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Background: Black carbon (BC) is an air pollutant of growing concern due to its adverse impacts on health and climate. Growing evidence suggests that BC could have a number of negative impacts on morbidity and mortality, but more evidence is needed.

Objective: The objectives of this study are to quantify any associations between BC exposure and cause-specific (cardiovascular and cancer) mortality outcomes.

Methods: Using the Malmö Diet and Cancer Cohort linked with a high-resolution dispersion model, we examined the association between long-term exposure to locally emitted BC, nitrogen oxides (NOx) and fine particulate matter (PM2.5) with cardiovascular and cancer mortality.

Results: In fully adjusted models, BC exposure was consistently associated with cardiovascular mortality (HR 1.15 [1.06–1.26] per IQR increase), an association that was stronger and more robust than for PM2.5 or NOx. This association was present across all models, all time periods and both sets of exposure intervals. This association was stronger than with the other pollutants. Less clear association was found between any pollutant and cancer mortality.

Conclusion: This study shows associations between BC exposure and especially cardiovascular mortality, consistent with international evidence showing similar impacts. For cancer mortality, there were tendencies of an association with BC but less clear than for cardiovascular mortality. These findings suggest a unique role of BC in air pollution-related cardiovascular mortality and support the need for action on mitigation of air pollution in general and BC in particular.

Background: Evidence suggests that a father’s smoking in puberty may adversely impact respiratory health in offspring, possibly through epigenetic changes in germ cells. This study investigates whether snus use starting in or after puberty influences respiratory health in future offspring.

Methods: We analysed Swedish data from RHINE (Respiratory Health in Northern Europe) parents and RHINESSA (Respiratory Health in Northern Europe, Spain and Australia) offspring by using mixed-effect logistic regression to assess the links between paternal snus initiation around puberty and offspring asthma, chronic bronchitis, rhinitis, and eczema, adjusting for paternal and offspring smoking.

Results: We identified 1090 offspring–father pairs. The offspring’s median age was 29 years (17–51) and 55% were women. The maternal line (n = 1421) was not analysed, as <1% of mothers used snus in puberty. The offspring of fathers starting snus use in puberty (n = 89) had a higher risk of current allergic asthma [odds ratio (OR) 1.42; 95% confidence interval (CI) 1.02–1.97], at least three asthma symptoms with allergy (OR 1.13; 95% CI 1.10–1.21), chronic bronchitis (OR 2.17; 95% CI 1.04–4.54), and eczema (OR 1.45; 95% CI 1.27–1.65). Fathers’ snus use starting after puberty (n = 252) showed no consistent associations with offspring outcomes. The effect estimates were consistent after excluding offspring using snus in puberty.

Conclusion: Paternal snus use starting in puberty was associated with a higher risk of asthma and other respiratory and allergic symptoms in offspring. These findings support the hypothesis that exposures in puberty may impact future generations’ respiratory health, possibly through epigenetic changes. This highlights the need for research on exposures during this period and actions to prevent habits that could negatively impact future offspring’s health.

Background: A large part of the Swedish population is exposed to higher levels of air pollution than the health-centered air quality guidelines recommended by the World Health Organization (WHO).

Aim: The aim of the study was to illustrate the potential health benefits of cleaner air in Sweden by conducting a comprehensive health impact assessment, using a population sample of 100,000 individuals representing the country’s demographics.

Methods: Exposure-response functions for various health outcomes were derived from epidemiological literature, mainly from systematic reviews and low-exposure settings. Two hypothetical scenarios were studied: a 1 µg/m³ decrease in particulate matter with an aerodynamic diameter <2.5µm (PM_2.5) and nitrogen dioxide (NO²), and a reduction in PM_2.5 or NO² from average exposure corresponding to Sweden’s Clean Air objectives to WHO’s air quality guidelines.

Results: The findings demonstrated that even a modest decrease in air pollution concentrations can yield significant health benefits. For example, reducing PM_2.5 by 1 µg/m³ was projected to correspond to a 1% to 2% decrease in mortality, a 2% reduction in myocardial infarction cases, a 4% decrease in stroke incidence, a 2% decline in chronic obstructive pulmonary disease, and a 1% decreases in lung cancer and type 2 diabetes annually. Moreover, this reduction is estimated to lower childhood asthma cases, incidences of hypertension during pregnancy, and premature births by 3%, 3% and 2%, respectively, each year.

Conclusions: The results highlighted that even minor enhancements in air quality would lead to substantial improvements in public health.

Background: To educate students and prepare them for life in society, school principals, teachers, and staff needproper work-related organizational preconditions, motivation, and good health. In this context, span of control(SoC, i.e., the number of employees a manager is accountable for) is an understudied modifiable organizationalprecondition that influences the relationships between managers and employees. Therefore, as a basis for futurepreventive actions, we examined (a) school principals’ SoC and (b) how SoC varied across gender, job title, years ofworking as a school principal, and school owner, and the extent to which SoC was associated with (c) the reporting ofexhaustion symptoms and perceived work ability, and (d) demanding and supportive managerial circumstances.

Methods: School principals (N = 2045; mean age 49 years [SD 7 years]; 77% women) in Sweden completed a crosssectionalweb survey including background information and the Lund University Checklist for Incipient Exhaustion,a brief version of the Gothenburg Manager Stress Inventory, and the Work Ability Score. SoC was assessed as thetotal number of employees the principal was accountable for. Median and quartile splits created four groups withincrementally wider SoC. Data were analysed using non-parametric tests as well as multivariate analyses of variance(MANOVAs).

Results: The mean SoC was 31.7 employees (SD 15.5). SoC differed across job titles, school levels, school owner, andyears of working as a school principal. There was no difference in SoC across gender, exhaustion symptoms, or workability. Adjusted MANOVAs and subsequent post-hoc testing indicated that principals with the narrowest SoC (i.e., ≤22 employees) reported less frequent role conflicts and role demands, and less frequent need to harbour employee’sfrustration as well as less access to support from colleagues at the same level.

Conclusions: Irrespective of school ownership, an SoC of no more than 22 employees was consistently associatedwith reports of perceiving less frequent role conflicts, role demands, and need to harbour employee frustrations

Som ansvarig chef och ledare för det pedagogiska arbetet samt för den interna organisationen,har rektorer breda ansvarsområden och en nyckelposition i utbildningsystemet. Eftersom rektorn genom sitt ledarskap skapar ramarna för hur personalen arbetar, kan överbelastning och ohälsa hos rektorer leda till bristande ledarskap som påverkar lärare, elever och i förlängningen hela förskolan, skolan och samhället. Det finns därför starka skäl till att vara uppmärksam på rektorernas hälsa och arbetssituation och att verka för att skapa goda förutsättningar för ett långsiktigt fungerande skolledarskap.

I denna rapport presenteras resultat och slutsatser från forskningsprojektet ”Skolledares arbetsmiljödel 2: Fördjupande undersökningar av rektorers organisatoriska förutsättningar för ett hållbart skolledarskap”som finansierats av AFA Försäkring. 

The number of people seeking help for mental illness is increasing across all ages, creating a major burden for individuals, families, and the society. While personalized medicine is advancing in other fields, diagnosis and treatment of mental disorders remain largely symptom-based and fail to capture individual, sex, and gender differences in risk, manifestation, and treatment response. Early signs of illness often go unnoticed due to the lack of monitoring tools, and stigma continues to hinder prevention and care. In some phases of life, an individual’s susceptibility to mental illness is heightened and may be influenced by changes in endocrine signalling. To address these challenges, the research project Building REsilience against MEntal illness during ENDocrine-sensitive life stages (RE-MEND) has implemented an interdisciplinary approach focusing on four critical endocrine-sensitive life stages: prenatal, puberty, peripartum, and older age. The project integrates longitudinal population-based cohorts with experimental and clinical studies to identify genetic, environmental, and endocrine factors shaping susceptibility and resilience to mental illness. Multi-omics data (genomics, epigenomics, transcriptomics, proteomics, metabolomics, lipidomics, and adductomics) will be combined with neurobiological, clinical, and behavioural measures, analysed using advanced biostatistics and machine learning. RE-MEND seeks to i) identify risk and resilience factors affecting mental health; ii) deliver biomarker panels for susceptibility, disease progression, and treatment response across sensitive life stages; iii) discover novel drug targets through repurposing strategies, and iv) promote mental health literacy and reduce stigma. The integration of biological research with communication science is anticipated to result in translatable findings, supporting earlier intervention and more effective care.

This chapter reviews the growing body of epidemiological evidence linking long-term exposure to ambient air pollution with increased risk of dementia, including Alzheimer’s disease (AD) and vascular dementia (VaD). With air pollution now recognized as a potentially modifiable risk factor, the chapter explores mechanistic pathways, such as neuroinflammation and oxidative stress, through which pollutants like PM2.5 and NO₂ may contribute to neurodegeneration. It discusses dementia subtypes, highlighting the need for subtype-specific analyses given their differing pathologies and risk factors. The chapter also emphasizes the importance of life course exposure assessment and the potential roles of co-exposures such as noise and lack of green space, which are often correlated with air pollution but understudied in relation to cognitive decline. A review of systematic reviews and meta-analyses reveals consistent associations between PM2.5 and dementia risk, though evidence remains limited for other pollutants. The chapter calls for future studies to adopt multi-exposure frameworks, improve exposure and outcome assessments, and include underrepresented populations in high-pollution areas, particularly in low- and middle-income countries. Establishing a causal link between air pollution and dementia could significantly strengthen the case for environmental interventions as a public health strategy to reduce the burden of dementia worldwide.

Air pollution is increasingly discussed as a risk factor for dementia, but the biological mechanisms are not yet fully understood. Biological markers like telomere length are relevant to study with air pollution, as they are associated with aging and dementia. The study aimed to investigate the relationship between source-specific air pollution exposure and telomere length in a low-level air pollution area, and whether this potential relationship depended on future dementia status. The data originated from the Betula study in Northern Sweden, where 509 participants recruited between 1988 and 1995 were included to investigate the association between annual mean air pollution concentrations at the participants’ residences and relative leukocyte telomere length using a linear regression model. No association was observed between air pollution and telomere length, with regression slope estimates close to zero and p-values > 0.10 (e.g. PM2.5_total: β = 0.01 (-0.011, 0.025) and BC_total: β = 0.03 (95% CI: -0.046, 0.114). There were indications of a positive association between longer telomere length and higher exposure to air pollution among individuals later diagnosed with dementia (N = 74), but these findings were not conclusive (p-values > 0.10) (PM2.5_total: β = 0.03, p-value = 0.12; BC_total: β = 0.11, p-value = 0.17). Although not statistically significant, our findings contribute to the evidence from low-exposure settings, and it is important to report these types of findings for a balanced understanding of potential health effects.

Background: Air pollution and greenness impact respiratory health, but intergenerational effects remain unclear.We investigated whether pre-conception parental residential exposure to air pollution and greenness at age 20–44 years is associated with offspring asthma outcomes in the Lifespan and inter-generational respiratory effects of exposures to greenness and air pollution (Life-GAP) project.

Methods: We analyzed data on 3684 RHINESSA study participants born after the year 1990 (mean age 19, standard deviation 4), offspring of 2689 RHINE study participants. Modelled annual concentrations of particulate matter (PM_2.5, PM₁₀), nitrogen dioxide (NO₂), elemental carbon (EC), and ozone (O₃), and greenness (Normalized Difference Vegetation Index, NDVI) were assigned to parental residential addresses in 1990, corresponding to 1–18 years prior to birth (mean: 6 years, SD: 5). We analyzed associations using generalized structural equation modelling (GSEM), with cluster-robust standard errors allowing for intra-family correlation, while adjusting for potential confounders.

Results: Among offspring participants, 18% reported lifetime asthma, 9% active asthma, 8% asthma medication, 5% asthma attacks, and 37% any asthma symptom. An interquartile range (IQR) increase in parental residential NDVI exposure was associated with less lifetime asthma (OR = 0.79, 95%CI: 0.64, 0.98 per 0.3 units). Similar associations were observed for active asthma and asthma medication use. Associations of air pollution with asthma outcomes were inconclusive.

Conclusion: Parental exposure to residential green spaces before conception was associated with lower asthma risk in offspring. Urban planning policies prioritizing green spaces may be a key public health intervention for future cities.

Airborne ultrafine particulate matter (PM0.1) can enter the brain, induce microglia activation, and promote the development of Alzheimer's disease (AD). Circular RNAs (circRNAs) are also involved in AD pathogenesis. However, the role of AD-related circRNAs in PM0.1-induced microglia activation remains unclear. Therefore, we explore cytotoxicity, microglia activation, and AD-associated circRNA expression in human microglial HMC3 cells treated with PM0.1, and further examined circRNA expression in mice and cognitively impaired individuals. The results revealed that PM0.1 exposure decreased cell viability, increased lactate dehydrogenase activity, caused microglia activation, elevated microglial M1 maker expression, downregulated microglial M2 maker expression, and reduced AD-related circ_0061183 expression in vitro. Functionally, circ_0061183 silencing enhanced microglia activation and microglial M1 polarization, but inhibited microglial M2 polarization. Mechanistically, circ_0061183 can bind to miR‐98‐5p to co-regulate M2 microglial-related IL10 expression, which may affect transforming growth factor-β signaling to regulate PM0.1-inhibited microglial M2 polarization. Moreover, circ_0061183 downregulation was observed in the brain of PM2.5-exposed mice and AD mice and in the blood of cognitively impaired individuals. Furthermore, circ_0061183 was positively related to mini–mental state examination scores and amyloid-β42 peptide expression in elderly individuals. Overall, the current work offers epigenetic insights into the regulatory mechanisms of circRNAs on microglial activation caused by environmental pollutants.