| 1. |
- 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 In the Nordic countries, recent pollution health impact assessments have had to rely on outdated studies.Aims: To investigate if air pollution exposure is associated with sick leave 20 years later.Methods: We analysed self-reported sick leave (all-cause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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| 2. |
- Kirkeleit, Jorunn, et al.
(författare)
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Early life exposures contributing to accelerated lung function decline in adulthood – a follow-up study of 11,000 adults from the general population
- 2023
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Ingår i: eClinicalMedicine. - : Elsevier. - 2589-5370. ; 66
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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)
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Early life origins of lung ageing : A study of lung function decline the ECRHS and NFBC1966 cohorts
- 2020
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Ingår i: European Respiratory Journal. - : ERS Publications. - 0903-1936 .- 1399-3003. ; 56
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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)
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Late Breaking Abstract - Associations of fathers and their offsprings weight gain with non-allergic asthma
- 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: 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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