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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.

Research on epigenetic‒environmental interactions in the development of Alzheimer's disease (AD) has accelerated rapidly in recent decades. Numerous studies have demonstrated the contribution of ambient particulate matter (PM) to the onset of AD. Emerging evidence indicates that non-coding RNAs (ncRNAs), including long non-coding RNAs, circular RNAs, and microRNAs, play a role in the pathophysiology of AD. In this review, we provide an overview of PM-altered ncRNAs in the brain, with emphasis on their potential roles in the pathogenesis of AD. These results suggest that these PM-altered ncRNAs are involved in the regulation of amyloid-beta pathology, microtubule-associated protein Tau pathology, synaptic dysfunction, damage to the blood‒brain barrier, microglial dysfunction, dysmyelination, and neuronal loss. In addition, we utilized in silico analysis to explore the biological functions of PM-altered ncRNAs in the development of AD. This review summarizes the knowns and unknowns of PM-altered ncRNAs in AD pathogenesis and discusses the current dilemma regarding PM-altered ncRNAs as promising biomarkers of AD. Altogether, this is the first thorough review of the connection between PM exposure and ncRNAs in AD pathogenesis, which may offer novel insights into the prevention, diagnosis, and treatment of AD associated with ambient PM exposure.

Per- and polyfluoroalkyl substances (PFAS) are endocrine disruptors with unambiguous neurotoxic effects. However, due to variability in experimental models, population characteristics, and molecular endpoints, the elucidation of mechanisms underlying PFAS-induced neurotoxicity remains incomplete. In this review, we utilized the adverse outcome pathway (AOP) framework, a comprehensive tool for evaluating toxicity across multiple biological levels (molecular, cellular, tissue and organ, individual, and population), to elucidate the mechanisms of neurotoxicity induced by PFAS. Based on 271 studies, the reactive oxygen species (ROS) generation emerged as the molecular initiating event 1 (MIE1). Subsequent key events (KEs) at the cellular level include oxidative stress, neuroinflammation, apoptosis, altered Ca²⁺ signal transduction, glutamate and dopamine signaling dyshomeostasis, and reduction of cholinergic and serotonin. These KEs culminate in synaptic dysfunction at organ and tissue levels. Further insights were offered into MIE2 and upstream KEs associated with altered thyroid hormone levels, contributing to synaptic dysfunction and hypomyelination at the organ and tissue levels. The inhibition of Na⁺/I⁻ symporter (NIS) was identified as the MIE2, initiating a cascade of KEs at the cellular level, including altered thyroid hormone synthesis, thyroid hormone transporters, thyroid hormone metabolism, and binding with thyroid hormone receptors. All KEs ultimately result in adverse outcomes (AOs), including cognition and memory impairment, autism spectrum disorders, attention deficit hyperactivity disorders, and neuromotor development impairment. To our knowledge, this review represents the first comprehensive and systematic AOP analysis delineating the intricate mechanisms responsible for PFAS-induced neurotoxic effects, providing valuable insights for risk assessments and mitigation strategies against PFAS-related health hazards.

Background: Parental allergic diseases and smoking influence respiratory disease in the offspring but it is not known whether they influence fractional exhaled nitric oxide (FeNO) in the offspring. We investigated whether parental allergic diseases, parental smoking and FeNO levels in parents were associated with FeNO levels in their offspring.

Methods: We studied 609 offspring aged 16–47 years from the Respiratory Health in Northern Europe, Spain and Australia generation (RHINESSA) study with parental information from the Respiratory Health in Northern Europe (RHINE) III study and the European Community Respiratory Health Survey (ECRHS) III. Linear regression models were used to assess the association between offspring FeNO and parental FeNO, allergic rhinitis, asthma and smoking, while adjusting for potential confounding factors.

Results: Parental allergic rhinitis was significantly associated with higher FeNO in the offspring, both on the paternal and maternal side (percent change: 20.3 % [95%CI 5.0–37.7], p = 0.008, and 13.8 % [0.4–28.9], p = 0.043, respectively). Parental allergic rhinitis with asthma in any parent was also significantly associated with higher offspring FeNO (16.2 % [0.9–33.9], p = 0.037). However, parental asthma alone and smoking were not associated with offspring FeNO. Parental FeNO was not associated with offspring FeNO after full adjustments for offspring and parental factors.

Conclusions: Parental allergic rhinitis but not parental asthma was associated with higher levels of FeNO in offspring. These findings suggest that parental allergic rhinitis status should be considered when interpreting FeNO levels in offspring beyond childhood.

Planetary health is being or should be added to medical training curricula in accordance with association consensus. Several articles published in recent years have addressed concern on the implementation, and the challenges that can occur if not addressed properly. This scoping narrative literature review focuses on planetary health as a concept, as well as challenges and suggested solutions to address these challenges. Planetary health is an important concept and needs to be addressed in all medical training. We found that one main challenge is implementation without ensuring the right competences and resources. Medically trained teachers set out to understand and teach complex natural and social systems. At some institutions the time allocated to teach planetary health is limited or non-existent. Case studies and student led teaching are solutions suggested, while other argue that true interdisciplinarity by inviting experts are more in line with what we expect from other subjects. In conclusion, the roots of planetary health, the enormous health risks at stake and nature of the subject requires medical training to adopt a true inter/trans-disciplinary approach to succeed. It might not be expected for all students to become planetary health experts, but all need a general understanding of the most important aspects and values.

Background: During the initial phase of the COVID-19 pandemic, reductions in air pollution were globally observed owing to decreased human activities, underscoring the potential for cleaner air through shifts in human behaviour.

Objectives: The objective of the present study was to hypothetically estimate the resulting population health impacts in Malmö, Sweden, if these improvements in air quality were to become permanent. Methods: We utilized air pollution data from two measurement campaigns conducted in the spring of 2019 and the spring of 2020 for our Health Impact Assessment, applying standard methods. This assessment involved making assumptions about baseline population risk and using established concentration-response functions.

Results: In the spring of 2020, the NO2 concentrations exhibited an average decrease of 6.6 μg/m3 (42%) decrease and PM2.5 concentrations a 1.9 μg/m3 (22%) decrease, compared to the spring of 2019. If sustained, such improvements could lead to an estimated 1–3% decrease in premature deaths, a 2% decrease in preeclampsia cases, a 6% decrease in low birthweight children, a 4% decrease in bronchitis cases among children, a 2% decrease in asthma cases, a 0.2% decrease in hospital admissions for respiratory diagnoses, and an estimated 11% decrease in dementia cases annually.

Conclusion: The findings illustrate the potential for enhanced health in Malmö due to improved air quality. Efforts to combat air pollution and implement long-term strategies, such as those targeting urban mobility and commuting patterns, are essential for the health and well-being of both local and global populations.

The aim of this study was to investigate the relationship between source-specific ambient particulate air pollution concentrations and the incidence of dementia. The study encompassed 70,057 participants from the Västerbotten intervention program cohort in Northern Sweden with a median age of 40 years at baseline. High-resolution dispersion models were employed to estimate source-specific particulate matter (PM) concentrations, such as PM10 and PM2.5 from traffic, exhaust, and biomass (mainly wood) burning, at the residential addresses of each participant. Cox regression models, adjusted for potential confounding factors, were used for the assessment. Over 884,847 person-years of follow-up, 409 incident dementia cases, identified through national registers, were observed. The study population’s average exposure to annual mean total PM10 and PM2.5 lag 1–5 years was 9.50 µg/m3 and 5.61 µg/m3, respectively. Increased risks were identified for PM10-Traffic (35% [95% CI 0–82%]) and PM2.5-Exhaust (33% [95% CI − 2 to 79%]) in the second exposure tertile for lag 1–5 years, although no such risks were observed in the third tertile. Interestingly, a negative association was observed between PM2.5-Wood burning and the risk of dementia. In summary, this register-based study did not conclusively establish a strong association between air pollution exposure and the incidence of dementia. While some evidence indicated elevated risks for PM10-Traffic and PM2.5-Exhaust, and conversely, a negative association for PM2.5-Wood burning, no clear exposure–response relationships were evident.

A prevalent solution to accommodate population growth due to urbanization is densification. However, this often pushes new residential housing closer to roads, increasing exposure to both noise and air pollution. The present study's aim was to estimate the health impacts of road traffic-related noise and air pollution for a low-income area (Drottninghög) in Helsingborg, Sweden, according to pre-densification (2012) and post-densification (2030) scenarios.

Road traffic noise was simulated at the façade of residential buildings using the Nordic prediction method, and exposure was assessed using SoundPLAN. Exposure-response functions (ERF) from the WHO were utilized for the following health outcomes associated with noise: annoyance, adverse sleep disturbance, ischemic heart disease (IHD) incidence and IHD mortality. Air pollution (nitrogen dioxide, NO2) was assessed using a Gaussian dispersion model (AERMODE). Health outcomes associated with NO2 included natural cause mortality, pediatric asthma, respiratory hospitalizations and low birth weight (LBW). ERFs were derived from meta-analyses. Health impact assessments were then performed for both scenarios.

Densifying Drottninghög according to the municipality's planned strategy would lead to a 15 % unit increase in the proportion of residents exposed to road traffic noise above the WHO's health-based guideline value (53 dB(A) Lden). This was estimated to markedly increase the proportion of residents highly annoyed by traffic noise (7.4–13.9 %) as well as those highly sleep disturbed (3.0–4.9 %). IHD incidence and IHD mortality attributed to noise would increase by an estimated 49 % and 44 %, respectively, post-densification. NO2 exposure was estimated to increase slightly (0.7 µg/m3) post-densification, which would contribute to an estimated 4–6 % increase in natural cause mortality, pediatric asthma, respiratory hospitalization and LBW.

Urban planning initiatives need to consider these prevalent urban environmental exposures and integrate a public health perspective into densification strategies. Doing so can create synergies in the built environment that promote healthy, sustainable cities.

Aim: Heritability of cough has not yet been studied. We aimed to evaluate if individuals with cough are more likely to have offspring who develop cough, and if these associations differ by type of cough (productive/nonproductive).

Methods: The RHINESSA Generation Study (Respiratory Health In Northern Europe, Spain and Australia) includes 7155 parents (initially aged 30–54) answering detailed questionnaires in 2000 and 2010, and 8176 offspring ⩾20 years answering similar questionnaires in 2012–2019. Chronic cough was categorised as productive or nonproductive (dry) cough. Associations between parental and offspring cough were analysed using mixed-effects logistic regression, adjusting for offspring age, sex, body mass index, smoking history, education level, current asthma, rhinitis, nocturnal gastroesophageal reflux; parent sex and smoking history; centre and family.

Results: Among parents with nonproductive cough, 11% of their offspring reported nonproductive cough, compared with 7% of offspring to parents without nonproductive cough, adjusted odds ratio (aOR) 1.59 (95% confidence interval 1.20–2.10). Among parents with productive cough, 14% of their offspring reported productive cough, compared with 11% of offspring to parents without productive cough, aOR 1.34 (1.07–1.67). No associations were found between parent productive cough–offspring nonproductive cough, nor between parent nonproductive cough–offspring productive cough.

Conclusions: Parents with chronic cough are more likely to have offspring with chronic cough independent of parental asthma, suggesting cough to be a separate heritable trait. The type of cough is important, as the nonproductive cough in parent associates only with nonproductive cough in offspring, and the same applied for productive cough.

Background and aims: Despite firm evidence for an association between long-term ambient air pollution exposure and cardiovascular morbidity and mortality, results from epidemiological studies on the association between air pollution exposure and atherosclerosis have not been consistent. We investigated associations between long-term low-level air pollution exposure and coronary atherosclerosis.

Methods: We performed a cross-sectional analysis in the large Swedish CArdioPulmonary bioImaging Study (SCAPIS, n = 30 154), a random general population sample. Concentrations of total and locally emitted particulate matter <2.5 μm (PM_2.5), <10 μm (PM₁₀), and nitrogen oxides (NO_x) at the residential address were modelled using high-resolution dispersion models. We estimated associations between air pollution exposures and segment involvement score (SIS), coronary artery calcification score (CACS), number of non-calcified plaques (NCP), and number of significant stenoses, using ordinal regression models extensively adjusted for potential confounders.

Results: Median 10-year average PM_2.5 exposure was 6.2 μg/m³ (range 3.5–13.4 μg/m³). 51 % of participants were women and 51 % were never-smokers. None of the assessed pollutants were associated with a higher SIS or CACS. Exposure to PM_2.5 was associated with NCP (adjusted OR 1.34, 95 % CI 1.13, 1.58, per 2.05 μg/m³). Associations with significant stenoses were inconsistent.

Conclusions: In this large, middle-aged general population sample with low exposure levels, air pollution was not associated with measures of total burden of coronary atherosclerosis. However, PM_2.5 appeared to be associated with a higher prevalence of non-calcified plaques. The results suggest that increased risk of early-stage atherosclerosis or rupture, but not increased total atherosclerotic burden, may be a pathway for long-term air pollution effects on cardiovascular disease.