| 1. |
- Janson, Emma, et al.
(author)
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Insomnia associated with traffic noise and proximity to traffic : a cross-sectional study of the Respiratory Health in Northern Europe III population
- 2020
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In: Journal of Clinical Sleep Medicine (JCSM). - : American Academy of Sleep Medicine. - 1550-9389 .- 1550-9397. ; 16:4, s. 545-552
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Journal article (peer-reviewed)abstract
- Study Objectives: Exposure to traffic noise increases the risk of sleeping disturbance, but little is known about the effect of traffic-related air pollution on insomnia symptoms. We aimed to investigate the separate associations of self-reported proximity to traffic and traffic noise with insomnia.Methods: This is a cross-sectional study of the population included in the Respiratory Health in Northern Europe study, consisting of randomly selected men and women born between 1945 and 1973, from 7 Northern European centers. Hearing traffic noise in the bedroom, bedroom window proximity to traffic, and insomnia symptoms were self-reported. Bedroom window proximity to traffic was used as a surrogate for exposure to traffic-related air pollution. The following insomnia symptoms were assessed: difficulty initiating sleep, difficulty maintaining sleep, and early morning awakening.Results: A total of 12,963 individuals was included. Traffic noise was positively associated with all three insomnia symptoms: difficulty initiating sleep (odds ratio [OR] = 3.54; 95% confidence interval [CI]: 1.85, 6.76), difficulty maintaining sleep (OR = 2.95; 95% CI: 1.62, 5.37), and early morning awakening (OR = 3.25; 95% CI: 1.97, 5.37). Proximity to traffic without disturbing noise was associated with difficulty initiating sleep (OR = 1.62; 95% CI: 1.45, 1.82).Conclusions: This study adds further support to the identification of traffic noise as a risk factor for insomnia. Proximity to traffic without being exposed to noise was associated with an increased risk of difficulty initiating sleep. Our findings indicate that insomnia may be associated with both traffic noise and traffic-related air pollution.
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| 2. |
- Accordini, Simone, et al.
(author)
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Incidence trends of airflow obstruction among European adults without asthma : a 20-year cohort study
- 2020
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In: Scientific Reports. - : NATURE PUBLISHING GROUP. - 2045-2322. ; 10:1
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Journal article (peer-reviewed)abstract
- Investigating COPD trends may help healthcare providers to forecast future disease burden. We estimated sex- and smoking-specific incidence trends of pre-bronchodilator airflow obstruction (AO) among adults without asthma from 11 European countries within a 20-year follow-up (ECRHS and SAPALDIA cohorts). We also quantified the extent of misclassification in the definition based on pre-bronchodilator spirometry (using post-bronchodilator measurements from a subsample of subjects) and we used this information to estimate the incidence of post-bronchodilator AO (AO(post-BD)), which is the primary characteristic of COPD. AO incidence was 4.4 (95% CI: 3.5-5.3) male and 3.8 (3.1-4.6) female cases/1,000/year. Among ever smokers (median pack-years: 20, males; 12, females), AO incidence significantly increased with ageing in men only [incidence rate ratio (IRR), 1-year increase: 1.05 (1.03-1.07)]. A strong exposure-response relationship with smoking was found both in males [IRR, 1-pack-year increase: 1.03 (1.02-1.04)] and females [1.03 (1.02-1.05)]. The positive predictive value of AO for AO(post-BD) was 59.1% (52.0-66.2%) in men and 42.6% (35.1-50.1%) in women. AO(post-BD) incidence was 2.6 (1.7-3.4) male and 1.6 (1.0-2.2) female cases/1,000/year. AO incidence was considerable in Europe and the sex-specific ageing-related increase among ever smokers was strongly related to cumulative tobacco exposure. AO(post-BD) incidence is expected to be half of AO incidence.
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| 3. |
- Accordini, S., et al.
(author)
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Prenatal and prepubertal exposures to tobacco smoke in men may cause lower lung function in future offspring: a three-generation study using a causal modelling approach
- 2021
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In: European Respiratory Journal. - : European Respiratory Society (ERS). - 0903-1936 .- 1399-3003. ; 58:4
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Journal article (peer-reviewed)abstract
- 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 (FEV1) and forced vital capacity (FVC), or FEV1/FVC z-scores as potential mediators (proxies of unobserved biological mechanisms that are true mediators); and offspring's FEV1 and FVC, or FEV1/FVC z-scores as outcomes. All effects were summarised as differences (Delta) 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 FEV1 (Delta z-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' FEV1/FVC -0.57, 95% CI -1.09--0.05) and a negative indirect effect on offspring's FEV1/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.
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| 4. |
- Amaral, Andre F. S., et al.
(author)
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Chronic airflow obstruction and ambient particulate air pollution
- 2021
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In: Thorax. - : BMJ Publishing Group Ltd. - 0040-6376 .- 1468-3296. ; 76:12, s. 1236-1241
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Journal article (peer-reviewed)abstract
- Smoking is the most well-established cause of chronic airflow obstruction (CAO) but particulate air pollution and poverty have also been implicated. We regressed sex-specific prevalence of CAO from 41 Burden of Obstructive Lung Disease study sites against smoking prevalence from the same study, the gross national income per capita and the local annual mean level of ambient particulate matter (PM2.5) using negative binomial regression. The prevalence of CAO was not independently associated with PM2.5 but was strongly associated with smoking and was also associated with poverty. Strengthening tobacco control and improved understanding of the link between CAO and poverty should be prioritised.
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| 5. |
- Amaral, Rita, et al.
(author)
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The influence of individual characteristics and non-respiratory diseases on blood eosinophil count
- 2021
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In: Clinical and Translational Allergy. - : John Wiley & Sons. - 2045-7022. ; 11:4
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Journal article (peer-reviewed)abstract
- BackgroundBlood eosinophil (B-Eos) count is an emerging biomarker in the management of respiratory disease but determinants of B-Eos count besides respiratory disease are poorly described. Therefore, we aimed to evaluate the influence of non-respiratory diseases on B-Eos count, in comparison to the effect on two other biomarkers: fraction of exhaled nitric oxide (FeNO) and C-reactive protein (CRP), and to identify individual characteristics associated with B-Eos count in healthy controls.MethodsChildren/adolescents (<18 years) and adults with complete B-Eos data from the US National Health and Nutritional Examination Surveys 2005–2016 were included, and they were divided into having respiratory diseases (n = 3333 and n = 7,894, respectively) or not having respiratory disease (n = 8944 and n = 15,010, respectively). After excluding any respiratory disease, the association between B-Eos count, FeNO or CRP, and non-respiratory diseases was analyzed in multivariate models and multicollinearity was tested. After excluding also non-respiratory diseases independently associated with B-Eos count (giving healthy controls; 8944 children/adolescents and 5667 adults), the independent association between individual characteristics and B-Eos count was analyzed.ResultsIn adults, metabolic syndrome, heart disease or stroke was independently associated with higher B-Eos count (12%, 13%, and 15%, respectively), whereas no associations were found with FeNO or CRP. In healthy controls, male sex or being obese was associated with higher B-Eos counts, both in children/adolescents (15% and 3% higher, respectively) and adults (14% and 19% higher, respectively) (p < 0.01 all). A significant influence of race/ethnicity was also noted, and current smokers had 17% higher B-Eos count than never smokers (p < 0.001).ConclusionsNon-respiratory diseases influence B-Eos count but not FeNO or CRP. Male sex, obesity, certain races/ethnicities, and current smoking are individual characteristics or exposures that are associated with higher B-Eos counts. All these factors should be considered when using B-Eos count in the management of respiratory disease.
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| 6. |
- Amid Hägg, Shadi, et al.
(author)
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Smokers with insomnia symptoms are less likely to stop smoking
- 2020
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In: Respiratory Medicine. - : Elsevier BV. - 0954-6111 .- 1532-3064. ; 170
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Journal article (peer-reviewed)abstract
- Objectives: Smoking is associated with sleep disturbances. The aim of this study was to analyze whether sleep disturbances are predictors of smoking cessation and whether continued smoking is associated with the development of sleep disturbances. Methods: A questionnaire was sent to randomly selected men and women in Northern Europe in 1999-2001 (RHINE II) and was followed up by a questionnaire in 2010-2012 (RHINE III). The study population consisted of 2568 participants who were smokers at baseline and provided data on smoking at follow-up. Insomnia symptoms were defined as having difficulty initiating and/or maintaining sleep and/or early morning awakening >= 3 nights/week. Multiple logistic regression analyses were performed to calculate odds ratios (OR). Results: Subjects with difficulty initiating sleep (adjusted odds ratio; 95% confidence interval: 0.6; 0.4-0.8), difficulty maintaining sleep (0.7; 0.5-0.9), early morning awakening (0.6; 0.4-0.8), any insomnia symptom (0.6; 0.5-0.8) or excessive daytime sleepiness (0.7; 0.5-0.8) were less likely to achieve long-term smoking cessation after adjustment for age, BMI, pack-years, hypertension, diabetes, chronic bronchitis, rhinitis, asthma, gender and BMI difference. There was no significant association between snoring and smoking cessation. In subjects without sleep disturbance at baseline, continued smoking increased the risk of developing difficulty initiating sleep during the follow-up period compared with those that had quit smoking (adj. OR 1.7, 95% CI 1.2-2.3). Conclusions: Insomnia symptoms and excessive daytime sleepiness negatively predict smoking cessation. Smoking is a risk factor for the development of difficulty initiating sleep. Treatment for sleep disturbances should be included in smoking-cessation programs.
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| 7. |
- Amin, Kawa, et al.
(author)
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Evidence for eosinophil and IL-17 mediated inflammation in allergic rhinitis
- 2020
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In: Clinical and Molecular Allergy. - : Springer Science and Business Media LLC. - 1476-7961. ; 18
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Journal article (peer-reviewed)abstract
- Background: The aim was to determine the level of inflammatory cytokines, eosinophil cationic protein and IgE in allergic rhinitis (AR) patients.Subjects and methods: Blood samples were taken from 88 AR patients and 88 healthy controls (HC). Each sample was analysed for eosinophil counts by flow cytometry, IgE by ECLIA, ECP, IL-17, and IL-33 by using ELISA test.Results: There was no significant difference between AR patients and the control group in age and gender. Levels of eosinophils, IgE, ECP, IL-17, IL-33 and the total symptom scores were significantly higher in AR patients than the HC (P = 0.0001). Serum ECP correlated with IL-17 (P = 0.041, r = 0.42), IL-33 (P = 0.0001, r = 080), and IgE levels (P = 0.017, r = 0.45) in the R patients. There was no correlation between IL-17 and IL-33. There was a correlation between symptom scores and eosinophils (P = 0.026, r = 0.52), and IgE (P = 0.001, r = 0.60) in the patients. No correlation was observed between symptom scores and ECP, IL-17, and IL-33 in the AR patient.Conclusions: Patients with AR have significant higher serum levels of ECP, IL-17, and IL-33 than healthy controls. This indicates that these markers could be used to in order to diagnose AR and to monitor disease. Inhibitory molecules to IL-17 and IL-33 may be considered as novel treatment strategies.
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| 8. |
- Andersson, Maria, et al.
(author)
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Cost effectiveness of benralizumab for severe, uncontrolled oral corticosteroid-dependent asthma in Sweden
- 2020
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In: Journal of Medical Economics. - : TAYLOR & FRANCIS LTD. - 1369-6998 .- 1941-837X. ; 23:8, s. 877-884
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Journal article (peer-reviewed)abstract
- Aim: We investigated cost effectiveness of benralizumab vs. standard of care (SOC) plus oral corticosteroids (OCS) for patients with severe, eosinophilic OCS-dependent asthma in Sweden. Materials and methods: A three-state, cohort-based Markov model of data from three Phase III benralizumab clinical trials (ZONDA [NCT02075255], SIROCCO [NCT01928771], and CALIMA [NCT01914757]) was used to assess the incremental cost-effectiveness ratio of benralizumab vs. SOC plus OCS. Health outcomes were estimated in terms of quality-adjusted life-years (QALYs). The model included costs and disutilities associated with extrapolated OCS-related adverse events. Patients with severe asthma were defined as those receiving OCS >= 5 mg/day. Results: Benralizumab demonstrated a cost-effectiveness ratio vs. SOC plus OCS of 2018 Swedish Kronor (SEK) 366,855 (euro34,127) per QALY gained, based on increases of 1.33 QALYs and SEK 488,742 (euro45,344) per patient. Benralizumab treatment costs contributed most to incremental costs. The probability of benralizumab's being cost-effective with willingness-to-pay (WTP) thresholds between SEK 429,972 (euro40,000) and SEK 752,452 (euro70,000) ranged from 75% to 99%. Limitations: Potential limitations of these analyses include the use of combined data from three different clinical trials, a one-way sensitivity analysis that did not include mortality and transition estimates, and Observational & Pragmatic Research Institute (OPRI) data from the UK as a proxy of the Swedish health care system. Conclusions: The results of these analyses demonstrate that benralizumab has a high probability of being cost-effective compared with SOC plus OCS for a subgroup of patients with severe, eosinophilic asthma receiving regular OCS treatment and may support clinicians, payers and patients in making treatment decisions.
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| 9. |
- Athlin, Åsa, 1971-, et al.
(author)
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Prediction of Mortality Using Different COPD Risk Assessments : A 12-Year Follow-Up
- 2021
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In: The International Journal of Chronic Obstructive Pulmonary Disease. - : Dove Medical Press Ltd.. - 1176-9106 .- 1178-2005. ; 16, s. 665-675
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Journal article (peer-reviewed)abstract
- Purpose: A multidimensional approach in the risk assessment of chronic obstructive pulmonary disease (COPD) is preferable. The aim of this study is to compare the prognostic ability for mortality by different COPD assessment systems; spirometric staging, classification by GOLD 2011, GOLD 2017, the age, dyspnea, obstruction (ADO) and the dyspnea, obstruction, smoking, exacerbation (DOSE) indices.Patients and Methods: A total of 490 patients diagnosed with COPD were recruited from primary and secondary care in central Sweden in 2005. The cohort was followed until 2017. Data for categorization using the different assessment systems were obtained through questionnaire data from 2005 and medical record reviews between 2000 and 2003. Kaplan-Meier survival analyses and Cox proportional hazard models were used to assess mortality risk. Receiver operating characteristic curves estimated areas under the curve (AUC) to evaluate each assessment systems´ ability to predict mortality.Results: By the end of follow-up, 49% of the patients were deceased. The mortality rate was higher for patients categorized as stage 3-4, GOLD D in both GOLD classifications and those with a DOSE score above 4 and ADO score above 8. The ADO index was most accurate for predicting mortality, AUC 0.79 (95% CI 0.75-0.83) for all-cause mortality and 0.80 (95% CI 0.75-0.85) for respiratory mortality. The AUC values for stages 1-4, GOLD 2011, GOLD 2017 and DOSE index were 0.73, 0.66, 0.63 and 0.69, respectively, for all-cause mortality.Conclusion: All of the risk assessment systems predict mortality. The ADO index was in this study the best predictor and could be a helpful tool in COPD risk assessment.
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| 10. |
- Bedard, Annabelle, et al.
(author)
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Physical activity and lung function-Cause or consequence?
- 2020
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In: PLOS ONE. - : PUBLIC LIBRARY SCIENCE. - 1932-6203. ; 15:8
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Journal article (peer-reviewed)abstract
- Concerns exist that the positive association of physical activity with better lung function, which has been suggested in previous longitudinal studies in smokers, is due to reverse causation. To investigate this, we applied structural equation modeling (SEM), an exploratory approach, and marginal structural modeling (MSM), an approach from the causal inference framework that corrects for reverse causation and time-dependent confounding and estimates causal effects, on data from participants in the European Community Respiratory Health Survey (ECRHS, a multicentre European cohort study initiated in 1991-1993 with ECRHS I, and with two follow-ups: ECRHS II in 1999-2003, and ECRHS III in 2010-2014). 753 subjects who reported current smoking at ECRHS II, with repeated data on lung function at ECRHS I, II and III, physical activity at ECRHS II and III, and potential confounders at ECRHS I and II, were included in the analyses. SEM showed positive associations between physical activity and lung function in both directions. MSM suggested a protectivecausaleffect of physical activity on lung function (overall difference in mean beta (95% CI), comparing active versus non-active individuals: 58 mL (21-95) for forced expiratory volume in one second and 83 mL (36-130) for forced vital capacity). Our results suggest bi-directional causation and support a true protective effect of physical activity on lung function in smokers, after accounting for reverse causation and time-dependent confounding.
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