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Sökning: WFRF:(Kirkeleit Jorunn)

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1.
  • Johannessen, Ane, et al. (författare)
  • Long-term air pollution exposure is associated with sick leave 20 years later
  • 2018
  • Ingår i: European Respiratory Journal. - : European Respiratory Society. - 0903-1936 .- 1399-3003. ; 52
  • 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 In the Nordic countries, recent pollution health impact assessments have had to rely on outdated studies.Aims: To investigate if air pollution exposure is associated with sick leave 20 years later.Methods: We analysed self-reported sick leave (all-cause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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2.
  • Kirkeleit, Jorunn, et al. (författare)
  • Early life exposures contributing to accelerated lung function decline in adulthood – a follow-up study of 11,000 adults from the general population
  • 2023
  • Ingår i: eClinicalMedicine. - : Elsevier. - 2589-5370. ; 66
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: We aimed to assess whether exposure to risk factors in early life from conception to puberty continue to contribute to lung function decline later in life by using a pooled cohort comprising approx. 11,000 adults followed for more than 20 years and with up to three lung function measurements. Methods: Participants (20–68 years) in the ECRHS and NFBC1966 cohort studies followed in the periods 1991–2013 and 1997–2013, respectively, were included. Mean annual decline in maximum forced expired volume in 1 s (FEV1) and forced vital capacity (FVC) were main outcomes. Associations between early life risk factors and change in lung function were estimated using mixed effects linear models adjusted for sex, age, FEV1, FVC and height at baseline, accounting for personal smoking. Findings: Decline in lung function was accelerated in participants with mothers that smoked during pregnancy (FEV1 2.3 ml/year; 95% CI: 0.7, 3.8) (FVC 2.2 ml/year; 0.2, 4.2), with asthmatic mothers (FEV1 2.6 ml/year; 0.9, 4.4) (FEV1/FVC 0.04 per year; 0.04, 0.7) and asthmatic fathers (FVC 2.7 ml/year; 0.5, 5.0), and in women with early menarche (FVC 2.4 ml/year; 0.4, 4.4). Personal smoking of 10 pack-years contributed to a decline of 2.1 ml/year for FEV1 (1.8, 2.4) and 1.7 ml/year for FVC (1.3, 2.1). Severe respiratory infections in early childhood were associated with accelerated decline among ever-smokers. No effect-modification by personal smoking, asthma symptoms, sex or cohort was found. Interpretation: Mothers’ smoking during pregnancy, parental asthma and early menarche may contribute to a decline of FEV1 and FVC later in life comparable to smoking 10 pack-years. Funding: European Union's Horizon 2020; Research Council of Norway; Academy of Finland; University Hospital Oulu; European Regional Development Fund; Spanish Ministry of Science and Innovation; Generalitat de Catalunya.
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3.
  • Kirkeleit, Jorunn, et al. (författare)
  • Early life origins of lung ageing : A study of lung function decline the ECRHS and NFBC1966 cohorts
  • 2020
  • Ingår i: European Respiratory Journal. - : ERS Publications. - 0903-1936 .- 1399-3003. ; 56
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Objective: To determine whether early life factors associated with poor lung growth and submaximal attained lung function contribute to accelerated lung function decline later in life.Methods: Participants in the European Community Respiratory Health Survey (ECRHS) and the Northern Finland Birth Cohort 1966 (NFBC1966) with lung function measured in a first (n=10,971), second (n=7,981) and third wave (n=4,849), aged 20 – 68 years, were included. Mean annual decline in maximum forced expired volume in 1 second (FEV1) and forced vital capacity (FVC) were main outcomes. Information on early life factors was provided by standardized interviews and questionnaires. We estimated the effect of early life factors including maternal age, parental smoking, season of birth, parental asthma and respiratory infections using mixed effects models, adjusted for age, FEV1 and FVC at baseline, height, and smoking habits.Results: Decline in FEV1 was accelerated in women born of a mother with asthma (β = 2.4 ml; 95% CI 0.6-4.3) or who smoked during pregnancy (1.9; 0.2-3.6), and in men having a father with asthma (3.5; 0.2-6.9) or born by Cesarean section (7.9; 1.6-14.2). Accelerated decline in FVC was associated with paternal asthma in men (4.3; 0.1-8.5) and early menarche (<12 years) in women (2.4; 0.4-4.4). No statistically significant effect on lung function decline was found for other investigated early life factors.Conclusion: Early life risk factors contribute to an accelerated lung function decline with ageing, following sex-specific patterns. Decline in FEV1 versus FVC showed slightly different patterns.
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4.
  • Lonnebotn, Marianne, et al. (författare)
  • Late Breaking Abstract - Associations of fathers and their offsprings weight gain with non-allergic asthma
  • 2018
  • Ingår i: European Respiratory Journal. - : European Respiratory Society. - 0903-1936 .- 1399-3003. ; 52
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
    • Background: We found that a father’s overweight in puberty was associated with non-allergic asthma in his future offspring.Aim: We explored the associations of both fathers and their offsprings own weight gain throughout the lifespan with offspring non-allergic asthma.Methods: We analysed questionnaire data from 3018 adult offspring (age 18-50) and their 2153 fathers (age 39-66) participating in the RHINESSA/RHINE generation study in 10 ECRHS centres in North Europe, Spain and Australia. The associations of fathers' and their offsprings weight gain was assessed by 9 body silhouettes (from lean to fat) self-reported for childhood, puberty and adult ages with non-allergic asthma in the offspring. It was analysed using a logistic regression model adjusted for parents and offspring variables, and cluster by family.Results: Non-allergic asthma was related to a weight gain of ≥2 body silhouettes from 8 years to puberty, both for fathers’ weight gain (OR 1.69; 95% CI 1.05-2.72; adjusted for fathers asthma, offspring body mass index, smoking and education) and for their offspring weight gain (1.77 [1.12-2.79], adjusted for parents´ education, smoking and asthma, and fathers´ weight gain from age 8 to puberty). If the father was overweight at puberty, in addition to having gained weight, non-allergic asthma in the offspring was more than tripled (3.53[1.80-6.94]; weight gain and adjustment as given above). No effect of weight gain from puberty or within adulthood in fathers’ or their offspring was observed.Conclusion: Non-allergic asthma was associated with weight gain from childhood to puberty. This was found both for personal weight gain and for having a father who gained weight.
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5.
  • Peters, Susan, et al. (författare)
  • Narrative review of occupational exposures and noncommunicable diseases
  • 2024
  • Ingår i: ANNALS OF WORK EXPOSURES AND HEALTH. - 2398-7308 .- 2398-7316. ; 68:6, s. 562-580
  • Forskningsöversikt (refereegranskat)abstract
    • Objective Within the scope of the Exposome Project for Health and Occupational Research on applying the exposome concept to working life health, we aimed to provide a broad overview of the status of knowledge on occupational exposures and associated health effects across multiple noncommunicable diseases (NCDs) to help inform research priorities.Methods We conducted a narrative review of occupational risk factors that can be considered to have "consistent evidence for an association," or where there is "limited/inadequate evidence for an association" for 6 NCD groups: nonmalignant respiratory diseases; neurodegenerative diseases; cardiovascular/metabolic diseases; mental disorders; musculoskeletal diseases; and cancer. The assessment was done in expert sessions, primarily based on systematic reviews, supplemented with narrative reviews, reports, and original studies. Subsequently, knowledge gaps were identified, e.g. based on missing information on exposure-response relationships, gender differences, critical time-windows, interactions, and inadequate study quality.Results We identified over 200 occupational exposures with consistent or limited/inadequate evidence for associations with one or more of 60+ NCDs. Various exposures were identified as possible risk factors for multiple outcomes. Examples are diesel engine exhaust and cadmium, with consistent evidence for lung cancer, but limited/inadequate evidence for other cancer sites, respiratory, neurodegenerative, and cardiovascular diseases. Other examples are physically heavy work, shift work, and decision latitude/job control. For associations with limited/inadequate evidence, new studies are needed to confirm the association. For risk factors with consistent evidence, improvements in study design, exposure assessment, and case definition could lead to a better understanding of the association and help inform health-based threshold levels.Conclusions By providing an overview of knowledge gaps in the associations between occupational exposures and their health effects, our narrative review will help setting priorities in occupational health research. Future epidemiological studies should prioritize to include large sample sizes, assess exposures prior to disease onset, and quantify exposures. Potential sources of biases and confounding need to be identified and accounted for in both original studies and systematic reviews.
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6.
  • Thompson, Paul, et al. (författare)
  • Supporting the working life exposome: Annotating occupational exposure for enhanced literature search
  • 2024
  • Ingår i: PLOS ONE. - 1932-6203. ; 19:8
  • Tidskriftsartikel (refereegranskat)abstract
    • An individual's likelihood of developing non-communicable diseases is often influenced by the types, intensities and duration of exposures at work. Job exposure matrices provide exposure estimates associated with different occupations. However, due to their time-consuming expert curation process, job exposure matrices currently cover only a subset of possible workplace exposures and may not be regularly updated. Scientific literature articles describing exposure studies provide important supporting evidence for developing and updating job exposure matrices, since they report on exposures in a variety of occupational scenarios. However, the constant growth of scientific literature is increasing the challenges of efficiently identifying relevant articles and important content within them. Natural language processing methods emulate the human process of reading and understanding texts, but in a fraction of the time. Such methods can increase the efficiency of both finding relevant documents and pinpointing specific information within them, which could streamline the process of developing and updating job exposure matrices. Named entity recognition is a fundamental natural language processing method for language understanding, which automatically identifies mentions of domain-specific concepts (named entities) in documents, e.g., exposures, occupations and job tasks. State-of-the-art machine learning models typically use evidence from an annotated corpus, i.e., a set of documents in which named entities are manually marked up (annotated) by experts, to learn how to detect named entities automatically in new documents. We have developed a novel annotated corpus of scientific articles to support machine learning based named entity recognition relevant to occupational substance exposures. Through incremental refinements to the annotation process, we demonstrate that expert annotators can attain high levels of agreement, and that the corpus can be used to train high-performance named entity recognition models. The corpus thus constitutes an important foundation for the wider development of natural language processing tools to support the study of occupational exposures.
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