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Background: Residential wood combustion (RWC) is one of the largest sources of fine particles (PM 2.5 ) in the Nordic cities. The current study aims to calculate the related health effects in four studied city areas in Sweden, Finland, Norway, and Denmark., Methods: Health impact assessment (HIA) was employed as the methodology to quantify the health burden. Firstly, the RWC induced annual average PM 2.5 concentrations from local sources were estimated with air pollution dispersion modelling. Secondly, the baseline mortality rates were retrieved from the national health registers. Thirdly, the concentration-response function from a previous epidemiological study was applied. For the health impact calculations, the WHO-developed tool AirQ + was used., Results: Amongst the studied city areas, the local RWC induced PM 2.5 concentration was lowest in the Helsinki Metropolitan Area (population-weighted annual average concentration 0.46 µg m - 3 ) and highest in Oslo (2.77 µg m - 3 ). Each year, particulate matter attributed to RWC caused around 19 premature deaths in Umeå (95% CI: 8-29), 85 in the Helsinki Metropolitan Area (95% CI: 35-129), 78 in Copenhagen (95% CI: 33-118), and 232 premature deaths in Oslo (95% CI: 97-346). The average loss of life years per premature death case was approximately ten years; however, in the whole population, this reflects on average a decrease in life expectancy by 0.25 (0.10-0.36) years. In terms of the relative contributions in cities, life expectancy will be decreased by 0.10 (95% CI: 0.05-0.16), 0.18 (95% CI: 0.07-0.28), 0.22 (95% CI: 0.09-0.33) and 0.63 (95% CI: 0.26-0.96) years in the Helsinki Metropolitan Area, Umeå, Copenhagen and Oslo respectively. The number of years of life lost was lowest in Umeå (172, 95% CI: 71-260) and highest in Oslo (2458, 95% CI: 1033-3669)., Conclusions: All four Nordic city areas have a substantial amount of domestic heating, and RWC is one of the most significant sources of PM 2.5 . This implicates a substantial predicted impact on public health in terms of premature mortality. Thus, several public health measures are needed to reduce the RWC emissions., (© 2022. The Author(s).)

Aims: To estimate the overall health impact of transferring commuting trips from car to bicycle., Methods: In this study registry information on the location of home and work for residents in Stockholm County was used to obtain the shortest travel route on a network of bicycle paths and roads. Current modes of travel to work were based on travel survey data. The relation between duration of cycling and distance cycled was established as a basis for selecting the number of individuals that normally would drive a car to work, but have a distance to work that they could bicycle within 30 minutes. The change in traffic flows was estimated by a transport model (LuTrans) and effects on road traffic injuries and fatalities were estimated by using national hospital injury data. Effects on air pollution concentrations were modelled using dispersion models., Results: Within the scenario, 111,000 commuters would shift from car to bicycle. On average the increased physical activity reduced the one-year mortality risk by 12% among the additional bicyclists. Including the number of years lost due to morbidity, the total number of disability adjusted life-years gained was 696. The amount of disability adjusted life-years gained in the general population due to reduced air pollution exposure was 471. The number of disability adjusted life-years lost by traffic injuries was 176. Also including air pollution effects among bicyclists, the net benefit was 939 disability adjusted life-years per year., Conclusions: Large health benefits were estimated by transferring commuting by car to bicycle.

The old Swedish city Visby, located on the island Gotland, has, for several years, reported higher PM 10 concentrations than any other city in Sweden. In Visby, local limestone is used, both in road paving and as sand used for anti-slip measures, resulting in a clear annual pattern of PM 10 with the highest concentrations during winter/spring when studded tires are allowed. This study analyzes the short-term associations between PM 10 and daily number of patients with acute respiratory problems (ICD-10 diagnoses: J00-J99) seeking care at the hospital or primary healthcare units in Visby during the period of 2013-2019. The daily mean of PM 10 was on average 45 µg m -3 during winter/spring and 18 µg m -3 during summer/autumn. Four outcome categories were analyzed using quasi-Poisson regression models, stratifying for period and adjusting for calendar variables and weather. An increase in respiratory visits was associated with increasing concentrations in PM 10 during the summer/autumn period, most prominent among children, where asthma visits increased by 5% (95% CI: 2-9%) per 10 µg m -3 increase in PM 10 . For the winter/spring period, no significant effects were observed, except for the diagnose group 'upper airways' in adults, where respiratory visits increased by 1% (95% CI: 0.1-1.9%) per 10 µg m -3 increase. According to the results, limestone in particles seem to be relatively harmless at the exposure concentrations observed in Visby, and this is in line with the results from a few experimental and occupational studies.

Background: Increased mortality risk is associated with short-term temperature variability. However, to our knowledge, there has been no comprehensive assessment of the temperature variability-related mortality burden worldwide. In this study, using data from the MCC Collaborative Research Network, we first explored the association between temperature variability and mortality across 43 countries or regions. Then, to provide a more comprehensive picture of the global burden of mortality associated with temperature variability, global gridded temperature data with a resolution of 0·5° × 0·5° were used to assess the temperature variability-related mortality burden at the global, regional, and national levels. Furthermore, temporal trends in temperature variability-related mortality burden were also explored from 2000-19., Methods: In this modelling study, we applied a three-stage meta-analytical approach to assess the global temperature variability-related mortality burden at a spatial resolution of 0·5° × 0·5° from 2000-19. Temperature variability was calculated as the SD of the average of the same and previous days' minimum and maximum temperatures. We first obtained location-specific temperature variability related-mortality associations based on a daily time series of 750 locations from the Multi-country Multi-city Collaborative Research Network. We subsequently constructed a multivariable meta-regression model with five predictors to estimate grid-specific temperature variability related-mortality associations across the globe. Finally, percentage excess in mortality and excess mortality rate were calculated to quantify the temperature variability-related mortality burden and to further explore its temporal trend over two decades., Findings: An increasing trend in temperature variability was identified at the global level from 2000 to 2019. Globally, 1 753 392 deaths (95% CI 1 159 901-2 357 718) were associated with temperature variability per year, accounting for 3·4% (2·2-4·6) of all deaths. Most of Asia, Australia, and New Zealand were observed to have a higher percentage excess in mortality than the global mean. Globally, the percentage excess in mortality increased by about 4·6% (3·7-5·3) per decade. The largest increase occurred in Australia and New Zealand (7·3%, 95% CI 4·3-10·4), followed by Europe (4·4%, 2·2-5·6) and Africa (3·3, 1·9-4·6)., Interpretation: Globally, a substantial mortality burden was associated with temperature variability, showing geographical heterogeneity and a slightly increasing temporal trend. Our findings could assist in raising public awareness and improving the understanding of the health impacts of temperature variability., Funding: Australian Research Council, Australian National Health & Medical Research Council., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

An unmet need for inguinal hernia repair is significant in Ghana where the number of specialist general surgeons is extremely limited. While surgical task sharing with medical doctors without formal specialist training in surgery has been adopted for inguinal hernia repair in Ghana, no prior research has been conducted on the long-term costs and health outcomes associated with expanding operations to repair all inguinal hernias among adult males in Ghana. The study aimed to estimate cost-effectiveness of elective open mesh repair performed by medical doctors and surgeons for adult males with primary inguinal hernia compared to no treatment in Ghana and to project costs and health gains associated with expanding operation services through task sharing between medical doctors and surgeons. The study analysis adopted a healthcare system perspective. A Markov model was constructed to assess 10-year differences in costs and outcomes between operations conducted by medical doctors or surgeons and no treatment. A 10-year budget impact analysis on service expansion for groin hernia repair through increasing task sharing between the providers was conducted. Incremental cost-effectiveness ratios for medical doctors and surgeons were USD 120 and USD 129 respectively per disability-adjusted life year (DALY) averted compared to no treatment, which are below the estimated threshold value for cost-effectiveness in Ghana of USD 371-491. Repairing all inguinal hernias (1.4 million) through task sharing between the providers in the same timeframe is estimated to cost USD 194 million. Total health gains of 1.5 million DALYs averted are expected. Inguinal hernia repair is cost-effective regardless of the type of surgical provider. Scaling up of inguinal hernia repair is worthwhile, with the potential to substantially reduce the disease burden in the country., Competing Interests: The authors declare that there is no conflict of interest., (Copyright: © 2022 Thet Lwin et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Studies have investigated the effects of heat and temperature variability (TV) on mortality. However, few assessed whether TV modifies the heat-mortality association. Data on daily temperature and mortality in the warm season were collected from 717 locations across 36 countries. TV was calculated as the standard deviation of the average of the same and previous days' minimum and maximum temperatures. We used location-specific quasi-Poisson regression models with an interaction term between the cross-basis term for mean temperature and quartiles of TV to obtain heat-mortality associations under each quartile of TV, and then pooled estimates at the country, regional, and global levels. Results show the increased risk in heat-related mortality with increments in TV, accounting for 0.70% (95% confidence interval [CI]: -0.33 to 1.69), 1.34% (95% CI: -0.14 to 2.73), 1.99% (95% CI: 0.29-3.57), and 2.73% (95% CI: 0.76-4.50) of total deaths for Q1-Q4 (first quartile-fourth quartile) of TV. The modification effects of TV varied geographically. Central Europe had the highest attributable fractions (AFs), corresponding to 7.68% (95% CI: 5.25-9.89) of total deaths for Q4 of TV, while the lowest AFs were observed in North America, with the values for Q4 of 1.74% (95% CI: -0.09 to 3.39). TV had a significant modification effect on the heat-mortality association, causing a higher heat-related mortality burden with increments of TV. Implementing targeted strategies against heat exposure and fluctuant temperatures simultaneously would benefit public health., Competing Interests: The authors declare no competing interests., (© 2022 The Author(s).)

Migratory species are the most important commercial fishes in the Amazon. They are also now the most threatened directly by some combination of overfishing, floodplain deforestation, and dam construction. Limited governmental monitoring and implemented regulations impede adequate management of the fisheries at adequate scale. We summarize the current stock status of the three most heavily exploited long-distance migratory species, which are two goliath catfishes (Brachyplatystoma rousseauxii and B. vaillantii) and the characiform Colossoma macropomum. In addition, we analyze impacts beyond overfishing on these species. Our results indicate: (i) the overfishing trends for these important species are either ominous or indicate the verge of collapse of the commercial fisheries based on them, and (ii) a dangerous synergy between overfishing, hydroelectric dams, and floodplain deforestation further challenge fisheries management of migratory species in the Amazon. We propose eight direct governmental actions as a proactive approach that addresses the main impacts on the fisheries. We consider that the most practical way to assess and manage overfishing of migratory species in the short run in an area as large as the main commercial fishing area in the Amazon is at market sites where enforced regulations can control fish catch. The management of the three species considered here has implications beyond just their sustainability. Their management would represent a paradigm shift where the governments assume their legal responsibilities in fishery management. These responsibilities include regulation enforcement, data collecting, inter-jurisdictional cooperation to protect migratory species at realistic life history scales, mitigation of the Madeira dams to assure goliath catfish passage to the largest western headwater region, and recognition of monitoring and managing wetland deforestation for the protection of fish and other aquatic and terrestrial biodiversity., Competing Interests: The authors have declared that no competing interests exist.

Background: The association between fine particulate matter (PM2.5) and mortality widely differs between as well as within countries. Differences in PM2.5 composition can play a role in modifying the effect estimates, but there is little evidence about which components have higher impacts on mortality., Methods: We applied a 2-stage analysis on data collected from 210 locations in 16 countries. In the first stage, we estimated location-specific relative risks (RR) for mortality associated with daily total PM2.5 through time series regression analysis. We then pooled these estimates in a meta-regression model that included city-specific logratio-transformed proportions of seven PM2.5 components as well as meta-predictors derived from city-specific socio-economic and environmental indicators., Results: We found associations between RR and several PM2.5 components. Increasing the ammonium (NH4+) proportion from 1% to 22%, while keeping a relative average proportion of other components, increased the RR from 1.0063 (95% confidence interval [95% CI] = 1.0030, 1.0097) to 1.0102 (95% CI = 1.0070, 1.0135). Conversely, an increase in nitrate (NO3-) from 1% to 71% resulted in a reduced RR, from 1.0100 (95% CI = 1.0067, 1.0133) to 1.0037 (95% CI = 0.9998, 1.0077). Differences in composition explained a substantial part of the heterogeneity in PM2.5 risk., Conclusions: These findings contribute to the identification of more hazardous emission sources. Further work is needed to understand the health impacts of PM2.5 components and sources given the overlapping sources and correlations among many components., Competing Interests: The authors report no conflicts of interest., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Long-term air pollution exposure increases the risk for cardiovascular disease, but little is known about the temporal relationships between exposure and health outcomes. This study aims to estimate the exposure-lag response between air pollution exposure and risk for ischemic heart disease (IHD) and stroke incidence by applying distributed lag non-linear models (DLNMs). Annual mean concentrations of particles with aerodynamic diameter less than 2.5 µm (PM 2.5 ) and black carbon (BC) were estimated for participants in five Swedish cohorts using dispersion models. Simultaneous estimates of exposure lags 1-10 years using DLNMs were compared with separate year specific (single lag) estimates and estimates for lag 1-5- and 6-10-years using moving average exposure. The DLNM estimated no exposure lag-response between PM 2.5 total, BC, and IHD. However, for PM 2.5 from local sources, a 20% risk increase per 1 µg/m 3 for 1-year lag was estimated. A risk increase for stroke was suggested in relation to lags 2-4-year PM 2.5 and BC, and also lags 8-9-years BC. No associations were shown in single lag models. Increased risk estimates for stroke in relation to lag 1-5- and 6-10-years BC moving averages were observed. Estimates generally supported a greater contribution to increased risk from exposure windows closer in time to incident IHD and incident stroke.

Background: Fractional exhaled nitric oxide (FeNO) is a well-known marker of type-2 inflammation. FeNO is elevated in asthma and allergic rhinitis, with IgE sensitization as a major determinant., Objective: We aimed to see whether there was an independent association between upper airway inflammatory disorders (UAID) and FeNO, after adjustment for asthma and sensitization, in a multi-centre population-based study., Methods: A total of 741 subjects with current asthma and 4155 non-asthmatic subjects participating in the second follow-up of the European Community Respiratory Health Survey (ECRHS III) underwent FeNO measurements. Sensitization status was based on measurement of IgE against airborne allergens; information on asthma, UAID and medication was collected through interview-led questionnaires. Independent associations between UAID and FeNO were assessed in adjusted multivariate regression models and test for interaction with perennial sensitization and asthma on the relation between UAID and FeNO were made., Results: UAID were associated with higher FeNO after adjusting for perennial sensitization, asthma and other confounders: with 4.4 (0.9-7.9) % higher FeNO in relation to current rhinitis and 4.8 (0.7-9.2) % higher FeNO in relation to rhinoconjunctivitis. A significant interaction with perennial sensitization was found in the relationship between current rhinitis and FeNO (p = .03) and between rhinoconjunctivitis and FeNO (p = .03). After stratification by asthma and perennial sensitization, the association between current rhinitis and FeNO remained in non-asthmatic subjects with perennial sensitization, with 12.1 (0.2-25.5) % higher FeNO in subjects with current rhinitis than in those without., Conclusions & Clinical Relevance: Current rhinitis and rhinoconjunctivitis was associated with higher FeNO, with an interaction with perennial sensitization. This further highlights the concept of united airway disease, with correlations between symptoms and inflammation in the upper and lower airways and that sensitization needs to be accounted for in the relation between FeNO and rhinitis., (© 2021 The Authors. Clinical & Experimental Allergy published by John Wiley & Sons Ltd.)

Background: The premenstrual syndrome (PMS) causes clinically relevant psychological and physical symptoms in up to 20% of women of reproductive age. To date, no studies have investigated the relationship between PMS and residential surrounding greenspace, although a green living environment has been reported to have beneficial associations with overall and reproductive health., Objective: To investigate whether lifelong exposure to residential surrounding greenspace is associated with PMS and whether such an association is mediated by BMI, air pollution or physical activity., Methods: This study used data collected in 2013-2015 from 1069 Scandinavian women aged 18-49 years, participating in RHINESSA, a European multi-centre and population-based cohort. Satellite-derived Normalised Difference Vegetation Index was used as a proxy of greenspace. Presence of eight common PMS symptoms and their sum (PMS symptom count) were used as outcomes. The associations were assessed by adjusted multilevel logistic and negative binomial regressions. Subsequently we carried out mediation analyses for physical activity, BMI and air pollution exposure., Results: Higher exposure to residential surrounding greenspace was associated with "Anxiety or tension" (Odds Ratio 0.82, 95% Confidence Interval (CI): 0.70 - 0.95), "Depression or hopelessness" (0.84, 0.73 - 0.98), "Difficulty with sleeping" (0.82, 0.68 - 1.00) and "Breast tenderness and abdominal bloating" (0.84, 0.71 - 0.99) before or around the start of the menstrual period. There was also an association with a lower PMS symptom count (Risk Ratio: 0.94, 95% CI: 0.91 - 0.99). These associations were robust to sensitivity analyses and were not mediated by BMI, physical activity or air pollution., Conclusions: Living in greener areas may be beneficial against PMS symptoms. Further studies are needed to confirm these novel findings and to explore the underlying biological mechanisms., (Copyright © 2021 The Author(s). Published by Elsevier Ltd.. All rights reserved.)

Background: Emerging research suggests health effects in offspring after parental chemical exposures before conception. Many future mothers are exposed to potent chemicals at work, but potential offspring health effects are hardly investigated., Objective: We sought to investigate childhood asthma in relation to mother's occupational exposure to cleaning products and disinfectants before conception., Methods: The multicenter Respiratory Health In Northern Europe/Respiratory Health In Northern Europe, Spain and Australia generation study investigated asthma and wheeze starting at age less than 10 years in 3318 mother-offspring pairs. From an asthma-specific Job-Exposure Matrix and mothers' occupational history, we defined maternal occupational exposure to indoor cleaning agents (cleaning products/detergents and disinfectants) starting before conception, in the 2-year period around conception and pregnancy, or after birth. Never-employed mothers were excluded. Exposed groups include cleaners, health care workers, cooks, and so forth. Associations were analyzed using mixed-effects logistic regression and ordinary logistic regression with clustered robust SEs and adjustment for maternal education., Results: Maternal occupational exposure to indoor cleaning starting preconception and continuing (n = 610) was associated with offspring's childhood asthma: odds ratio 1.56 (95% CI, 1.05-2.31), childhood asthma with nasal allergies: 1.77 (1.13-2.77), and childhood wheeze and/or asthma: 1.71 (95% CI, 1.19-2.44). Exposure starting around conception and pregnancy (n = 77) was associated with increased childhood wheeze and/or asthma: 2.25 (95% CI, 1.03-4.91). Exposure starting after birth was not associated with asthma outcomes (1.13 [95% CI, 0.71-1.80], 1.15 [95% CI, 0.67-1.97], 1.08 [95% CI, 0.69-1.67])., Conclusions: Mother's occupational exposure to indoor cleaning agents starting before conception, or around conception and pregnancy, was associated with more childhood asthma and wheeze in offspring. Considering potential implications for vast numbers of women in childbearing age using cleaning agents, and their children, further research is imperative., (Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.)

Mechanistic research suggests that lifestyle and environmental factors impact respiratory health across generations by epigenetic changes transmitted through male germ cells. Evidence from studies on humans is very limited.We investigated multigeneration causal associations to estimate the causal effects of tobacco smoking on lung function within the paternal line. We analysed data from 383 adult offspring (age 18-47 years; 52.0% female) and their 274 fathers, who had participated in the European Community Respiratory Health Survey (ECRHS)/Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study and had provided valid measures of pre-bronchodilator lung function. Two counterfactual-based, multilevel mediation models were developed with: paternal grandmothers' smoking in pregnancy and fathers' smoking initiation in prepuberty as exposures; fathers' forced expiratory volume in 1 s (FEV 1 ) and forced vital capacity (FVC), or FEV 1 /FVC z-scores as potential mediators (proxies of unobserved biological mechanisms that are true mediators); and offspring's FEV 1 and FVC, or FEV 1 /FVC z-scores as outcomes. All effects were summarised as differences (Δ) in expected z-scores related to fathers' and grandmothers' smoking history.Fathers' smoking initiation in prepuberty had a negative direct effect on both offspring's FEV 1 (Δz-score -0.36, 95% CI -0.63- -0.10) and FVC (-0.50, 95% CI -0.80- -0.20) compared with fathers' never smoking. Paternal grandmothers' smoking in pregnancy had a negative direct effect on fathers' FEV 1 /FVC (-0.57, 95% CI -1.09- -0.05) and a negative indirect effect on offspring's FEV 1 /FVC (-0.12, 95% CI -0.21- -0.03) compared with grandmothers' not smoking before fathers' birth nor during fathers' childhood.Fathers' smoking in prepuberty and paternal grandmothers' smoking in pregnancy may cause lower lung function in offspring. Our results support the concept that lifestyle-related exposures during these susceptibility periods influence the health of future generations., Competing Interests: Conflict of interest: S. Accordini has nothing to disclose. Conflict of interest: L. Calciano has nothing to disclose. Conflict of interest: A. Johannessen has nothing to disclose. Conflict of interest: B. Benediktsdóttir has nothing to disclose. Conflict of interest: R.J. Bertelsen has nothing to disclose. Conflict of interest: L. Bråbäck has nothing to disclose. Conflict of interest: S.C. Dharmage has nothing to disclose. Conflict of interest: B. Forsberg has nothing to disclose. Conflict of interest: F. Gómez Real has nothing to disclose. Conflict of interest: J.W. Holloway reports grants from the European Union's Horizon 2020 research and innovation programme, and from the Research Council of Norway, during the conduct of the study. Conflict of interest: M. Holm has nothing to disclose. Conflict of interest: C. Janson has nothing to disclose. Conflict of interest: N.O. Jõgi has nothing to disclose. Conflict of interest: R. Jõgi reports grants from the Estonian Research Council (personal research grant number 562), during the conduct of the study; personal fees for consultancy and lectures from GSK, Boehringer and Novartis, personal fees for travel/accommodation/meeting expenses from GSK and Boehringer, outside the submitted work. Conflict of interest: A. Malinovschi has nothing to disclose. Conflict of interest: A. Marcon has nothing to disclose. Conflict of interest: J. Martínez-Moratalla Rovira has nothing to disclose. Conflict of interest: J.L. Sánchez-Ramos has nothing to disclose. Conflict of interest: V. Schlünssen has nothing to disclose. Conflict of interest: K. Torén has nothing to disclose. Conflict of interest: D. Jarvis reports grants from the European Union, during the conduct of the study. Conflict of interest: C. Svanes has nothing to disclose., (Copyright ©The authors 2021.)

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.)

Exposure to air pollution is of great concern for public health although studies on the associations between exposure estimates and personal exposure are limited and somewhat inconsistent. The aim of this study was to quantify the associations between personal nitrogen oxides (NO x ), ozone (O 3 ) and particulate matter (PM 10 ) exposure levels and ambient levels, and the impact of climate and time spent outdoors in two cities in Sweden. Subjects (n = 65) from two Swedish cities participated in the study. The study protocol included personal exposure measurements at three occasions, or waves. Personal exposure measurements were performed for NO x and O 3 for 24 h and PM 10 for 24 h, and the participants kept an activity diary. Stationary monitoring stations provided hourly data of NO x , O 3 and PM, as well as data on air temperature and relative humidity. Data were analysed using mixed linear models with the subject-id as a random effect and stationary exposure and covariates as fixed effects. Personal exposure levels of NO x , O 3 and PM 10 were significantly associated with levels measured at air pollution monitoring stations. The associations persisted after adjusting for temperature, relative humidity, city and wave, but the modelled estimates were slightly attenuated from 2.4% (95% CI 1.8-2.9) to 2.0% (0.97-2.94%) for NO x , from 3.7% (95% CI 3.1-4.4) to 2.1% (95% CI 1.1-2.9%) for O 3 and from 2.6% (95% 0.9-4.2%) to 1.3% (95% CI - 1.5-4.0) for PM 10 . After adding covariates, the degree of explanation offered by the model (coefficient of determination, or R 2 ) did not change for NO x (0.64 to 0.63) but increased from 0.46 to 0.63 for O 3 , and from 0.38 to 0.43 for PM 10 . Personal exposure to NO x , O 3 and PM has moderate to good association with levels measured at urban background sites. The results indicate that stationary measurements are valid as measure of exposure in environmental health risk assessments, especially if they can be refined using activity diaries and meteorological data. Approximately 50-70% of the variation of the personal exposure was explained by the stationary measurement, implying occurrence of misclassification in studies using more crude exposure metrics, potentially leading to underestimates of the effects of exposure to ambient air pollution., (© 2021. The Author(s).)

Background: Minimum mortality temperature (MMT) is an important indicator to assess the temperature-mortality association, indicating long-term adaptation to local climate. Limited evidence about the geographical variability of the MMT is available at a global scale., Methods: We collected data from 658 communities in 43 countries under different climates. We estimated temperature-mortality associations to derive the MMT for each community using Poisson regression with distributed lag nonlinear models. We investigated the variation in MMT by climatic zone using a mixed-effects meta-analysis and explored the association with climatic and socioeconomic indicators., Results: The geographical distribution of MMTs varied considerably by country between 14.2 and 31.1 °C decreasing by latitude. For climatic zones, the MMTs increased from alpine (13.0 °C) to continental (19.3 °C), temperate (21.7 °C), arid (24.5 °C), and tropical (26.5 °C). The MMT percentiles (MMTPs) corresponding to the MMTs decreased from temperate (79.5th) to continental (75.4th), arid (68.0th), tropical (58.5th), and alpine (41.4th). The MMTs indreased by 0.8 °C for a 1 °C rise in a community's annual mean temperature, and by 1 °C for a 1 °C rise in its SD. While the MMTP decreased by 0.3 centile points for a 1 °C rise in a community's annual mean temperature and by 1.3 for a 1 °C rise in its SD., Conclusions: The geographical distribution of the MMTs and MMTPs is driven mainly by the mean annual temperature, which seems to be a valuable indicator of overall adaptation across populations. Our results suggest that populations have adapted to the average temperature, although there is still more room for adaptation., Competing Interests: The authors declare that they have no conflicts of interest with regard to the content of this report., (Copyright © 2021 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of The Environmental Epidemiology. All rights reserved.)

Objectives: To estimate concentration-response relationships for particulate matter (PM) and black carbon (BC) in relation to mortality in cohorts from three Swedish cities with comparatively low pollutant levels., Setting: Cohorts from Gothenburg, Stockholm and Umeå, Sweden., Design: High-resolution dispersion models were used to estimate annual mean concentrations of PM with aerodynamic diameter ≤10 µm (PM10) and ≤2.5 µm (PM2.5), and BC, at individual addresses during each year of follow-up, 1990-2011. Moving averages were calculated for the time windows 1-5 years (lag1-5) and 6-10 years (lag6-10) preceding the outcome. Cause-specific mortality data were obtained from the national cause of death registry. Cohort-specific HRs were estimated using Cox regression models and then meta-analysed including a random effect of cohort., Participants: During the study period, 7 340 cases of natural mortality, 2 755 cases of cardiovascular disease (CVD) mortality and 817 cases of respiratory and lung cancer mortality were observed among in total 68 679 individuals and 689 813 person-years of follow-up., Results: Both PM10 (range: 6.3-41.9 µg/m 3 ) and BC (range: 0.2-6.8 µg/m 3 ) were associated with natural mortality showing 17% (95% CI 6% to 31%) and 9% (95% CI 0% to 18%) increased risks per 10 µg/m 3 and 1 µg/m 3 of lag1-5 exposure, respectively. For PM2.5 (range: 4.0-22.4 µg/m 3 ), the estimated increase was 13% per 5 µg/m 3 , but less precise (95% CI -9% to 40%). Estimates for CVD mortality appeared higher for both PM10 and PM2.5. No association was observed with respiratory mortality., Conclusion: The results support an effect of long-term air pollution on natural mortality and mortality in CVD with high relative risks also at low exposure levels. These findings are relevant for future decisions concerning air quality policies., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ.)

Background: Many regions of the world are now facing more frequent and unprecedentedly large wildfires. However, the association between wildfire-related PM 2·5 and mortality has not been well characterised. We aimed to comprehensively assess the association between short-term exposure to wildfire-related PM 2·5 and mortality across various regions of the world., Methods: For this time series study, data on daily counts of deaths for all causes, cardiovascular causes, and respiratory causes were collected from 749 cities in 43 countries and regions during 2000-16. Daily concentrations of wildfire-related PM 2·5 were estimated using the three-dimensional chemical transport model GEOS-Chem at a 0·25° × 0·25° resolution. The association between wildfire-related PM 2·5 exposure and mortality was examined using a quasi-Poisson time series model in each city considering both the current-day and lag effects, and the effect estimates were then pooled using a random-effects meta-analysis. Based on these pooled effect estimates, the population attributable fraction and relative risk (RR) of annual mortality due to acute wildfire-related PM 2·5 exposure was calculated., Findings: 65·6 million all-cause deaths, 15·1 million cardiovascular deaths, and 6·8 million respiratory deaths were included in our analyses. The pooled RRs of mortality associated with each 10 μg/m 3 increase in the 3-day moving average (lag 0-2 days) of wildfire-related PM 2·5 exposure were 1·019 (95% CI 1·016-1·022) for all-cause mortality, 1·017 (1·012-1·021) for cardiovascular mortality, and 1·019 (1·013-1·025) for respiratory mortality. Overall, 0·62% (95% CI 0·48-0·75) of all-cause deaths, 0·55% (0·43-0·67) of cardiovascular deaths, and 0·64% (0·50-0·78) of respiratory deaths were annually attributable to the acute impacts of wildfire-related PM 2·5 exposure during the study period., Interpretation: Short-term exposure to wildfire-related PM 2·5 was associated with increased risk of mortality. Urgent action is needed to reduce health risks from the increasing wildfires., Funding: Australian Research Council, Australian National Health & Medical Research Council., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2021 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.)

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: Exposure to cold or hot temperatures is associated with premature deaths. We aimed to evaluate the global, regional, and national mortality burden associated with non-optimal ambient temperatures., Methods: In this modelling study, we collected time-series data on mortality and ambient temperatures from 750 locations in 43 countries and five meta-predictors at a grid size of 0·5° × 0·5° across the globe. A three-stage analysis strategy was used. First, the temperature-mortality association was fitted for each location by use of a time-series regression. Second, a multivariate meta-regression model was built between location-specific estimates and meta-predictors. Finally, the grid-specific temperature-mortality association between 2000 and 2019 was predicted by use of the fitted meta-regression and the grid-specific meta-predictors. Excess deaths due to non-optimal temperatures, the ratio between annual excess deaths and all deaths of a year (the excess death ratio), and the death rate per 100 000 residents were then calculated for each grid across the world. Grids were divided according to regional groupings of the UN Statistics Division., Findings: Globally, 5 083 173 deaths (95% empirical CI [eCI] 4 087 967-5 965 520) were associated with non-optimal temperatures per year, accounting for 9·43% (95% eCI 7·58-11·07) of all deaths (8·52% [6·19-10·47] were cold-related and 0·91% [0·56-1·36] were heat-related). There were 74 temperature-related excess deaths per 100 000 residents (95% eCI 60-87). The mortality burden varied geographically. Of all excess deaths, 2 617 322 (51·49%) occurred in Asia. Eastern Europe had the highest heat-related excess death rate and Sub-Saharan Africa had the highest cold-related excess death rate. From 2000-03 to 2016-19, the global cold-related excess death ratio changed by -0·51 percentage points (95% eCI -0·61 to -0·42) and the global heat-related excess death ratio increased by 0·21 percentage points (0·13-0·31), leading to a net reduction in the overall ratio. The largest decline in overall excess death ratio occurred in South-eastern Asia, whereas excess death ratio fluctuated in Southern Asia and Europe., Interpretation: Non-optimal temperatures are associated with a substantial mortality burden, which varies spatiotemporally. Our findings will benefit international, national, and local communities in developing preparedness and prevention strategies to reduce weather-related impacts immediately and under climate change scenarios., Funding: Australian Research Council and the Australian National Health and Medical Research Council., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2021 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

During the summer of 2018 Sweden experienced a high occurrence of wildfires, most intense in the low-densely populated Jämtland Härjedalen region. The aim of this study was to investigate any short-term respiratory health effects due to deteriorated air quality generated by the smoke from wildfires. For each municipality in the region Jämtland Härjedalen, daily population-weighted concentrations of fine particulate matter (PM 2.5 ) were calculated through the application of the MATCH chemistry transport model. Modelled levels of PM 2.5 were obtained for two summer periods (2017, 2018). Potential health effects of wildfire related levels of PM 2.5 were examined by studying daily health care contacts concerning respiratory problems in each municipality in a quasi-Poisson regression model, adjusting for long-term trends, weekday patterns and weather conditions. In the municipality most exposed to wildfire smoke, having 9 days with daily maximum 1-h mean of PM 2.5 > 20 μg/m 3 , smoke days resulted in a significant increase in daily asthma visits the same and two following days (relative risk (RR) = 2.64, 95% confidence interval (CI): 1.28-5.47). Meta-estimates for all eight municipalities revealed statistically significant increase in asthma visits (RR = 1.68, 95% CI: 1.09-2.57) and also when grouping all disorders of the lower airways (RR = 1.40, 95% CI: 1.01-1.92).

When mortality or other health outcomes attributable to fine particulate matter (PM 2.5 ) are estimated, the same exposure-response function (ERF) is usually assumed regardless of the source and composition of the particles, and independently of the spatial resolution applied in the exposure model. While several recent publications indicate that ERFs based on exposure models resolving within-city gradients are steeper per concentration unit (μgm -3 ), the ERF for PM 2.5 recommended by the World Health Organization does not reflect this observation and is heavily influenced by studies based on between-city exposure estimates. We evaluated the potential health benefits of three air pollution abatement strategies: electrification of light vehicles, reduced use of studded tires, and introduction of congestion charges in Stockholm and Gothenburg, using different ERFs. We demonstrated that using a single ERF for PM 2.5 likely results in an underestimation of the effect of local measures and may be misleading when evaluating abatement strategies. We also suggest applying ERFs that distinguish between near-source and regional contributions of exposure to PM 2.5 . If separate ERFs are applied for near-source and regional PM 2.5 , congestion charges as well as a reduction of studded tire use are estimated to be associated with a significant reduction in the mortality burden in both Gothenburg and Stockholm. In some scenarios the number of premature deaths is more than 10 times higher using separate ERFs in comparison to using a single ERF irrespective of sources as recommended by the WHO. For electrification, the net change in attributable deaths is small or within the uncertainty range depending on the choice of ERF.

Objective: Habitual snoring is associated with fatigue, headaches and low work performance. This cross-sectional study aimed to investigate if snoring is affected by environmental factors such as home dampness and exposure to air pollution., Setting: General population sample from four Swedish cities., Participants: 25 848 participants from the Swedish part of the epidemiological Global Asthma and Allergy and European network of excellence study carried out in 2008. The participants completed a postal questionnaire on snoring and, indoor and outdoor environmental exposure as well as potential confounders including smoking, weight, height and educational level., Results: Of the participants, 4211 (16.3%) were habitual snorers. Habitual snorers reported water damage (8.3% vs 7.0% p<0.0001), floor dampness (4.6% vs 3.8% % p<0.0001) and visible mould (5.2% vs 3.8% p<0.0001) in their homes more often than non-snorers. Habitual snorers stated being annoyed by air pollution more often than non-snorers with habitual snorers reporting being irritated with the air in their residential area to a higher extent (sometimes 16.2% vs 13.9%, and daily 4.6% vs 3.1%) as well as annoyance from traffic fumes (somewhat 19% vs 18.5% and very 5% vs 3.6%) (p<0.0001). These results remained significant after adjustment for age, body mass index, smoking history and educational level., Conclusion: Snoring is more prevalent in subjects reporting home dampness and air pollution. These association should be confirmed in further research using objective measurements and a longitudinal approach., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

We investigated the prevalence of chronic cough and its association with work ability and sick leave in the general population.Data were analysed from the Respiratory Health In Northern Europe (RHINE) III cohort (n=13 500), of which 11 252 participants had also participated in RHINE II 10 years earlier, a multicentre study in Northern Europe. Participants answered a questionnaire on chronic cough, employment factors, smoking and respiratory comorbidities.Nonproductive chronic cough was found in 7% and productive chronic cough in 9% of the participants. Participants with nonproductive cough were more often female and participants with productive cough were more often smokers and had a higher body mass index (BMI) than those without cough. Participants with chronic cough more often reported >7 days of sick leave in the preceding year than those without cough ("nonproductive cough" 21% and "productive cough" 24%; p<0.001 for comparisons with "no cough" 13%). This pattern was consistent after adjusting for age, sex, BMI, education level, smoking status and comorbidities. Participants with chronic cough at baseline reported lower work ability and more often had >7 days of sick leave at follow-up than those without cough. These associations remained significant after adjusting for cough at follow-up and other confounding factors.Chronic cough was found in around one in six participants and was associated with more sick leave. Chronic cough 10 years earlier was associated with lower work ability and sick leave at follow-up. These associations were not explained by studied comorbidities. This indication of negative effects on employment from chronic cough needs to be recognised., Competing Interests: Conflict of interest: A. Johannessen has nothing to disclose. Conflict of interest: M. Holm has nothing to disclose. Conflict of interest: B. Forsberg has nothing to disclose. Conflict of interest: V. Schlünssen has nothing to disclose. Conflict of interest: R. Jõgi has nothing to disclose. Conflict of interest: M. Clausen has nothing to disclose. Conflict of interest: E. Lindberg has nothing to disclose. Conflict of interest: A. Malinovschi has nothing to disclose. Conflict of interest: Ö.I. Emilsson has nothing to disclose. Conflict of interest: H. Johansson has nothing to disclose., (Copyright ©ERS 2021.)

Climate change affects human health; however, there have been no large-scale, systematic efforts to quantify the heat-related human health impacts that have already occurred due to climate change. Here, we use empirical data from 732 locations in 43 countries to estimate the mortality burdens associated with the additional heat exposure that has resulted from recent human-induced warming, during the period 1991-2018. Across all study countries, we find that 37.0% (range 20.5-76.3%) of warm-season heat-related deaths can be attributed to anthropogenic climate change and that increased mortality is evident on every continent. Burdens varied geographically but were of the order of dozens to hundreds of deaths per year in many locations. Our findings support the urgent need for more ambitious mitigation and adaptation strategies to minimize the public health impacts of climate change., Competing Interests: Competing interests The authors declare no competing interests.

Background: Alzheimer's disease (AD) and other dementias currently represent the fifth most common cause of death in the world, according to the World Health Organization, with a projected future increase as the proportion of the elderly in the population is growing. Air pollution has emerged as a plausible risk factor for AD, but studies estimating dementia cases attributable to exposure to fine particulate matter (PM 2.5 ) air pollution and resulting monetary estimates are lacking., Methods: We used data on average population-weighted exposure to ambient PM 2.5 for the entire population of Sweden above 30 years of age. To estimate the annual number of dementia cases attributable to air pollution in the Swedish population above 60 years of age, we used the latest concentration response functions (CRF) between PM 2.5 exposure and dementia incidence, based on ten longitudinal cohort studies, for the population above 60 years of age. To estimate the monetary burden of attributable cases, we calculated total costs related to dementia, including direct and indirect lifetime costs and intangible costs by including quality-adjusted life years (QALYs) lost. Two different monetary valuations of QALYs in Sweden were used to estimate the monetary value of reduced quality-of-life from two different payer perspectives., Results: The annual number of dementia cases attributable to PM 2.5 exposure was estimated to be 820, which represents 5% of the annual dementia cases in Sweden. Direct and indirect lifetime average cost per dementia case was estimated to correspond € 213,000. A reduction of PM 2.5 by 1 μg/m 3 was estimated to yield 101 fewer cases of dementia incidences annually, resulting in an estimated monetary benefit ranging up to 0.01% of the Swedish GDP in 2019., Conclusion: This study estimated that 5% of annual dementia cases could be attributed to PM 2.5 exposure, and that the resulting monetary burden is substantial. These findings suggest the need to consider airborne toxic pollutants associated with dementia incidence in public health policy decisions.

Background: Fractional exhaled nitric oxide (FeNO) is a marker of type-2 inflammation used both to support diagnosis of asthma and follow up asthma patients. The associations of FeNO with lung function decline and bronchodilator (BD) response have been studied only scarcely in large populations., Objectives: To study the association between FeNO and a) retrospective lung function decline over 20 years, and b) lung function response to BD among asthmatic subjects compared with non-asthmatic subjects and with regards to current smoking and sex., Methods: Longitudinal analyses of previous lung function decline and FeNO level at follow-up and cross-sectional analyses of BD response and FeNO levels in 4257 participants (651 asthmatics) from the European Community Respiratory Health Survey., Results: Among asthmatic subjects, higher percentage declines of FEV 1 and FEV 1 /FVC were associated with higher FeNO levels (p = 0.001 for both) at follow-up. These correlations were found mainly among non-smoking individuals (p = 0.001) and females (p = 0.001) in stratified analyses.Percentage increase in FEV 1 after BD was positively associated with FeNO levels in non-asthmatic subjects. Further, after stratified for sex and smoking separately, a positive association was seen between FEV 1 and FeNO levels in non-smokers and women, regardless of asthma status., Conclusions: We found a relationship between elevated FeNO and larger FEV 1 decline over 20 years among subjects with asthma who were non-smokers or women. The association between elevated FeNO levels and larger BD response was found in both non-asthmatic and asthmatic subjects, mainly in women and non-smoking subjects., Competing Interests: DF reports grants from Asthma Foundation of Victoria, grants from Allen and Hanbury’s, grants from National Health & Medical Research Council, during the conduct of the study. VS reports grants from The Wood Dust Foundation (Project No. 444508795), during the conduct of the study. RJ reports grants from Estonian Research Council Personal Research Grant no 562, during the conduct of the study; personal fees from Consultancy, grants from Grants/grants pending, personal fees from Payment for lectures, personal fees from Travel/accommodations/meeting expenses, outside the submitted work. PD reports grants from ALK, Stallergenes Greer, grants from AstraZeneca, ThermoFisherScientific, Ménarini, grants from Bausch & Lomb, personal fees from Sanofi, Regeneron, outside the submitted work. RN reports grants and personal fees from AstraZeneca, grants from Novartis, grants from Boehringer Ingelheim, grants and personal fees from GlaxoSmithKline, outside the submitted work. IP reports other from NOVARTIS, other from ASTRA ZENECA, personal fees from AGIRadom, outside the submitted work. All other authors declare no conflicts of interests. The following grants contributed to funding ECRHS I. Australia: Asthma Foundation of Victoria, Allen and Hanbury’s. Belgium: Belgian Science Policy Office, National Fund for Scientific Research. Denmark: The Danish Lung Association. Estonia: Estonian Science Foundation, grant no 1088. France: Ministère de la Santé, Glaxo France, Institut Pneumologique d'Aquitaine, Contrat de Plan Etat-Région Languedoc-Rousillon, CNMATS, CNMRT (90MR/10, 91AF/6), Ministre delegué de la santé, RNSP, France; GSF. Germany: Bundesminister für Forschung und Technologie. Greece: The Greek Secretary General of Research and Technology, Fisons, Astra and Boehringer-Ingelheim. India: Bombay Hospital Trust. Italy: Ministero dell'Università e della Ricerca Scientifica e Tecnologica, CNR, Regione Veneto grant RSF n. 381/05.93. New Zealand: Asthma Foundation of New Zealand, Lotteries Grant Board, Health Research Council of New Zealand. Norway: Norwegian Research Council project no. 101422/310. Portugal: Glaxo Farmacêutica Lda, Sandoz Portugesa. Spain: Fondo de Investigación Sanitaria (#91/0016-060-05/E, 92/0319 and #93/0393), Hospital General de Albacete, Hospital General Juan Ramón Jiménez, Dirección Regional de Salud Pública (Consejería de Sanidad del Principado de Asturias), CIRIT (1997 SGR 00079), and Servicio Andaluz de Salud. Sweden: The Swedish Medical Research Council, the Swedish Heart Lung Foundation, and the Swedish Association against Asthma and Allergy. Switzerland: Swiss National Science Foundation grant 4026-28099. UK: National Asthma Campaign, British Lung Foundation, Department of Health, South Thames Regional Health Authority. USA: United States Department of Health, Education and Welfare Public Health Service (grant #2 S07 RR05521-28). The coordination of this work was supported by the European Commission. The following grants contributed to funding ECRHS III. Australia: National Health & Medical Research Council. Belgium: Antwerp South, Antwerp City – Research Foundation Flanders (FWO), grant code G.0.410.08.N.10 (both sites). Estonia: Tartu – SF0180060s09 from the Estonian Ministry of Education. France: (All) Ministère de la Santé, Programme Hospitalier de Recherche Clinique (PHRC) national 2010. Bordeaux: INSERM U897 Université Bordeaux Segalen. Grenoble: Comite Scientifique AGIRadom 2011. Paris: Agence Nationale de la Santé, Région Ile de France, domaine d’intérêt majeur (DIM). Germany: Erfurt: German Research Foundation HE 3294/10-1. Hamburg: German Research Foundation MA 711/6-1, NO 262/7-1. Iceland: Reykjavik, The Landspítali University Hospital Research Fund, University of Iceland Research Fund, ResMed Foundation, California, USA, Orkuveita Reykjavíkur (Geothermal plant), Vegagerðin (The Icelandic Road Administration (ICERA). Italy: All Italian centres were funded by the Italian Ministry of Health, Chiesi Farmaceutici SpA. Verona received additional funding from the Cariverona foundation, Education Ministry (MIUR). Norway: Norwegian Research Council grant no 214123, Western Norway Regional Health Authorities grant no 911631, Bergen Medical Research Foundation. Spain: Fondo de Investigación Sanitaria (PS09/02457, PS09/00716 09/01511) PS09/02185 PS09/03190), Servicio Andaluz de Salud, Sociedad Española de Neumología y Cirurgía Torácica (SEPAR 1001/2010), Fondo de Investigación Sanitaria (PS09/02457). Barcelona: Fondo de Investigación Sanitaria (FIS PS09/00716). Galdakao:Fondo de Investigación Sanitaria (FIS 09/01511). Huelva: Fondo de Investigación Sanitaria (FIS PS09/02185) and Servicio Andaluz de Salud. Oviedo: Fondo de Investigación Sanitaria(FIS PS09/03190). Sweden: All centres were funded by the Swedish Heart and Lung Foundation, the Swedish Asthma and Allergy Association, the Swedish Association against Lung and Heart Disease, and the Swedish Research Council for Health, Working Life and Welfare (FORTE). Göteborg also received further funding from the Swedish Council for Working Life and Social Research. Umeå also received funding from a Västerbotten County Council ALF grant. Switzerland: The Swiss National Science Foundation (grants no 33CSCO-134276/1, 33CSCO-108796, 3247BO-104283, 3247BO-104288, 3247BO-104284, 3247-065896, 3100-059302, 3200-052720, 3200-042532, 4026-028099), The Federal office for Forest, Environment and Landscape, The Federal Office of Public Health, The Federal Office of Roads and Transport, the canton’s government of Aargan, Basel-Stadt, Basel-Land, Geneva, Luzern, Ticino, Valais, and Zürich, the Swiss Lung League, the canton’s Lung League of Basel Stadt/ Basel, Landschaft, Geneva, Ticino, Valais, and Zurich, SUVA, Freiwillige Akademische Gesellschaft, UBS Wealth Foundation, Talecris Biotherapeutics GmbH, Abbott Diagnostics, European Commission 018996 (GABRIEL), Wellcome Trust WT 084703MA, UK: Medical Research Council (Grant Number 92091). Support was also provided by the National Institute for Health Research through the Primary Care Research Network., (© 2021 The Author(s).)

Objective: To assess a possible interaction effect between physical activity and air pollution on first incidence of ischaemic heart disease (IHD)., Design: Prospective cohort study., Setting: Umeå, Northern Sweden., Participants: We studied 34 748 adult participants of Västerbotten Intervention Programme cohort from 1990 to January 2014. Annual particulate matter concentrations (PM 2.5 and PM 10 ) at the participants' residential addresses were modelled and a questionnaire on frequency of exercise and active commuting was completed at baseline. Cox proportional hazards modelling was used to estimate (1) association with physical activity at different levels of air pollution and (2) the association with particulate matter at different levels of physical activity., Outcome: First incidence of IHD., Results: Over a mean follow-up of 12.4 years, there were 1148 IHD cases. Overall, we observed an increased risk of IHD among individuals with higher concentrations of particles at their home address. Exercise at least twice a week was associated with a lower risk of IHD among participants with high residential PM 2.5 (hazard ratio (HR) 0.60; 95% CI: 0.44 to 0.82) and PM 10 (HR 0.55; 95% CI: 0.4 to 0.76). The same beneficial effect was not observed with low residential PM 2.5 (HR 0.94; 95% CI: 0.72 to 1.22) and PM 10 (HR 0.99; 95% CI: 0.76 to 1.29). An increased risk associated with higher long-term exposure to particles was only observed among participants that exercised in training clothes at most one a week and among those not performing any active commuting. However, only the interaction effect on HRs for exercise was statistically significant., Conclusion: Exercise was associated with a lower risk of first incidence of IHD among individuals with higher residential particle concentrations. An air pollution-associated risk was only observed among those who exercised less. The findings support the promotion of physical activity and a mitigation of air pollution., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ.)

Background: Epidemiological evidence on short-term association between ambient carbon monoxide (CO) and mortality is inconclusive and limited to single cities, regions, or countries. Generalisation of results from previous studies is hindered by potential publication bias and different modelling approaches. We therefore assessed the association between short-term exposure to ambient CO and daily mortality in a multicity, multicountry setting., Methods: We collected daily data on air pollution, meteorology, and total mortality from 337 cities in 18 countries or regions, covering various periods from 1979 to 2016. All included cities had at least 2 years of both CO and mortality data. We estimated city-specific associations using confounder-adjusted generalised additive models with a quasi-Poisson distribution, and then pooled the estimates, accounting for their statistical uncertainty, using a random-effects multilevel meta-analytical model. We also assessed the overall shape of the exposure-response curve and evaluated the possibility of a threshold below which health is not affected., Findings: Overall, a 1 mg/m 3 increase in the average CO concentration of the previous day was associated with a 0·91% (95% CI 0·32-1·50) increase in daily total mortality. The pooled exposure-response curve showed a continuously elevated mortality risk with increasing CO concentrations, suggesting no threshold. The exposure-response curve was steeper at daily CO levels lower than 1 mg/m 3 , indicating greater risk of mortality per increment in CO exposure, and persisted at daily concentrations as low as 0·6 mg/m 3 or less. The association remained similar after adjustment for ozone but was attenuated after adjustment for particulate matter or sulphur dioxide, or even reduced to null after adjustment for nitrogen dioxide., Interpretation: This international study is by far the largest epidemiological investigation on short-term CO-related mortality. We found significant associations between ambient CO and daily mortality, even at levels well below current air quality guidelines. Further studies are warranted to disentangle its independent effect from other traffic-related pollutants., Funding: EU Horizon 2020, UK Medical Research Council, and Natural Environment Research Council., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2021 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.)

We aimed to assess a possible interaction effect between physical activity and particulate air pollution exposure on recurrence of ischemic heart disease (IHD) and stroke. We followed 2221 adult participants comprising first time IHD (1403) and stroke (818) cases from the Västerbotten Intervention Program between 1 January 1990 to 31 December 2013. During mean follow-up times of 5.5 years, 428 and 156 participants developed IHD and stroke recurrence, respectively. PM2.5 concentrations above the median (5.48 µg/m 3 ) were associated with increased risk of IHD and stroke recurrence by 13% (95% CI -17-45%) and 21% (95% CI -19-80%), respectively. These risk increases were however only observed among those that exercised at most once a week at 21% (95% CI -5-50%) and 25% (95% CI -19-90%) for IHD and stroke recurrence, respectively. Higher frequency of exercise at recruitment was positively associated with IHD and stroke recurrence but only the association with IHD recurrence among participants with low residential PM2.5 was statistically significant (96% increased risk (95%-CI 22-215%)). However, no interaction effect between physical activity and PM2.5 exposure was found. Our findings suggest that physical activity may reduce the air pollution exposure associated risk for recurrent cardiovascular disease, likely by reducing the inflammatory response.

Background: Solar ultraviolet radiation (UVR) affects the body through pathways that exhibit positive as well as negative health effects such as immunoregulation and vitamin D production. Different vitamin D metabolites are associated with higher or lower concentrations of estrogens and may thus alter the female sex hormone balance., Objective: To study whether exposure to UVR, as a modifiable lifestyle factor, is associated with levels of sex hormones (17β-estradiol, estrone, estrone 3-sulfate, testosterone, dehydroepiandrosterone sulfate), gonadotropins (follicle stimulating hormone, luteinizing hormone) as well as sex hormone binding globulin in postmenopausal women, and thus investigate whether managing UVR exposure can influence the hormone balance, with potential benefits for the biological aging process., Methods: The study included 580 postmenopausal women from six European countries, participating in the European Community Respiratory Health Survey (2010-2014). Average UVR exposure during the month before blood sampling was estimated based on personal sun behavior and ambient levels. Hormone concentrations were measured in serum using state-of-the-art methods. Subsequently we applied linear mixed-effects models, including center as random intercept, hormone concentrations (one at a time) as outcome and UVR, age, skin type, body mass index, vitamin D from dietary sources, smoking, age at completed full-time education and season of blood sampling as fixed-effect predictors., Results: One interquartile range increase in UVR exposure was associated with decreased levels of 17β-estradiol (-15.6 pmol/L, 95 % Confidence Interval (CI): -27.69, -3.51) and estrone (-13.36 pmol/L, 95 % CI: -26.04, -0.68) and increased levels of follicle stimulating hormone (9.34IU/L, 95 % CI: 2.91, 15.77) and luteinizing hormone (13.86 IU/daL, 95 % CI: 2.48, 25.25)., Conclusions: Exposure to UVR is associated with decreased estrogens and increased gonadotropins in postmenopausal women, a status associated with osteoporosis, lung function decline and other adverse health effects. This study indicates that managing UVR exposure has potential to influence the hormone balance and counteract adverse health conditions after menopause., (Copyright © 2020 The Author(s). Published by Elsevier B.V. All rights reserved.)

Rationale: Few longitudinal studies have assessed the relationship between occupational exposures and lung-function decline in the general population with a sufficiently long follow-up. Objectives: To examine the potential association in two large cohorts: the ECRHS (European Community Respiratory Health Survey) and the SAPALDIA (Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults). Methods: General-population samples of individuals aged 18 to 62 were randomly selected in 1991-1993 and followed up approximately 10 and 20 years later. Spirometry (without bronchodilation) was performed at each visit. Coded complete job histories during follow-up visits were linked to a job-exposure matrix, generating cumulative exposure estimates for 12 occupational exposures. Forced expiratory volume in 1 second (FEV 1 ) and forced vital capacity (FVC) were jointly modeled in linear mixed-effects models, fitted in a Bayesian framework, taking into account age and smoking. Results: A total of 40,024 lung-function measurements from 17,833 study participants were analyzed. We found accelerated declines in FEV 1 and the FEV 1 /FVC ratio for exposure to biological dust, mineral dust, and metals (FEV 1  = -15.1 ml, -14.4 ml, and -18.7 ml, respectively; and FEV 1 /FVC ratio = -0.52%, -0.43%, and -0.36%, respectively; per 25 intensity-years of exposure). These declines were comparable in magnitude with those associated with long-term smoking. No effect modification by sex or smoking status was identified. Findings were similar between the ECRHS and the SAPALDIA cohorts. Conclusions: Our results greatly strengthen the evidence base implicating occupation, independent of smoking, as a risk factor for lung-function decline. This highlights the need to prevent or control these exposures in the workplace.

Objectives: The study aims to make use of individual data to estimate the impact on premature mortality due to both existing commuter bicycling and the potential impact due to increased physical activity through shifting transport mode from car commuting to bicycling., Methods: Using registry data on home and work addresses for the population of Stockholm County the shortest bicycling route on a network of bicycle paths and roads was retrieved. Travel survey data were used to establish current modes of commuting. The relation between duration of bicycling and distance bicycled within the general population in 2015 was established as a basis for identifying individuals that currently drive a car to work but were estimated to have the physical capacity to bicycle to work within 30 min. Within this mode-shift scenario from car-to-bike the duration of bicycling per week was estimated, both among current and potential bicycle commuters. The health impact assessment (HIA) on mortality due to bicycle commuting physical activity was estimated using the same relative risk as within the WHO Health Economic Assessment Tool., Results: The current number of bicycle commuters were 53 000, and the scenario estimated an additional 111 000. Their mean bicycle distances were 4.5 and 3.4 km, respectively. On average these respective amounts of physical activity reduced the yearly mortality by 16% and 12%, resulting in 11.3 and 16.2 fewer preterm deaths per year., Conclusion: The HIA of transferring commuting by car to bicycle estimated large health benefits due to increased physical activity., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: While direct effects of occupational exposures on an individual's respiratory health are evident, a new paradigm is emerging on the possible effects of pre-conception occupational exposure on respiratory health in offspring. We aimed to study the association between parental occupational exposure starting before conception and asthma in their offspring (at 0-15 years of age)., Methods: We studied 3985 offspring participating in the Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study. Their mothers or fathers (n = 2931) previously participated in the European Community Respiratory Health Survey (ECRHS). Information was obtained from questionnaires on parental job history pre- and post-conception which was linked to an asthma-specific job-exposure matrix (JEM). We assessed the association between parental occupational exposure and offspring asthma, applying logistic regression models, clustered by family and adjusted for study centre, offspring sex, parental characteristics (age, asthma onset, place of upbringing, smoking) and grandparents' level of education., Results: Parental occupational exposure to microorganisms, pesticides, allergens or reactive chemicals pre-conception or both pre- and post-conception was not related to offspring asthma; in general, subgroup analyses confirmed this result. However, maternal exposure both pre- and post-conception to allergens and reactive chemicals was associated with increased odds for early-onset asthma in offspring (0-3 years of age); odds ratio 1.70 (95% CI: 1.02-2.84) and 1.65 (95% CI: 0.98-2.77), respectively., Conclusions: This study did not find evidence that parental occupational exposure, defined by an asthma JEM before conception only or during pre- and post-conception vs non-exposed, was associated with offspring asthma., (© The Author(s) 2020. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Exposure to fine particulate air pollution (PM2.5) is emerging as a risk factor for Alzheimer's disease (AD), but existing studies are still limited and heterogeneous. We have previously studied the association between dementia (AD and vascular dementia) and PM2.5 stemming from vehicle exhaust and wood-smoke in the Betula cohort in Northern Sweden. The aim of this commentary is to estimate the association between total PM2.5 and dementia in the Betula cohort, which is more relevant to include in future meta-estimates than the source-specific estimates. The hazard ratio for incident dementia associated with a 1μg/m3 increase in local PM2.5 was 1.38 (95% confidence interval: 0.99 -1.92). The interpretation of our results is that they indicate an association between local contrasts in concentration of PM2.5 at the residential address and incidence of dementia in a low-level setting.

We studied associations between tobacco smoke, home environment and respiratory health in a 10 year follow up of a cohort of 11,506 adults in Northern Europe. Multilevel logistic regression models were applied to estimate onset and remission of symptoms. Current smokers at baseline developed more respiratory symptoms (OR = 1.39-4.43) and rhinitis symptoms (OR = 1.35). Starting smoking during follow up increased the risk of new respiratory symptoms (OR = 1.54-1.97) and quitting smoking decreased the risk (OR = 0.34-0.60). ETS at baseline increased the risk of wheeze (OR = 1.26). Combined ETS at baseline or follow up increased the risk of wheeze (OR = 1.27) and nocturnal cough (OR = 1.22). Wood painting at baseline reduced remission of asthma (OR 95%CI: 0.61, 0.38-0.99). Floor painting at home increased productive cough (OR 95%CI: 1.64, 1.15-2.34) and decreased remission of wheeze (OR 95%CI: 0.63, 0.40-0.996). Indoor painting (OR 95%CI: 1.43, 1.16-1.75) and floor painting (OR 95%CI: 1.77, 1.11-2.82) increased remission of allergic rhinitis. Living in the oldest buildings (constructed before 1960) was associated with higher onset of nocturnal cough and doctor diagnosed asthma. Living in the newest buildings (constructed 1986-2001) was associated with higher onset of nocturnal breathlessness (OR = 1.39) and rhinitis (OR = 1.34). In conclusion, smoking, ETS and painting indoor can be risk factors for respiratory symptoms. Wood painting and floor painting can reduce remission of respiratory symptoms. Smoking can increase rhinitis. Living in older buildings can be a risk factor for nocturnal cough and doctor diagnosed asthma. Living in new buildings can increase nocturnal dyspnoea and rhinitis., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

Objectives: To investigate if air pollution and greenness exposure from birth till adulthood affects adult asthma, rhinitis and lung function., Methods: We analysed data from 3428 participants (mean age 28) in the RHINESSA study in Norway and Sweden. Individual mean annual residential exposures to nitrogen dioxide (NO 2 ), particulate matter (PM 10 and PM 2.5 ), black carbon (BC), ozone (O 3 ) and greenness (normalized difference vegetation index (NDVI)) were averaged across susceptibility windows (0-10 years, 10-18 years, lifetime, adulthood (year before study participation)) and analysed in relation to physician diagnosed asthma (ever/allergic/non-allergic), asthma attack last 12 months, current rhinitis and low lung function (lower limit of normal (LLN), z-scores of forced expiratory volume in one second (FEV 1 ), forced vital capacity (FVC) and FEV 1 /FVC below 1.64). We performed logistic regression for asthma attack, rhinitis and LLN lung function (clustered with family and study centre), and conditional logistic regression with a matched case-control design for ever/allergic/non-allergic asthma. Multivariable models were adjusted for parental asthma and education., Results: Childhood, adolescence and adult exposure to NO 2 , PM 10 and O 3 were associated with an increased risk of asthma attacks (ORs between 1.29 and 2.25), but not with physician diagnosed asthma. For rhinitis, adulthood exposures seemed to be most important. Childhood and adolescence exposures to PM 2.5 and O 3 were associated with lower lung function, in particular FEV 1 (range ORs 2.65 to 4.21). No associations between NDVI and asthma or rhinitis were revealed, but increased NDVI was associated with lower FEV 1 and FVC in all susceptibility windows (range ORs 1.39 to 1.74)., Conclusions: Air pollution exposures in childhood, adolescence and adulthood were associated with increased risk of asthma attacks, rhinitis and low lung function in adulthood. Greenness was not associated with asthma or rhinitis, but was a risk factor for low lung function., (Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.)

We estimated the association between regular physical activity and the incidence of restrictive spirometry pattern. Forced expiratory volume in 1 second (FEV1), forced vital capacity (FVC), and physical activity were assessed in 2 population-based European cohorts (European Community Respiratory Health Survey: n = 2,757, aged 39-67 years; and Swiss Study on Air Pollution and Lung and Heart Diseases in Adults: n = 2,610, aged 36-82 years) first in 2000-2002 and again approximately 10 years later (2010-2013). Subjects with restrictive or obstructive spirometry pattern at baseline were excluded. We assessed the association of being active at baseline (defined as being physically active at least 2-3 times/week for ≥1 hour) with restrictive spirometry pattern at follow-up (defined as a postbronchodilation FEV1/FVC ratio of at least the lower limit of normal and FVC of <80% predicted) using modified Poisson regression, adjusting for relevant confounders. After 10 years of follow-up, 3.3% of participants had developed restrictive spirometry pattern. Being physically active was associated with a lower risk of developing this phenotype (relative risk = 0.76, 95% confidence interval: 0.59, 0.98). This association was stronger among those who were overweight and obese than among those of normal weight (P for interaction = 0.06). In 2 large European studies, adults practicing regular physical activity were at lower risk of developing restrictive spirometry pattern over 10 years., (© The Author(s) 2020. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

This study aims to use dispersion-modeled concentrations of nitrogen oxides (NOx) and black carbon (BC) to estimate bicyclist exposures along a network of roads and bicycle paths. Such modeling was also performed in a scenario with increased bicycling. Accumulated concentrations between home and work were thereafter calculated for both bicyclists and drivers of cars. A transport model was used to estimate traffic volumes and current commuting preferences in Stockholm County. The study used individuals' home and work addresses, their age, sex, and an empirical model estimate of their expected physical capacity in order to establish realistic bicycle travel distances. If car commuters with estimated physical capacity to bicycle to their workplace within 30 min changed their mode of transport to bicycle, >110,000 additional bicyclists would be achieved. Time-weighted mean concentrations along paths were, among current bicyclists, reduced from 25.8 to 24.2 μg/m 3 for NOx and 1.14 to 1.08 μg/m 3 for BC. Among the additional bicyclists, the yearly mean NOx dose from commuting increased from 0.08 to 1.03 μg/m 3 . This would be expected to yearly cause 0.10 fewer deaths for current bicycling levels and 1.7 more deaths for additional bicycling. This increased air pollution impact is much smaller than the decrease in the total population.

We investigated if greenness and air pollution exposure in parents' childhood affect offspring asthma and hay fever, and if effects were mediated through parental asthma, pregnancy greenness/pollution exposure, and offspring exposure. We analysed 1106 parents with 1949 offspring (mean age 35 and 6) from the Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) generation study. Mean particulate matter (PM 2.5 and PM 10 ), nitrogen dioxide (NO 2 ), black carbon (BC), ozone (O 3 ) (µg/m 3 ) and greenness (normalized difference vegetation index (NDVI)) were calculated for parents 0-18 years old and offspring 0-10 years old, and were categorised in tertiles. We performed logistic regression and mediation analyses for two-pollutant models (clustered by family and centre, stratified by parental lines, and adjusted for grandparental asthma and education). Maternal medium PM 2.5 and PM 10 exposure was associated with higher offspring asthma risk (odds ratio (OR) 2.23, 95%CI 1.32-3.78, OR 2.27, 95%CI 1.36-3.80), and paternal high BC exposure with lower asthma risk (OR 0.31, 95%CI 0.11-0.87). Hay fever risk increased for offspring of fathers with medium O 3 exposure (OR 4.15, 95%CI 1.28-13.50) and mothers with high PM 10 exposure (OR 2.66, 95%CI 1.19-5.91). The effect of maternal PM 10 exposure on offspring asthma was direct, while for hay fever, it was mediated through exposures in pregnancy and offspring's own exposures. Paternal O 3 exposure had a direct effect on offspring hay fever. To conclude, parental exposure to air pollution appears to influence the risk of asthma and allergies in future offspring.

Emerging evidence suggests that parents' preconception exposures may influence offspring health. We aimed to investigate maternal and paternal smoking onset in specific time windows in relation to offspring body mass index (BMI) and fat mass index (FMI). We investigated fathers (n = 2111) and mothers (n = 2569) aged 39-65 years, of the population based RHINE and ECRHS studies, and their offspring aged 18-49 years (n = 6487, mean age 29.6 years) who participated in the RHINESSA study. BMI was calculated from self-reported height and weight, and FMI was estimated from bioelectrical impedance measures in a subsample. Associations with parental smoking were analysed with generalized linear regression adjusting for parental education and clustering by study centre and family. Interactions between offspring sex were analysed, as was mediation by parental pack years, parental BMI, offspring smoking and offspring birthweight. Fathers' smoking onset before conception of the offspring (onset ≥15 years) was associated with higher BMI in the offspring when adult (β 0.551, 95%CI: 0.174-0.929, p = 0.004). Mothers' preconception and postnatal smoking onset was associated with higher offspring BMI (onset <15 years: β1.161, 95%CI 0.378-1.944; onset ≥15 years: β0.720, 95%CI 0.293-1.147; onset after offspring birth: β2.257, 95%CI 1.220-3.294). However, mediation analysis indicated that these effects were fully mediated by parents' postnatal pack years, and partially mediated by parents' BMI and offspring smoking. Regarding FMI, sons of smoking fathers also had higher fat mass (onset <15 years β1.604, 95%CI 0.269-2.939; onset ≥15 years β2.590, 95%CI 0.544-4.636; and onset after birth β2.736, 95%CI 0.621-4.851). There was no association between maternal smoking and offspring fat mass. We found that parents' smoking before conception was associated with higher BMI in offspring when they reached adulthood, but that these effects were mediated through parents' pack years, suggesting that cumulative smoking exposure during offspring's childhood may elicit long lasting effects on offspring BMI., Competing Interests: The authors have declared that no competing interests exist.

Background: Emerging evidence suggests that androgens and estrogens have a role in respiratory health, but it is largely unknown whether levels of these hormones can affect lung function in adults from the general population. This study investigated whether serum dehydroepiandrosterone sulfate (DHEA-S), a key precursor of both androgens and estrogens in peripheral tissues, was related to lung function in adult women participating in the European Community Respiratory Health Survey (ECRHS)., Methods: Lung function and serum DHEA-S concentrations were measured in n  = 2,045 and n  = 1,725 women in 1999-2002 and in 2010-2013, respectively. Cross-sectional associations of DHEA-S levels (expressed as age-adjusted z-score) with spirometric outcomes were investigated, adjusting for smoking habits, body mass index, menopausal status, and use of corticosteroids. Longitudinal associations of DHEA-S levels in 1999-2002 with incidence of restrictive pattern and airflow limitation in 2010-2013 were also assessed., Findings: Women with low DHEA-S (z-score<-1) had lower FEV1 (% of predicted, adjusted difference: -2.2; 95%CI: -3.5 to -0.9) and FVC (-1.7; 95%CI: -2.9 to -0.5) and were at a greater risk of having airflow limitation and restrictive pattern on spirometry than women with higher DHEA-S levels. In longitudinal analyses, low DHEA-S at baseline was associated with a greater incidence of airflow limitation after an 11-years follow-up (incidence rate ratio, 3.43; 95%CI: 1.91 to 6.14)., Interpretation: Low DHEA-S levels in women were associated with impaired lung function and a greater risk of developing airflow limitation later in adult life. Our findings provide new evidence supporting a role of DHEA-S in respiratory health., Funding: EU H2020, grant agreement no.633212., Competing Interests: Dr Demoly reports presentation honoraria from Stallergène Greer, ALK, Mylan, Astra Zeneca, Bausch&Lomb and personal fees as board advisor from Chiesi, Sanofi, Thermo Fisher Scientific, outside the submitted work. Dr Jogi reports personal grants from the Estonian Research Council [personal research grant no.562], and reports travel grants and presentation honoraria from GSK, Novartis, Boehringer, outside the submitted work. Dr Pin reports travel grants and presentation honoraria from GSK, Novartis, Astra Zeneca, Zambon Pharma, outside the submitted work. All the authors declare no competing interests., (© 2020 The Authors.)

Aims: The present study aimed to investigate if set thresholds in the Swedish heat-wave warning system are valid for all parts of Sweden and if the heat-wave warning system captures a potential increase in all-cause mortality and coronary heart disease (CHD) mortality. An additional aim was to investigate whether neighbourhood deprivation modifies the relationship between heat waves and mortality. Methods : From 1990 until 2014, in 14 municipalities in Sweden, we collected data on daily maximum temperatures and mortality for the five warmest months. Heat waves were defined according to the categories used in the current Swedish heat-wave warning system. Using a case-crossover approach, we investigated the association between heat waves and mortality in Sweden, as well as a modifying effect of neighbourhood deprivation. Results : On a national as well as a regional level, heat waves significantly increased both all-cause mortality and CHD mortality by approximately 10% and 15%, respectively. While neighbourhood deprivation did not seem to modify heat wave-related all-cause mortality, CHD mortality did seem to modify the risk. Conclusions : It may not be appropriate to assume that heat waves in Sweden will have the same impact in a northern setting as in a southern, or that the impact of heat waves will be the same in affluent and deprived neighbourhoods. When designing and implementing heat-wave warning systems, neighbourhood, regional and national information should be incorporated.

We have studied the associations between exhaust particles and birth weight. Adjustments were made for ozone and potential confounding factors at the individual level. The study included all singletons conceived between August 2003 and February 2013 with mothers living in Greater Stockholm. We obtained record-based register data from the Swedish Medical Birth Register. Data concerning the parents were provided by Statistics Sweden. Exposure levels for nearly 187,000 pregnancies were calculated using a validated air quality dispersion model with input from a detailed emission database. A higher socioeconomic status was associated with higher levels of exhaust particles at the home address. In this region, with rather low air pollution levels, the associations between levels of exhaust particles and birth weight were negative for all three of the studied exposure windows (i.e., first and second trimester and full pregnancy). For the entire pregnancy, the linear decrease in birth weight was 7.5 grams (95% CI-12.0; -2.9) for an increase in exposure, corresponding to the inter quartile range (IQR = 209 ng/m3). We also found that the risk of being born small for gestational age increased with the level of exhaust particles in all three exposure windows, but these associations were not statistically significant., Competing Interests: The authors declare no conflict of interest

Background: Previous studies have reported an association between weight increase and excess lung function decline in young adults followed for short periods. We aimed to estimate lung function trajectories during adulthood from 20-year weight change profiles using data from the population-based European Community Respiratory Health Survey (ECRHS)., Methods: We included 3673 participants recruited at age 20-44 years with repeated measurements of weight and lung function (forced vital capacity (FVC), forced expiratory volume in 1 s (FEV 1 )) in three study waves (1991-93, 1999-2003, 2010-14) until they were 39-67 years of age. We classified subjects into weight change profiles according to baseline body mass index (BMI) categories and weight change over 20 years. We estimated trajectories of lung function over time as a function of weight change profiles using population-averaged generalised estimating equations., Results: In individuals with normal BMI, overweight and obesity at baseline, moderate (0.25-1 kg/year) and high weight gain (>1 kg/year) during follow-up were associated with accelerated FVC and FEV 1 declines. Compared with participants with baseline normal BMI and stable weight (±0.25 kg/year), obese individuals with high weight gain during follow-up had -1011 mL (95% CI -1.259 to -763) lower estimated FVC at 65 years despite similar estimated FVC levels at 25 years. Obese individuals at baseline who lost weight (<-0.25 kg/year) exhibited an attenuation of FVC and FEV 1 declines. We found no association between weight change profiles and FEV 1 /FVC decline., Conclusion: Moderate and high weight gain over 20 years was associated with accelerated lung function decline, while weight loss was related to its attenuation. Control of weight gain is important for maintaining good lung function in adult life., Competing Interests: Competing interests: JG-A reports personal fees from Esteve, Chiesi and AstraZeneca, outside the submitted work. MJA reports grants from Pfizer, grants from Boehringer-Ingelheim and personal fees from Sanofi, outside the submitted work. PD reports personal fees from ALK, Stallergenes Greer, IQVIA, Chiesi, AstraZeneca, Thermo Fisher Scientific, Menarini, Bausch & Lomb, Mylan, ASIT Biotech, Novartis, Sanofi and Regeneron, outside the submitted work. RJ reports grants from Estonian Research Council (Personal Research Grant no 562) and personal fees from GSK, Boehringer and Novartis, outside the submitted work., (© Author(s) (or their employer(s)) 2020. Re-use permitted under CC BY. Published by BMJ.)

Background: Very few studies have examined the association between long-term outdoor air pollution and rhinitis severity in adults., Objective: We sought to assess the cross-sectional association between individual long-term exposure to air pollution and severity of rhinitis., Methods: Participants with rhinitis from 2 multicenter European cohorts (Epidemiological Study on the Genetics and Environment on Asthma and the European Community Respiratory Health Survey) were included. Annual exposure to NO 2 , PM 10 , PM 2.5 , and PM coarse (calculated by subtracting PM 2.5 from PM 10 ) was estimated using land-use regression models derived from the European Study of Cohorts for Air Pollution Effects project, at the participants' residential address. The score of rhinitis severity (range, 0-12), based on intensity of disturbance due to symptoms reported by questionnaire, was categorized into low (reference), mild, moderate, and high severity. Polytomous logistic regression models with a random intercept for city were used., Results: A total of 1408 adults with rhinitis (mean age, 52 years; 46% men, 81% from the European Community Respiratory Health Survey) were included. The median (1st quartile-3rd quartile) score of rhinitis severity was 4 (2-6). Higher exposure to PM 10 was associated with higher rhinitis severity (adjusted odds ratio [95% CI] for a 10 μg/m 3 increase in PM 10 : for mild: 1.20 [0.88-1.64], moderate: 1.53 [1.07-2.19], and high severity: 1.72 [1.23-2.41]). Similar results were found for PM 2.5 . Higher exposure to NO 2 was associated with an increased severity of rhinitis, with similar adjusted odds ratios whatever the level of severity. Adjusted odds ratios were higher among participants without allergic sensitization than among those with, but interaction was found only for NO 2. CONCLUSIONS: People with rhinitis who live in areas with higher levels of pollution are more likely to report more severe nasal symptoms. Further work is required to elucidate the mechanisms of this association., (Copyright © 2019 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.)

Background : A corruption event in 2009 led to changes in how donors supported the Zambian health system. Donor funding was withdrawn from the district basket mechanism, originally designed to pool donor and government financing for primary care. The withdrawal of these funds from the pooled financing mechanism raised questions from Government and donors regarding the impact on primary care financing during this period of aid volatility. Objectives : To examine the budgets and actual expenditure allocated from central Government to the district level, for health, in Zambia from 2006 to 2017 and determine trends in funding for primary care. Methods : Financial data were extracted from Government documents and adjusted for inflation. Budget and expenditure for the district level over the period 2006 to 2017 were disaggregated by programmatic area for analysis. Results : Despite the withdrawal of donor funding from the district basket after 2009, funding for primary care allocated to the district level more than doubled from 2006 to 2017. However, human resources accounted for this increase. The operational grant, on the other hand, declined. Conclusion : The increase in the budget allocated to primary care could be an example of 'reverse fungibility', whereby Government accounted for the gap left by donors. However, the decline in the operational grant demonstrates that this period of aid volatility continued to have an impact on how primary care was planned and financed, with less flexible budget lines most affected during this period. Going forward, Government and donors must consider how funding is allocated to ensure that primary care is resilient to aid volatility; and that the principles of aid effectiveness are prioritised to continue to provide primary health care and progress towards achieving health for all.

Genetic and environmental factors both contribute to the development of Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD). One suggested environmental risk factor for ASD and ADHD is air pollution, but knowledge of its effects, especially in low-exposure areas, are limited. Here, we investigate risks for ASD and ADHD associated with prenatal exposure to air pollution in an area with air pollution levels generally well below World Health Organization (WHO) air quality guidelines. We used an epidemiological database (MAPSS) consisting of virtually all (99%) children born between 1999 and 2009 (48,571 births) in the study area, in southern Sweden. MAPSS consists of data on modelled nitrogen oxide (NO x ) levels derived from a Gaussian dispersion model; maternal residency during pregnancy; perinatal factors collected from a regional birth registry; and socio-economic factors extracted from Statistics Sweden. All ASD and ADHD diagnoses in our data were undertaken at the Malmö and Lund Departments of Child and Adolescent Psychiatry, using standardized diagnostic instruments. We used logistic regression analyses to obtain estimates of the risk of developing ASD and ADHD associated with different air pollution levels, with adjustments for potential perinatal and socio-economic confounders. In this longitudinal cohort study, we found associations between air pollution exposure during the prenatal period and and the risk of developing ASD. For example, an adjusted Odds Ratio (OR) of 1.40 and its 95% Confidence Interval (CI) (95% CI: 1.02-1.93) were found when comparing the fourth with the first quartile of NO x exposure. We did not find similar associations on the risk of developing ADHD. This study contributes to the growing evidence of a link between prenatal exposure to air pollution and autism spectrum disorders, suggesting that prenatal exposure even below current WHO air quality guidelines may increase the risk of autism spectrum disorders., (Copyright © 2019 The Authors. Published by Elsevier Ltd.. All rights reserved.)

Background: Subarachnoid haemorrhage (SAH) is a devastating disease, with high mortality rate and substantial disability among survivors. Its causes are poorly understood. We aimed to investigate risk factors for SAH using a novel nationwide cohort consortium., Methods: We obtained individual participant data of 949 683 persons (330 334 women) between 25 and 90 years old, with no history of SAH at baseline, from 21 population-based cohorts. Outcomes were obtained from the Swedish Patient and Causes of Death Registries., Results: During 13 704 959 person-years of follow-up, 2659 cases of first-ever fatal or non-fatal SAH occurred, with an age-standardized incidence rate of 9.0 [95% confidence interval (CI) (7.4-10.6)/100 000 person-years] in men and 13.8 [(11.4-16.2)/100 000 person-years] in women. The incidence rate increased exponentially with higher age. In multivariable-adjusted Poisson models, marked sex interactions for current smoking and body mass index (BMI) were observed. Current smoking conferred a rate ratio (RR) of 2.24 (95% CI 1.95-2.57) in women and 1.62 (1.47-1.79) in men. One standard deviation higher BMI was associated with an RR of 0.86 (0.81-0.92) in women and 1.02 (0.96-1.08) in men. Higher blood pressure and lower education level were also associated with higher risk of SAH., Conclusions: The risk of SAH is 45% higher in women than in men, with substantial sex differences in risk factor strengths. In particular, a markedly stronger adverse effect of smoking in women may motivate targeted public health initiatives., (© The Author(s) 2019; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.)

Diabetes risk can be controlled and even reversed by making dietary changes. The aim of this study was to improve the understanding of how older persons with a high risk of developing Type 2 diabetes manage and relate to information about diabetes risk over a ten-year period. Fifteen qualitative interviews were conducted among participants from the Stockholm Diabetes Prevention Program (SDPP). The participants were asked to recall the health examinations conducted by the SDPP related to their prediabetes and to describe their experiences and potential changes related to diet and physical activity. Data were analyzed using qualitative content analysis. The main theme found was that T2D (type 2 diabetes) risk is not perceived as concrete enough to motivate lifestyle modifications, such as changing dietary patterns, without other external triggers. Diagnosis was recognized as a reason to modify diet, and social interactions were found to be important for managing behavior change. Diagnosis was also a contributing factor to lifestyle modification, while prognosis of risk was not associated with efforts to change habits. The results from this study suggest that the potential of reversing prediabetes needs to be highlighted and more clearly defined for older persons to serve as motivators for lifestyle modification.