60) per 10 μg/m 3 increase., Conclusion: We found evidence of an association between the investigated air pollutants and breast cancer, especially PM 2.5 . There were indications that the association differed by age at diagnosis. We were not able to include all potential confounders and thus, results should be interpreted with caution., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Joergen Brandt reports financial support was provided by NordForsk., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: Ambient fine particulate matter (PM 2.5 ) causes millions of deaths every year worldwide. Identification of the most harmful types of PM 2.5 would facilitate efficient prevention strategies., Objectives: The aim of this study was to investigate associations between components of PM 2.5 and mortality in a nation-wide Danish population., Methods: Our study base was Danes born 1921-1985 and aged 30-85 years, who were followed up for mortality from 1991 to 2015. We included 678,465 natural cause mortality cases and selected five age, sex and calendar time matched controls to each case from the study base. We retrieved the address history of the study population from Danish registries and assessed five-year average concentrations of eight PM 2.5 components using deterministic Chemistry-Transport Models air pollution models. We estimated mortality rate ratios (MRRs) by conditional logistic regression and adjusted for socio-demographical factors at individual and neighborhood level., Results: Single pollutant models showed the strongest associations between natural cause mortality and an interquartile increase in sulfate particles (SO 4 - - ) (MRR: 1.123; 95 % CI: 1.100-1.147 per 1.5 µg/m 3 ) and secondary organic aerosol (SOA) (MRR: 1.054; 95 % CI: 1.048-1.061 per 0.050 µg/m 3 ). Two-pollutant models showed robust associations between SO 4 - - and SOA and natural cause mortality. Elemental carbon and mineral dust showed robust associations with higher respiratory and lung cancer mortality., Conclusion: This nation-wide study found robust associations between natural cause mortality and SO 4 - - particles and SOA, which is in line with the results of previous studies. Elemental carbon and mineral dust showed robust associations with higher respiratory and lung cancer mortality., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

We used the EVAv6.0 system to estimate the present (2015) and future (2015-2050) global PM 2.5 and O 3 -related premature mortalities, using simulated surface concentrations from the GISS-E2.1-G Earth system model. The PM 2.5 -related global premature mortality is estimated to be 4.3 and 4.4 million by the non-linear and linear models, respectively. Ischemic heart diseases are found to be the leading cause of PM 2.5 -related premature deaths, contributing by 35% globally. Both long-term and short-term O 3 -related premature deaths are estimated to be around 1 million, globally. Overall, PM 2.5 and O 3 -related premature mortality leads to 5.3-5.4 million premature deaths, globally. The global burden of premature deaths is mainly driven by the Asian region, which in 2015 contributes by 75% of the total global premature deaths. An increase from 6.2% to 8% in the PM 2.5 relative risk as recommended by the WHO leads to an increase of PM 2.5 -related premature mortality by 28%, to 5.7 million. Finally, bias correcting the simulated PM 2.5 concentrations in 2015 leads to an increase of up to 73% in the global PM 2.5 -related premature mortality, leading to a total number of global premature deaths of up to 7.7 million, implying the necessity of bias correction to get more robust health burden estimates. PM 2.5 and O 3 -related premature mortality in 2050 decreases by up to 57% and 18%, respectively, due to emission reductions alone. However, the projected increase and aging of the population leads to increases of premature mortality by up to a factor of 2, showing that the population exposed to air pollution is more important than the level of air pollutants, highlighting that the population dynamics should be considered when setting up health assessment systems., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.)

Background: Only few epidemiological studies have investigated whether chronic exposure to air pollution from different sources have different impacts on risk of diabetes. We aimed to investigate associations between air pollution from traffic versus non-traffic sources and risk of type 2 diabetes in the Danish population., Methods: We estimated long-term exposure to traffic and non-traffic contributions of particulate matter with a diameter <2.5 µg (PM2.5), elemental carbon (EC), ultrafine particles (UFP) and nitrogen dioxide (NO2) for all persons living in Denmark for the period 2005-17. In total, 2.6 million persons aged >35 years were included, of whom 148 020 developed type 2 diabetes during follow-up. We applied Cox proportional hazards models for analyses, using 5-year time-weighted running means of air pollution and adjustment for individual- and area-level demographic and socioeconomic covariates., Results: We found that 5-year exposure to all particle measures (PM2.5, UFP and EC) and NO2 were associated with higher type 2 diabetes risk. We observed that for UFP, EC and potentially PM2.5, the pollution originating from traffic was associated with higher risks than the non-traffic contributions, whereas for NO2 similar hazard ratios (HR) were observed. For example, in two-source models, hazard ratios (HRs) per interquartile change in traffic UFP, EC and PM2.5 were 1.025, 1.045 and 1.036, respectively, whereas for non-traffic UFP, EC and PM2.5, the HRs were 1.013, 1.018 and 1.001, respectively., Conclusions: Our finding of stronger associations with particulate matter from traffic compared with non-traffic sources implies that prevention strategies should focus on limiting traffic-related particulate matter air pollution., (© The Author(s) 2022; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Background: The provision of different types of mortality metrics (e.g., mortality rate ratios [MRRs] and life expectancy) allows the research community to access a more informative set of health metrics. The aim of this study was to provide a panel of mortality metrics associated with a comprehensive range of disorders and to design a web page to visualize all results., Methods and Findings: In a population-based cohort of all 7,378,598 persons living in Denmark at some point between 2000 and 2018, we identified individuals diagnosed at hospitals with 1,803 specific categories of disorders through the International Classification of Diseases-10th Revision (ICD-10) in the National Patient Register. Information on date and cause of death was obtained from the Registry of Causes of Death. For each of the disorders, a panel of epidemiological and mortality metrics was estimated, including incidence rates, age-of-onset distributions, MRRs, and differences in life expectancy (estimated as life years lost [LYLs]). Additionally, we examined models that adjusted for measures of air pollution to explore potential associations with MRRs. We focus on 39 general medical conditions to simplify the presentation of results, which cover 10 broad categories: circulatory, endocrine, pulmonary, gastrointestinal, urogenital, musculoskeletal, hematologic, mental, and neurologic conditions and cancer. A total of 3,676,694 males and 3,701,904 females were followed up for 101.7 million person-years. During the 19-year follow-up period, 1,034,273 persons (14.0%) died. For 37 of the 39 selected medical conditions, mortality rates were larger and life expectancy shorter compared to the Danish general population. For these 37 disorders, MRRs ranged from 1.09 (95% confidence interval [CI]: 1.09 to 1.10) for vision problems to 7.85 (7.77 to 7.93) for chronic liver disease, while LYLs ranged from 0.31 (0.14 to 0.47) years (approximately 16 weeks) for allergy to 17.05 (16.95 to 17.15) years for chronic liver disease. Adjustment for air pollution had very little impact on the estimates; however, a limitation of the study is the possibility that the association between the different disorders and mortality could be explained by other underlying factors associated with both the disorder and mortality., Conclusions: In this study, we show estimates of incidence, age of onset, age of death, and mortality metrics (both MRRs and LYLs) for a comprehensive range of disorders. The interactive data visualization site (https://nbepi.com/atlas) allows more fine-grained analysis of the link between a range of disorders and key mortality estimates., Competing Interests: I have read the journal’s policy and the authors of this manuscript have the following competing interests: JWD has been involved in projects funded by the Novo Nordisk Foundation (NNF16OC0019126), The Central Denmark Region, and the Danish Epilepsy Association during the conduct of this study.

Background: Exposure to outdoor air pollution is associated with adverse health effects. Previous studies have indicated higher levels of air pollution in socially deprived areas., Aim: To investigate associations between air pollution and socio-demographic variables, comorbidity, stress, and green space at the residence in Denmark., Methods: We included 2,237,346 persons living in Denmark, aged 35 years or older in 2017. We used the high resolution, multi-scale DEHM/UBM/AirGIS air pollution modelling system to calculate mean concentrations of air pollution with PM 2.5 , elemental carbon, ultrafine particles and NO 2 at residences held the preceding five years. We used nationwide registries to retrieve information about socio-demographic indicators at the individual and neighborhood levels. We used general linear regression models to analyze associations between socio-demographic indicators and air pollution at the residence., Results: Individuals with high SES (income, higher white-collar worker and high educational level) and of non-Danish origin were exposed to higher levels of air pollution than individuals of low SES and of Danish origin, respectively. We found comparable levels of air pollution according to sex, stress events and morbidity. For neighborhood level SES indicators, we found high air pollution levels in neighborhoods with low SES measured as proportion of social housing, sole providers, low income and unemployment. In contrast, we found higher air pollution levels in neighborhoods with higher educational level and a low proportion of manual labor. People living in an apartment and/or with little green space had higher air pollution levels., Conclusion: In Denmark, high levels of residential air pollution were associated with higher individual SES and non-Danish origin. For neighborhood-level indicators of SES, no consistent pattern was observed. These results highlight the need for analyzing many different socio-demographic indicators to understand the complex associations between SES and exposure to air pollution., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Background: While air pollution has been linked to the development of chronic obstructive pulmonary disease (COPD), evidence on the role of environmental noise is just emerging. We examined the associations of long-term exposure to air pollution and road traffic noise with COPD incidence., Methods: We defined COPD incidence for 24 538 female nurses from the Danish Nurse Cohort (age >44 years) as the first hospital contact between baseline (1993 or 1999) and 2015. We estimated residential annual mean concentrations of particulate matter with an aerodynamic diameter <2.5 µm (PM 2.5 ) since 1990 and nitrogen dioxide (NO 2 ) since 1970 using the Danish Eulerian Hemispheric Model/Urban Background Model/Air Geographic Information System modelling system, and road traffic noise (L den ) since 1970 using the Nord2000 model. Time-varying Cox regression models were applied to assess the associations of air pollution and road traffic noise with COPD incidence., Results: 977 nurses developed COPD during a mean of 18.6 years' follow-up. We observed associations with COPD for all three exposures with HRs and 95% CIs of 1.19 (1.01-1.41) per 6.26 µg·m -3 for PM 2.5 , 1.13 (1.05-1.20) per 8.19 µg·m -3 for NO 2 and 1.15 (1.06-1.25) per 10 dB for L den . Associations with NO 2 and L den attenuated slightly after mutual adjustment, but were robust to adjustment for PM 2.5 . Associations with PM 2.5 were attenuated to null after adjustment for either NO 2 or L den . No potential interaction effect was observed between air pollutants and noise., Conclusion: Long-term exposure to air pollution, especially traffic-related NO 2 , and to road traffic noise were independently associated with COPD., Competing Interests: Conflict of interest: S. Liu has nothing to disclose. Conflict of interest: Y-H. Lim has nothing to disclose. Conflict of interest: M. Pedersen has nothing to disclose. Conflict of interest: J.T. Jørgensen has nothing to disclose. Conflict of interest: H. Amini has nothing to disclose. Conflict of interest: T. Cole-Hunter has nothing to disclose. Conflict of interest: A.J. Mehta has nothing to disclose. Conflict of interest: R. So has nothing to disclose. Conflict of interest: L.H. Mortensen has nothing to disclose. Conflict of interest: R.G.J. Westendorp has nothing to disclose. Conflict of interest: S. Loft has nothing to disclose. Conflict of interest: E.V. Bräuner has nothing to disclose. Conflict of interest: M. Ketzel has nothing to disclose. Conflict of interest: O. Hertel has nothing to disclose. Conflict of interest: J. Brandt has nothing to disclose. Conflict of interest: S.S. Jensen has nothing to disclose. Conflict of interest: J.H. Christensen has nothing to disclose. Conflict of interest: T. Sigsgaard has nothing to disclose. Conflict of interest: C. Geels has nothing to disclose. Conflict of interest: L.M. Frohn has nothing to disclose. Conflict of interest: M. Brborić has nothing to disclose. Conflict of interest: J. Radonić has nothing to disclose. Conflict of interest: M. Turk Sekulic has nothing to disclose. Conflict of interest: K. Bønnelykke has nothing to disclose. Conflict of interest: C. Backalarz has nothing to disclose. Conflict of interest: M.K. Simonsen has nothing to disclose. Conflict of interest: Z.J. Andersen has nothing to disclose., (Copyright ©The authors 2021. For reproduction rights and permissions contact permissions@ersnet.org.)

A growing body of evidence indicates that exposure to air pollution not only impacts on physical health but is also linked with a deterioration in mental health. We conducted the first study to investigate exposure to ambient particulate matter with an aerodynamic diameter of less than 2.5 μm (PM 2.5 ) and nitrogen dioxide (NO 2 ) during childhood and subsequent self-harm risk. The study cohort included persons born in Denmark between January 1, 1979 and December 31, 2006 (N = 1,424,670), with information on daily exposures to PM 2.5 and NO 2 at residence from birth to 10th birthday. Follow-up began from 10th birthday until first hospital-presenting self-harm episode, death, or December 31, 2016, whichever came first. Incidence rate ratios estimated by Poisson regression models revealed a dose relationship between increasing PM 2.5 exposure and rising self-harm risk. Exposure to 17-19 μg/m 3 of PM 2.5 on average per day from birth to 10th birthday was associated with a 1.45 fold (95% CI 1.37-1.53) subsequently elevated self-harm risk compared with a mean daily exposure of <13 μg/m 3 , whilst those exposed to 19 μg/m 3 or above on average per day had a 1.59 times (1.45-1.75) elevated risk. Higher mean daily exposure to NO 2 during childhood was also linked with increased self-harm risk, but the dose-response relationship observed was less evident than for PM 2.5 . Covariate adjustment attenuated the associations, but risk remained independently elevated. Although causality cannot be assumed, these novel findings indicate a potential etiological involvement of ambient air pollution in the development of mental ill health., (Copyright © 2021. Published by Elsevier Inc.)

Introduction: Asthma is a complex, heterogeneous disease and one of the most common chronic diseases among children. Exposure to ambient air pollution in early life and childhood may influence asthma aetiology, but it is uncertain which specific components of air pollution and exposure windows are of importance. The role of socio-economic status (SES) is also unclear. The aims of the present study are, therefore, to investigate how various exposure windows of different pollutants affect risk-induced asthma in early life and to explore the possible effect SES has on that relationship., Methods: The study population was constructed using register data on all singleton births in the greater Stockholm area between 2006 and 2013. Exposure to ambient black carbon (BC), fine particulate matter (PM 2.5 ), primary organic carbon (pOC) secondary organic aerosols (SOA), secondary inorganic aerosols, and oxidative potential at the residential address was modelled as mean values for the entire pregnancy period, the first year of life and the first three years of life. Swedish national registers were used to define the outcome: asthma diagnosis assessed at hospital during the first six years of life. Hazard ratios (HRs) and their 95% confidence intervals (CIs) were modelled with Cox proportional hazards model with age as the underlying time-scale, adjusting for relevant potential confounding variables., Results: An increased risk for developing childhood asthma was observed in association with exposure to PM 2.5 , pOC and SOA during the first three years of life. With an interquartile range increase in exposure, the HRs were 1.06 (95% CI: 1.01-1.10), 1.05 (95% CI: 1.02-1.09) and 1.02 (95% CI: 1.00-1.04), for PM 2.5 , pOC and SOA, respectively, in the fully adjusted models. Exposure during foetal life or the first year of life was not associated with asthma risk, and the other pollutants were not statistically significantly associated with increased risk. Furthermore, the increase in risk associated with PM 2.5 and the components BC, pOC and SOA were stronger in areas with lower SES., Conclusion: Our results suggest that exposure to air pollution during the first three years of life may increase the risk for asthma in early childhood. The findings further imply a possible increased vulnerability to air pollution-attributed asthma among low SES children., (Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Purpose: The etiology of Hodgkin lymphoma (HL) is obscure. Research on air pollution and risk of HL provides inconsistent results. We aimed to investigate the association between long-term residential exposure to air pollution and risk of adult Hodgkin lymphoma in Denmark., Methods: We performed a nationwide register-based case-control study, including all (n = 2,681) Hodgkin lymphoma cases registered in the nationwide Danish Cancer Registry between 1989 and 2014. We randomly selected 8,853 age- and sex-matched controls from the entire Danish population using the Civil Registration System, and identified 20-year residential address history for all cases and controls. We modeled outdoor air pollution concentrations at all these addresses using the high-resolution multiscale air pollution model system DEHM/UBM/AirGIS. We used conditional logistic regression to estimate odds ratios adjusted for individual and neighborhood level sociodemographic variables., Results: There was no association between 1, 5, 10, and 20 years' time-weighted average exposure to fine particles (PM 2.5 ), O 3 , SO 2, NO 2, or the PM 2.5 constituents OC, NH 4 , NO 3 , and SO 4 and risk of Hodgkin lymphoma., Conclusion: Residential exposure to ambient air pollution does not seem to increase the risk of developing Hodgkin lymphoma., (© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)

This study aims to estimate the mortality risk associated with air pollution in a Swedish cohort with relatively low exposure. Air pollution models were used to estimate annual mean concentrations of particulate matter with aerodynamic diameter ≤ 2.5 µm (PM 2.5 ), primary emitted carbonaceous particles (BC/pOC), sea salt, chemically formed particles grouped as secondary inorganic and organic aerosols (SIA and SOA) as well as ozone (O 3 ) and nitrogen dioxide (NO 2 ). The exposure, as a moving average was calculated based on home address for the time windows 1 year (lag 1), 1-5 years (lag 1-5) and 1-10 years (lag 1-10) preceding the death. During the study period, 1151 cases of natural mortality, 253 cases of cardiovascular disease (CVD) mortality and 113 cases of respiratory and lung cancer mortality were observed during 369,394 person-years of follow-up. Increased natural mortality was observed in association with NO 2 (3% [95% CI -8-14%] per IQR) and PM 2.5 (2% [95% CI -5-9%] for an IQR increase) and its components, except for SOA where a decreased risk was observed. Higher risk increases were observed for CVD mortality (e.g., 18% [95% CI 1-39%] per IQR for NO 2 ). These findings at low exposure levels are relevant for future decisions concerning air quality policies.

Background: Associations between long-term exposure to air pollution and road traffic noise have been established for ischemic heart disease, but findings have been mixed for atrial fibrillation (AF)., Objectives: The goal of the study was to examine associations of long-term exposure to road traffic noise and air pollution with AF., Methods: Time-varying Cox regression models were used to estimate associations of 1-, 3-, and 23-y mean road traffic noise and air pollution exposures with AF incidence in 23,528 women enrolled in the Danish Nurse Cohort (age > 44 y at baseline in 1993 or 1999). AF diagnoses were ascertained via the Danish National Patient Register. Annual mean weighted 24-h average road traffic noise levels ( L den ) at the nurses' residences, since 1970, were estimated using the Nord2000 model, and annual mean levels of particulate matter with a diameter < 2.5 μ m ( PM 2.5 ) and nitrogen dioxide ( NO 2 ) were estimated using the DEHM/UBM/AirGIS model., Results: Of 23,528 nurses with no prior AF diagnosis at the cohort baseline, 1,522 developed AF during follow-up. In a fully adjusted model (including PM 2.5 ), the estimated risk of AF was 18% higher [hazard ratio (HR); 95% confidence interval (CI): 1.18; 1.02, 1.36] in nurses with residential 3-y mean L den levels > 58  dB vs. < 48  dB , with similar findings for 1-y mean exposures. A 3.9 - μ g / m 3 increase in 3-y mean PM 2.5 was associated with incident AF before and after adjustment for concurrent exposure to road traffic noise (HR 1.09; 95% CI: 1.00, 1.20 and 1.08; 95% CI: 0.97, 1.19, respectively). Associations with 1-y mean PM 2.5 exposures were positive but closer to the null and not significant. Associations with NO 2 were null for all time periods before and after adjustment for road traffic noise and inverse when adjusted for concurrent PM 2.5 ., Conclusion: Our analysis of prospective data from a cohort of Danish female nurses followed for up to 14 y provided suggestive evidence of independent associations between incident AF and 1- and 3-y exposures to road traffic noise and PM 2.5 . https://doi.org/10.1289/EHP8090.

The World Health Organization estimates that around 7 million people die every year from exposure to fine particles (PM 2.5 ) inpolluted air. Here, the number of premature deaths in Europe from different diseases associated to the ambient exposure to PM 2.5 have here been studied both for present (1991-2010) and future periods (2031-2050, RCP8.5 scenario). This contribution combines different state-of-the-art approaches (use of high-resolution climate/chemistry simulations over Europe for providing air quality data; use of different baseline mortality data for specific European regions; inclusion of future population projections and dynamical changes for 2050 obtained from the United Nations (UN) Population Projections or use of non-linear exposure-response functions) to estimate the premature mortality due to PM 2.5 . The mortality endpoints included in this study are Lung Cancer (LC), Chronic Obstructive Pulmonary Disease (COPD), Cerebrovascular Disease (CEV), Ischemic Heart Disease (IHD), Lower Respiratory Infection (LRI) and other Non-Communicable Diseases (other NCDs). Different risk ratio and baseline mortalities for each disease end each age range have been estimated individually. The results indicate that the annual excess mortality rate from fine particulate matter in Europe is 904,000 [95% confidence interval (95% CI) 733,100-1,067,800], increasing by 73% in 2050s (1,560,000; 95% CI 1,260,000-1,840,000); meanwhile population decreases from 808 to 806 million according to the UN estimations. The results show that IHD is the main cause of premature mortality in Europe associated to PM 2.5 (around 48%) both for the present and future periods. Despite several marked regional differences, premature deaths associated to all the endpoints included in this study will increase in the future period due to the climate penalty but especially because of changes in the population projected and its aging., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Ambient air pollution is likely a risk factor for asthma, and recent evidence suggests the possible relevance of road traffic noise., Objectives: We examined the associations of long-term exposure to air pollution and road traffic noise with adult-asthma incidence., Methods: We followed 28,731 female nurses (age > 44 years) from the Danish Nurse Cohort, recruited in 1993 and 1999, for first hospital contact for asthma from 1977 until 2015. We estimated residential annual mean concentrations of particulate matter with diameter < 2.5 µm (PM 2.5 ) since 1990 and nitrogen dioxide (NO 2 ) since 1970 with the Danish DEHM/UBM/AirGIS modeling system, and road traffic noise (L den ) since 1970 with the Nord2000 model. Time-varying Cox regression models were used to associate air pollution and road traffic noise exposure with asthma incidence., Results: During 18.6 years' mean follow-up, 528 out of 23,093 participants had hospital contact for asthma. The hazard ratios (HR) and 95% confidence intervals for asthma incidence associated with 3-year moving average exposures were 1.29 (1.03, 1.61) per 6.3 µg/m 3 for PM 2.5 , 1.16 (1.07, 1.27) per 8.2 µg/m 3 for NO 2 , and 1.12 (1.00, 1.25) per 10 dB for L den . The HR for NO 2 remained unchanged after adjustment for either PM 2.5 or L den , while the HRs for PM 2.5 and L den attenuated to unity after adjustment for NO 2 ., Conclusions: Long-term exposure to air pollution was associated with adult-asthma incidence independently of road traffic noise, with NO 2 most relevant. Road traffic noise was not independently associated with adult-asthma incidence., (Copyright © 2021. Published by Elsevier Ltd.)

Background: Leukemia is one of the most common forms of hematologic malignancy, which can affect people of all ages. We previously showed an association between exposure to ambient particulate matter 2.5 μg (PM 2.5 ) and risk for leukemia in adults. The aim of this study was to investigate which PM 2.5 constituents were responsible for our previous observation., Methods: This is a nationwide register-based case-control study. We identified 14,983 persons diagnosed with leukemia at age 20 or above, 1989-2014, in the Danish Cancer Registry. We selected up to four sex and age-matched controls per case at random from the entire Danish population (n = 51,613). We modelled concentrations of ambient PM 2.5 and its constituents at the addresses of cases and controls for the 10-year period before index date with a state-of-the-art multiscale air pollution modeling system. We used conditional logistic regression to estimate odds ratios (ORs) adjusted for individual and neighborhood level socio-demographic variables., Result: The results showed higher risk for overall leukemia in association with interquartile range exposure to PM 2.5 (OR = 1.09; 95% CI: 1.02, 1.17), black carbon (BC) (OR = 1.02; 95% CI: 1.00, 1.03), secondary inorganic aerosols (SIA) (OR = 1.15; 95% CI: 1.03, 1.29) and its components ammonium (NH 4 ) (OR = 1.08; 95% CI: 1.00, 1.17) and nitrate (NO 3 ) (OR = 1.08; 95% CI: 1.02, 1.14). In leukemia subtype analysis, statistically significant associations were found for AML with PM 2.5 (OR = 1.14; 95% CI: 1.00, 1.29), BC (OR = 1.03; 95% CI: 1.00, 1.07), SIA (OR = 1.23; 95% CI: 1.01, 1.51), NH 4 (OR = 1.16; 95% CI: 1.01, 1.34) and NO 3 (OR = 1.12; 95% CI: 1.01, 1.24). The association between PM 2.5 and leukemia persisted in two pollutants models including sum of primary emitted black and organic carbon (BC + OC), secondary organic aerosols (SOA), or sea-salt. The association between black carbon (BC) and leukemia persisted in two pollutants models including organic carbon (OC). The three pollutant model with sulfate (SO 4 ), NH 4 and NO 3 showed an association with NO 3 but not with SO 4 or NH 4 ., Conclusion: Ambient concentrations of the PM 2.5 components BC, NH 4 and NO 3 at the residence showed associations with risk of incident leukemia in adults., (Copyright © 2020 Elsevier Inc. All rights reserved.)

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 (PM 2.5 ), black carbon (BC), nitrogen dioxide (NO 2 ) and ozone (O 3 ) 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 PM 2.5 prior to diagnosis (e.g. OR per 10 µg/m 3 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/m 3 for 10-year average: 1.35, 95% CI: 1.15-1.58). Null findings for younger participants. Higher 1-year average PM 2.5 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 PM 2.5 concentrations averaged over 1, 5 and 10 years prior to diagnosis.

In a recent study, we observed an increased risk of childhood non-Hodgkin lymphoma (NHL) associated with exposure to fine atmospheric particulate matter (PM 2.5 ) and black carbon (BC). In this nationwide register-based case-control study, we focus on specific components of PM 2.5 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 PM 2.5 concentrations and the following sub-components: secondary organic aerosols (SOA), secondary inorganic aerosols (SIA; i.e., NO 3 - , NH 4 + and SO 4 2- ), 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/m 3 ) PM 2.5 and 1.73 (0.68, 4.41) per IQR (3.71 µg/m 3 ) SIA, 0.95 (0.71, 1.29) per IQR (0.05 µg/m 3 ) SOA, 1.22 (1.02, 1.46) per IQR (0.39 µg/m 3 ) BC, 1.02 (0.83, 1.26) per IQR (0.56 µg/m 3 ) OC and 1.01 (0.79, 1.30) per IQR (0.87 µg/m3) sea salt, respectively. The estimates were attenuated after adjustment for PM 2.5 , whereas the OR for PM 2.5 remained increased regardless of adjustment for specific components. The findings indicate that the previously observed relation between PM 2.5 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 PM 2.5 remains ambiguous.

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., (Copyright © 2020. Published by Elsevier Ltd.)

There is limited evidence regarding a possible association between exposure to ambient air pollutants and the risk of non-Hodgkin lymphoma (NHL). Previous epidemiological studies have relied on crude estimations for air pollution exposure and/or small numbers of NHL cases. The objective of our study was to analyze this association based on air pollution modeled at the address level and NHL cases identified from the nationwide Danish Cancer Registry. We identified 20,874 incident NHL cases diagnosed between 1989 and 2014 and randomly selected 41,749 controls matched on age and gender among the entire Danish population. We used conditional logistic regression to estimate odds ratios (ORs) and adjusted for individual and neighborhood level sociodemographic variables. There was no association between exposure to PM 2.5 , BC, O 3 , SO 2 or NO 2 and overall risk of NHL but several air pollutants were associated with higher risk of follicular lymphoma, but statistically insignificant, for example, PM 2.5 (OR = 1.15 per 5 μg/m 3 ; 95% CI: 0.98-1.34) and lower risk for diffuse large B-cell lymphoma (OR = 0.92 per 5 μg/m 3 ; 95% CI: 0.82-1.03). In this population-based study, we did not observe any convincing evidence of a higher overall risk for NHL with higher exposure to ambient air pollutants., (© 2020 UICC.)

Background: The association between air pollution and mortality is well established, yet some uncertainties remain: there are few studies that account for road traffic noise exposure or that consider in detail the shape of the exposure-response function for cause-specific mortality outcomes, especially at low-levels of exposure., Objectives: We examined the association between long-term exposure to particulate matter [(PM) with a diameter of <2.5 µm (PM 2.5 ), <10 µm (PM 10 )], and nitrogen dioxide (NO 2 ) and total and cause-specific mortality, accounting for road traffic noise., Methods: We used data on 24,541 females (age > 44 years) from the Danish Nurse Cohort, who were recruited in 1993 or 1999, and linked to the Danish Causes of Death Register for follow-up on date of death and its cause, until the end of 2013. Annual mean concentrations of PM 2.5, PM 10, and NO 2 at the participants' residences since 1990 were estimated using the Danish DEHM/UBM/AirGIS dispersion model, and annual mean road traffic noise levels (L den ) were estimated using the Nord2000 model. We examined associations between the three-year running mean of PM 2.5 , PM 10 , and NO 2 with total and cause-specific mortality by using time-varying Cox Regression models, adjusting for individual characteristics and residential road traffic noise., Results: During the study period, 3,708 nurses died: 843 from cardiovascular disease (CVD), 310 from respiratory disease (RD), and 64 from diabetes. In the fully adjusted models, including road traffic noise, we detected associations of three-year running mean of PM 2.5 with total (hazard ratio; 95% confidence interval: 1.06; 1.01-1.11), CVD (1.14; 1.03-1.26), and diabetes mortality (1.41; 1.05-1.90), per interquartile range of 4.39 μg/m 3 . In a subset of the cohort exposed to PM 2.5  < 20 µg/m 3 , we found even stronger association with total (1.19; 1.11-1.27), CVD (1.27; 1.01-1.46), RD (1.27; 1.00-1.60), and diabetes mortality (1.44; 0.83-2.48). We found similar associations with PM 10 and none with NO 2 . All associations were robust to adjustment for road traffic noise., Discussion: Long-term exposure to low-levels of PM 2.5 and PM 10 is associated with total mortality, and mortality from CVD, RD, and diabetes. Associations were even stronger at the PM 2.5 levels below EU limit values and were independent of road traffic noise., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Particulate matter (PM) air pollution is a complex mixture and the various PM constituents likely affect health differently. The literature on the relationships among specific PM constituents and the risk of cancer is sparse. In this study, we aimed to evaluate the association of PM 2.5 and its constituents with the incidence of non-Hodgkin lymphoma (NHL) and the two main NHL subtypes., Methods: We undertook a nationwide register-based case-control study including 20,847 cases registered in the Danish Cancer Registry with NHL between 1989 and 2014. Among the entire Danish population, we selected 41,749 age and sex-matched controls randomly from the Civil Registration System. We assessed modelled outdoor PM concentrations at addresses of cases and controls with a state-of-the-art multi scale air pollution modelling system and used conditional logistic regression to estimate odds ratios (ORs) adjusted for individual and neighborhood level socio-demographic variables., Results: The 10-year time-weighted average concentrations of PM 2.5 , primary carbonaceous particles (BC/OC), secondary inorganic aerosols (SIA), secondary organic aerosols (SOA) and sea salt were 17.4, 2.3, 7.8, 0.3, and 4.1 μg/m 3 , respectively among controls. The results showed higher risk for NHL in association with exposure to BC/OC (OR = 1.03; 95% CI: 1.00, 1.07, per interquartile range (IQR)) and SOA (OR = 1.54; 95% CI: 1.13, 2.09, per IQR). The results indicated a higher risk for follicular lymphoma in association with several PM components. Including PM 2.5 (OR = 1.16; 95% CI: 0.98-1.38), BC/OC (OR = 1.05; 95% CI: 0.97-1.14), SIA (OR = 1.44; 95% CI: 0.80-1.08), SOA (OR = 4.52; 95% CI: 0.86-23.83) per IQR., Conclusion: This is the first study on PM constituents and the risk of NHL. The results indicated an association with primary carbonaceous and secondary organic PM. The results need replication in other settings before any firm conclusion can be reached., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Natural environments have been associated with mental health benefits worldwide. However, how different elements and types of natural environments associate with mental health is still largely unknown. In this study, we perform a detailed analysis on a large, nation-wide data set of mental health records (908 553 individuals) for Denmark combined with remotely-sensed land cover and vegetation density data. We explore associations between growing up surrounded by different environments and rates of a spectrum of 18 psychiatric disorders. Childhood land cover exposure for urban, agricultural, near-natural green space, and blue space was determined around the residence of each individual. Vegetation density and air pollution were evaluated as potential pathways. Cox proportional hazards models were used to estimate rates as hazard ratios and then adjusted for potential confounding from other known risk factors. For 12 of 18 disorders, rates were lower for children growing up in environments with more natural elements (near-natural green space, blue space, and agriculture) compared to children growing up in urban environments. High vegetation density was associated with lower rates for most disorders within all the examined environments, whereas mitigation of air pollution by natural environments seemed a less important potential pathway. Rates were not notably changed by adjustment for urbanization, parental and municipal socioeconomic status, family history of mental illness, and parents' age. In conclusion, we found that growing up surrounded by a range of natural environments such as near-natural green space, blue space, and agriculture may lower rates of psychiatric disorders. Our results show the importance of ensuring access to natural environments from as nature-based solutions for improved public health and sustainable, livable cities., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Ambient air pollution has been linked to stroke, but few studies have examined in detail stroke subtypes and confounding by road traffic noise, which was recently associated with stroke. Here we examined the association between long-term exposure to air pollution and incidence of stroke (overall, ischemic, hemorrhagic), adjusting for road traffic noise. In a nationwide Danish Nurse Cohort consisting of 23,423 nurses, recruited in 1993 or 1999, we identified 1,078 incident cases of stroke (944 ischemic and 134 hemorrhagic) up to December 31, 2014, defined as first-ever hospital contact. The full residential address histories since 1970 were obtained for each participant and the annual means of air pollutants (particulate matter with diameter < 2.5 µm and < 10 µm (PM 2.5 and PM 10 ), nitrogen dioxide (NO 2 ), nitrogen oxides (NOx)) and road traffic noise were determined using validated models. Time-varying Cox regression models were used to estimate hazard ratios (HR) (95% confidence intervals (CI)) for the associations of one-, three, and 23-year running mean of air pollutants with stroke adjusting for potential confounders and noise. In fully adjusted models, the HRs (95% CI) per interquartile range increase in one-year running mean of PM 2.5 and overall, ischemic, and hemorrhagic stroke were 1.12 (1.01-1.25), 1.13 (1.01-1.26), and 1.07 (0.80-1.44), respectively, and remained unchanged after adjustment for noise. Long-term exposure to ambient PM 2.5 was associated with the risk of stroke independent of road traffic noise., Competing Interests: Declaration of Competing Interest The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article., (Copyright © 2020 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Exposure to air pollution in early life has been linked to cognitive deficits and adverse neurodevelopmental effects. However, studies examining associations between air pollutants and Attention-Deficit/Hyperactivity Disorder (ADHD) have had conflicting findings., Methods: Individuals born in Denmark 1992-2007 (n = 809,654) were followed for the development of ADHD from 1997 to 2013. Data on daily concentrations of nitrogen dioxide (NO 2 ) and fine particulate matter (PM 2.5 ) from air-modeling data at a 1 km × 1 km resolution at residences within the first five years of life, was linked with population-based data from the Danish national registers, including data on clinical diagnoses of ADHD. We estimated incidence rate ratios (IRRs) with 95% confidence intervals (CI) for ADHD, according to increases in exposures, adjusting for age, year, sex, and parental education and income., Results: Exposure to NO 2 and PM 2.5 during early life was associated with a significantly increased risk of ADHD: IRR of 1.38 (Cl: 1.35 to 1.42) per 10 μg/m 3 increase in NO 2 and an IRR of 1.51 (Cl: 1.41 to 1.62) per 5 μg/m 3 increase in PM 2.5 . In two-pollutant models, the association between NO 2 and ADHD did not change (IRR 1.35; 95% CI: 1.31 to 1.39), while the association with PM 2.5 was substantially attenuated (IRR 1.07; 95% CI: 0.98 to 1.16), although in stratified models an elevated association with PM 2.5 was found in the lowest quintile of NO 2 exposure., Conclusions: In this large nationwide prospective cohort study, residential air pollution exposure, specifically NO 2 , during early childhood was associated with the development of ADHD, even when adjusted for parental level of income and education., Competing Interests: Declaration of competing interest None., (Copyright © 2019 Elsevier Inc. All rights reserved.)

High exposure to green space and natural environments has previously been associated with lower schizophrenia rates possibly through low air pollution and improved psychological restoration. Exposure to natural environments could explain the negative urban-rural gradient of schizophrenia, but it is unclear if all natural environments are associated with schizophrenia rates. We investigated the association between schizophrenia and growing up surrounded by environments classified as mainly urban, agricultural, near-natural green space, and blue space. Vegetation density and air pollution were assessed as potential pathways. We used the Danish population (943 027 people) and remotely-sensed environmental data to determine land cover exposure and vegetation density around each individual's residence. Effect sizes were estimated using Cox regression and adjusted for air pollution, socioeconomic status, and urbanization. Our results show that growing up surrounded by non-urban environments is associated with lower schizophrenia rates. Firstly, growing up surrounded by non-built-up areas (agricultural areas, near-natural green and blue space) is associated with lower schizophrenia rates compared to urban areas. Secondly, rates decrease with vegetation density in a dose-response relationship for urban and agricultural areas. Air pollution mitigation more strongly explained the protective association in near-natural green spaces, implying that restorative pathways together with air pollution mitigation may explain lower rates in natural environments. This study suggests that ensuring access to natural environments during childhood may be important for schizophrenia prevention, whilst being the first study to show that natural environments may influence schizophrenia rates through multiple pathways., Competing Interests: Declaration of competing interest All authors declare that they have no conflict of interest., (Copyright © 2019 Elsevier B.V. All rights reserved.)

Background: Ambient air pollution affects neurological function, but its association with schizophrenia risk is unclear. We investigated exposure to nitrogen oxides (NO X ) as a whole and nitrogen dioxide (NO 2 ) specifically, as well as PM 10 , and PM 2·5 , during childhood and subsequent schizophrenia risk., Methods: People born in Denmark from 1980 to 1984 (N=230 844), who were residing in the country on their tenth birthday, and who had two Danish-born parents were followed-up from their tenth birthday until schizophrenia diagnosis or Dec 31, 2016. Mean daily exposure to each pollutant (NO 2 , NO X , PM 10 , and PM 2·5 ) at all of an individual's residential addresses from birth to their tenth birthday was modelled. Incidence rate ratios, cumulative incidence, and population attributable risks were calculated using survival analysis techniques., Findings: We analysed data between Aug 1, 2018, and Nov 15, 2019. Of 230 844 individuals included, 2189 cohort members were diagnosed with schizophrenia during follow-up. Higher concentrations of residential NO 2 and NO X exposure during childhood were associated with subsequent elevated schizophrenia risk. People exposed to daily mean concentrations of more than 26·5 μg/m 3 NO 2 had a 1·62 (95% CI 1·41-1·87) times increased risk compared with people exposed to a mean daily concentration of less than 14·5 μg/m 3 . The absolute risks of developing schizophrenia by the age of 37 years when exposed to daily mean concentrations of more than 26·5 μg/m 3 NO 2 between birth and 10 years were 1·45% (95% CI 1·30-1·62%) for men and 1·03% (0·90-1·17) for women, whereas when exposed to a mean daily concentration of less than 14·5 μg/m 3 , the risk was 0·80% (95% CI 0·69-0·92%) for men and 0·67% (0·57-0·79) for women. Associations between exposure to PM 2·5 or PM 10 and schizophrenia risk were less consistent., Interpretation: If the association between air pollution and schizophrenia is causal, reducing ambient air pollution including NO 2 and NO X could have a potentially considerable effect on lowering schizophrenia incidence at the population level. Further investigations are necessary to establish a causal relationship., Funding: Lundbeck Foundation, Stanley Medical Research Institute, European Research Council, NordForsk, Novo Nordisk Foundation, National Health and Medical Research Council, Danish National Research Foundation., (Copyright © 2020 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Existing descriptions of bi-directional ammonia (NH3) land-atmosphere exchange incorporate temperature and moisture controls, and are beginning to be used in regional chemical transport models. However, such models have typically applied simpler emission factors to upscale the main NH3 emission terms. While this approach has successfully simulated the main spatial patterns on local to global scales, it fails to address the environment- and climate-dependence of emissions. To handle these issues, we outline the basis for a new modelling paradigm where both NH3 emissions and deposition are calculated online according to diurnal, seasonal and spatial differences in meteorology. We show how measurements reveal a strong, but complex pattern of climatic dependence, which is increasingly being characterized using ground-based NH3 monitoring and satellite observations, while advances in process-based modelling are illustrated for agricultural and natural sources, including a global application for seabird colonies. A future architecture for NH3 emission-deposition modelling is proposed that integrates the spatio-temporal interactions, and provides the necessary foundation to assess the consequences of climate change. Based on available measurements, a first empirical estimate suggests that 5°C warming would increase emissions by 42 per cent (28-67%). Together with increased anthropogenic activity, global NH3 emissions may increase from 65 (45-85) Tg N in 2008 to reach 132 (89-179) Tg by 2100.