| 1. |
- Ekström, Magnus, et al.
(författare)
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Breathlessness across generations : results from the RHINESSA generation study
- 2022
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Ingår i: Thorax. - : BMJ. - 0040-6376 .- 1468-3296. ; 77:2, s. 172-177
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Tidskriftsartikel (refereegranskat)abstract
- Background: Breathlessness is a major cause of suffering and disability globally. The symptom relates to multiple factors including asthma and lung function, which are influenced by hereditary factors. No study has evaluated potential inheritance of breathlessness itself across generations.Methods: We analysed the association between breathlessness in parents and their offspring in the Respiratory Health in Northern Europe, Spain and Australia generation study. Data on parents and offspring aged ≥18 years across 10 study centres in seven countries included demographics, self-reported breathlessness, asthma, depression, smoking, physical activity level, measured Body Mass Index and spirometry. Data were analysed using multivariable logistic regression accounting for clustering within centres and between siblings.Results: A total of 1720 parents (mean age at assessment 36 years, 55% mothers) and 2476 offspring (mean 30 years, 55% daughters) were included. Breathlessness was reported by 809 (32.7%) parents and 363 (14.7%) offspring. Factors independently associated with breathlessness in parents and offspring included obesity, current smoking, asthma, depression, lower lung function and female sex. After adjusting for potential confounders, parents with breathlessness were more likely to have offspring with breathlessness, adjusted OR 1.8 (95% CI 1.1 to 2.9). The association was not modified by sex of the parent or offspring.Conclusion: Parents with breathlessness were more likely to have children who developed breathlessness, after adjusting for asthma, lung function, obesity, smoking, depression and female sex in both generations. The hereditary components of breathlessness need to be further explored.
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| 2. |
- Emilsson, Össur Ingi, et al.
(författare)
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Heritability of cough across two generations : the RHINESSA study.
- 2024
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Ingår i: ERJ open research. - : European Respiratory Society. - 2312-0541. ; 10:4
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Tidskriftsartikel (refereegranskat)abstract
- 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.
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| 3. |
- Johannessen, Ane, et al.
(författare)
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Long-term air pollution exposure is associated with sick leave 20 years later
- 2018
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Ingår i: European Respiratory Journal. - : European Respiratory Society. - 0903-1936 .- 1399-3003. ; 52
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Background: Little is known on outdoor air pollution in a long-term perspective and societal costs such as sick leave. In the Nordic countries, recent pollution health impact assessments have had to rely on outdated studies.Aims: To investigate if air pollution exposure is associated with sick leave 20 years later.Methods: We analysed self-reported sick leave (all-cause and respiratory) in 7 466 subjects from Bergen, Gothenburg, Umea, Uppsala in the RHINE3 study in 2010-12. Home addresses were geocoded and linked to annual average concentrations of PM2.5, PM10 and NO2 at RHINE3, 10 years earlier and 20 years earlier, using existing land-use regression (LUR) models. We performed multilevel logistic regression clustered by centre, and adjusted for sex, smoking, education and previous health-related workplace change.Results: Age range in RHINE3 was 40-66 yrs, 34% and 4% reported all-cause and respiratory sick leave during the last year. In the adjusted analyses all-cause sick leave was associated with PM2.520 years earlier (OR per interquartile range (IQR) difference (2.6 µg/m³) 1.12 (95%CI 1.01, 1.24)), and borderline with NO2 (OR per IQR diff (8.1 µg/m³) 1.09 (95%CI 0.99, 1.19)). Respiratory sick leave was associated with PM10 20 years earlier (OR per IQR diff (3.92 µg/m³) 1.54 (95%CI 1.06, 2.25)), and borderline with PM2.5 (OR per IQR diff 1.31 (95%CI 0.97, 1.76)). Pollution exposures at present as well as 10 years earlier were not significantly associated with sick leave.Conclusions: Air pollution exposure in a general population is associated with sick leave in a 20-year perspective. Our findings suggest that even low air pollution levels such as in Northern Europe have societal costs over time.
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| 4. |
- Kuiper, Ingrid Nordeide, et al.
(författare)
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Lung health in adulthood after childhood exposure to air pollution and greenness
- 2018
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Ingår i: European Respiratory Journal. - : European Respiratory Society. - 0903-1936 .- 1399-3003. ; 52
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Background: Little is known on childhood exposure to air pollution and adult chronic respiratory outcomes.Aim: To investigate associations between air pollution and greenness in childhood and adult lung health.Methods: In selected centres of the RHINESSA study (age 18-52) we analysed the outcomes respiratory symptoms (≥3 symptoms), severe wheeze (wheeze last year with breathlessness, no cold) and late onset asthma (>10 years). We calculated mean annual exposures of PM2.5, PM10, NO2 (µg/m³) and greenness (Normalized Difference Vegetation Index, 100m buffer) from offspring's birth till age 18, categorised into mean exposure <10 years and 11-18 years. We performed multilevel logistic regression clustered by family, stratified by centre and adjusted for childhood passive smoke and parental asthma.Results: 12% had ≥3 respiratory symptoms, 7.7% severe wheeze, and 9.4% late onset asthma. Overall estimates: greenness was associated with less respiratory symptoms, PM2.5 and NO2 with more late onset asthma. Exposure <10 years: Greenness was associated with less wheeze in Tartu (OR 0.29, 95%CI 0.11-0.73). PM2.5 (OR 1.22, 95%CI 1.00-1.48) and NO2 (OR 1.06, 95%CI 1.01-1.11) were risk factors for late onset asthma in Bergen. PM10 was a risk factor for respiratory symptoms (OR 1.21, 95%CI 1.04-1.41) in Uppsala and late onset asthma (OR 1.23, 95%CI 1.02-1.45) in Bergen. Exposure 11-18 years: Greenness was protective for respiratory symptoms (OR 0.29, 95%CI 0.10-0.86) and wheeze (OR 0.39, 95%CI 0.19-0.80) in Tartu.Conclusions: Childhood exposure to greenness was associated with less respiratory symptoms, while air pollutants were associated with more respiratory symptoms (some centres) and late onset asthma.
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| 5. |
- López-Cervantes, Juan Pablo, et al.
(författare)
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Use of oral moist tobacco (snus) in puberty and its association with asthma in the population-based RHINESSA study.
- 2024
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Ingår i: BMJ Open Respiratory Research. - : BMJ Publishing Group Ltd. - 2052-4439. ; 11:1
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To investigate the association of early snus use initiation (≤15 years of age) with asthma and asthma symptoms.DESIGN: Cross-sectional analysis of a population-based cohort.SETTING: Study centres in Norway, Sweden, Iceland, Denmark and Estonia, from 2016 to 2019.PARTICIPANTS: 9002 male and female participants above 15 years of age of the Respiratory Health in Northern Europe, Spain and Australia study.MAIN OUTCOME MEASURES: Current asthma and asthma symptoms.RESULTS: The median age of study participants was 28 years (range 15-53) and 58% were women. 20% had used snus, 29% men and 14% women. Overall, 26% of males and 14% of females using snus started ≤15 years of age. Early snus use initiation was associated with having three or more asthma symptoms (OR 2.70; 95% CI 1.46 to 5.00) and a higher asthma symptom score (β-coefficient (β) 0.35; 95% CI 0.07 to 0.63) in women. These associations were weak in men (OR 1.23; 95% CI 0.78 to 1.94; β 0.16; 95% CI -0.06 to 0.38, respectively). There was evidence for an association of early snus initiation with current asthma (OR 1.72; 95% CI 0.88 to 3.37 in women; OR 1.31; 95% CI 0.84 to 2.06 in men). A sensitivity analysis among participants without smoking history showed stronger estimates for all three outcomes, in both men and women, statistically significant for three or more asthma symptoms in women (OR 3.28; 95% CI 1.18 to 9.10). Finally, no consistent associations with asthma outcomes were found for starting snus after age 15 years.CONCLUSIONS: Snus initiation in puberty was associated with higher likelihood of asthma and asthma symptoms, with the highest estimates in females and those without smoking history. These results raise concerns about the health adversities of early snus initiation and emphasise the need for public health initiatives to protect young people from this tobacco product.
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| 6. |
- Vogt, Elinor Chelsom, et al.
(författare)
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Premature menopause and autoimmune primary ovarian insufficiency in two international multi-center cohorts
- 2022
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Ingår i: Endocrine Connections. - : Bioscientifica. - 2049-3614. ; 11:5
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To investigate markers of premature menopause (<40 years) and specifically the prevalence of autoimmune primary ovarian insufficiency (POI) in European women.Design: Postmenopausal women were categorized according to age at menopause and self-reported reason for menopause in a cross-sectional analysis of 6870 women.Methods: Variables associated with the timing of menopause and hormone measurements of 17β-estradiol and follicle-stimulating hormone were explored using multivariable logistic regression analysis. Specific immunoprecipitating assays of steroidogenic autoantibodies against 21-hydroxylase (21-OH), side-chain cleavage enzyme (anti-SCC) and 17alpha-hydroxylase (17 OH), as well as NACHT leucine-rich-repeat protein 5 were used to identify women with likely autoimmune POI.Results: Premature menopause was identified in 2.8% of women, and these women had higher frequencies of nulliparity (37.4% vs 19.7%), obesity (28.7% vs 21.4%), osteoporosis (17.1% vs 11.6%), hormone replacement therapy (59.1% vs 36.9%) and never smokers (60.1% vs 50.9%) (P < 0.05), compared to women with menopause ≥40 years. Iatrogenic causes were found in 91 (47%) and non-ovarian causes in 27 (14%) women, while 77 (39%) women were classified as POI of unknown cause, resulting in a 1.1% prevalence of idiopathic POI. After adjustments nulliparity was the only variable significantly associated with POI (odds ratio 2.46; 95% CI 1.63-3.42). Based on the presence of autoantibodies against 21 OH and SCC, 4.5% of POI cases were of likely autoimmune origin.Conclusion: Idiopathic POI affects 1.1% of all women and almost half of the women with premature menopause. Autoimmunity explains 4.5% of these cases judged by positive steroidogenic autoantibodies.
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