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Post coronavirus disease-19 (post COVID-19) is mainly studied in clinical populations and less is known about post COVID-19 in a young general population. The aim of the study is to investigate the prevalence and symptoms of post COVID-19 and its potential risk factors in young adults. Participants from the Swedish population-based birth cohort BAMSE were included (n = 2022, mean age 26.5 years). Post COVID-19 was assessed through a questionnaire and defined as symptoms after confirmed COVID-19 (registry-based or self-reported positive test) lasting for ≥ 2 months. In total, 681 participants had had confirmed COVID-19. Among them, 112 (16.5%) fulfilled the definition of post COVID-19 (17.8% in females, 14.5% in males, p = 0.26). The most common post COVID-19 symptoms were altered smell and taste (68.8%), dyspnea (33.7%) and fatigue (30.4%). Overall, no major risk factors for post COVID-19 were identified except for being bedbound during COVID-19. However, asthma and rhinitis were associated with the post COVID-19 symptom dyspnea, migraine with altered smell and taste, and lower self-rated health with fatigue. In conclusion, post COVID-19 symptoms are common, also among young adults in the general population. Although not life-threatening, it could have a considerable impact on public health due to the high prevalence and long-term symptoms. [ABSTRACT FROM AUTHOR]

Background: The understanding of the influence of smoking and sex on lung function and symptoms is important for understanding diseases such as COPD. The influence of both genes and environment on lung function, smoking behaviour and the presence of respiratory symptoms has previously been demonstrated for each of these separately. Hence, smoking can influence lung function by co-varying not only as an environmental factor, but also by shared genetic pathways. Therefore, the objective was to evaluate heritability for different aspects of lung function, and to investigate how the estimates are affected by adjustments for smoking and respiratory symptoms. Methods: The current study is based on a selected sample of adult twins from the Swedish Twin Registry. Pairs were selected based on background data on smoking and respiratory symptoms collected by telephone interview. Lung function was measured as FEV1, VC and DLco. Pack years were quantified, and quantitative genetic analysis was performed on lung function data adjusting stepwise for sex, pack years and respiratory symptoms. Results: Fully adjusted heritability for VC was 59% and did not differ by sex, with smoking and symptoms explaining only a small part of the total variance. Heritabilities for FEV1 and DLco were sex specific. Fully adjusted estimates were10 and 15% in men and 46% and 39% in women, respectively. Adjustment for smoking and respiratory symptoms altered the estimates differently in men and women. For FEV1 and DLco, the variance explained by smoking and symptoms was larger in men. Further, smoking and symptoms explained genetic variance in women, but was primarily associated with shared environmental effects in men. Conclusion: Differences between men and women were found in how smoking and symptoms influence the variation in lung function. Pulmonary gas transfer variation related to the menstrual cycle has been shown before, and the findings regarding DLco in the present study indicates gender specific environmental susceptibility not shown before. As a consequence the results suggest that patients with lung diseases such as COPD could benefit from interventions that are sex specific. [ABSTRACT FROM AUTHOR]

There are a number of evidences suggesting that lung perfusion distribution is under active regulation and determined by several factors in addition to gravity. In this work, we hypothesised that autoinhalation of nitric oxide (NO), produced in the human nasal airways, may be one important factor regulating human lung perfusion distribution in the upright position. In 15 healthy volunteers, we used single-photon emission computed tomography technique and two tracers (99mTc and 113mIn) labeled with human macroaggregated albumin to assess pulmonary blood flow distribution. In the sitting upright position, subjects first breathed NO free air through the mouth followed by the administration of the first tracer. Subjects then switched to either nasal breathing or oral breathing with the addition of exogenous NO-enriched air followed by the administration of the second tracer. Compared with oral breathing, nasal breathing induced a blood flow redistribution of ∼4% of the total perfusion in the caudal to cranial and dorsal to ventral directions. For low perfused lung regions like the apical region, this represents a net increase of 24% in blood flow. Similar effects were obtained with the addition of exogenous NO during oral breathing, indicating that NO and not the breathing condition was responsible for the blood flow redistribution. In conclusion, these results provide evidence that autoinhalation of endogenous NO from the nasal airways may ameliorate the influence of gravity on pulmonary blood flow distribution in the upright position. The presence of nasal NO only in humans and higher primates suggest that it may be an important part of the adaptation to bipedalism. [ABSTRACT FROM AUTHOR]

Background: Bronchopulmonary dysplasia (BPD) is a risk factor for respiratory disease in adulthood. Despite the differences in underlying pathology, patients with a history of BPD are often treated as asthmatics. We hypothesized that pulmonary outcomes and health-related quality of life (HRQoL) were different in adults born preterm with and without a history of BPD compared to asthmatics and healthy individuals. Methods: We evaluated 96 young adults from the LUNAPRE cohort (clinicaltrials.gov/ct2/show/NCT02923648), including 26 individuals born preterm with a history of BPD (BPD), 23 born preterm without BPD (preterm), 23 asthmatics and 24 healthy controls. Extensive lung function testing and HRQoL were assessed. Results: The BPD group had more severe airway obstruction compared to the preterm-, (FEV1− 0.94 vs. 0.28 z-scores; p ≤ 0.001); asthmatic- (0.14 z-scores, p ≤ 0.01) and healthy groups (0.78 z-scores, p ≤ 0.001). Further, they had increased ventilation inhomogeneity compared to the preterm- (LCI 6.97 vs. 6.73, p ≤ 0.05), asthmatic- (6.75, p = 0.05) and healthy groups (6.50 p ≤ 0.001). Both preterm groups had lower DLCO compared to healthy controls (p ≤ 0.001 for both). HRQoL showed less physical but more psychological symptoms in the BPD group compared to asthmatics. Conclusions: Lung function impairment and HRQoL in adults with a history of BPD differed from that in asthmatics highlighting the need for objective assessment of lung health. [ABSTRACT FROM AUTHOR]

Background Little is known about early-life risk factors for food allergy in children. Objectives We examined the association between perinatal characteristics and future risk of food allergy in offspring. Methods This nationwide Swedish cohort study of 1,086,378 children born in Sweden in 2001-2012 used prospectively recorded data from health care registers. Using Cox regression, we estimated hazard ratios (HRs) with 95% CIs for the association between perinatal characteristics (eg, cesarean delivery and preterm birth) and food allergy as defined by diagnoses in the National Patient Register, adjusting for infant sex and maternal factors (age at delivery, country of birth, parity, smoking, body mass index, and asthma/pulmonary disease). Results During the 13-year follow-up, 26,732 (2.5%) children were given a diagnosis of food allergy. Food allergy was positively associated with cesarean delivery (HR, 1.21; 95% CI, 1.18-1.25), large for gestational age (HR, 1.15; 95% CI, 1.10-1.19), and low 5-minute Apgar score (HR, 1.22; 95% CI, 1.10-1.36) but negatively associated with very preterm birth (<32 weeks of gestation: HR, 0.74; 95% CI, 0.56-0.98). No association was found between food allergy and moderately preterm birth, low birth weight, or small for gestational age. Risk estimates were similar when the outcome was restricted to 2 records of diagnosed food allergy. In 1,000 children undergoing cesarean delivery, an extra 5 developed food allergy compared with the reference group, suggesting that 17% of food allergy in children born by means of cesarean delivery can be explained by this exposure (attributable fraction). Conclusions Cesarean delivery was associated with increased risk of food allergy, whereas very preterm birth decreased risk. Graphical abstract [ABSTRACT FROM AUTHOR]

Lung development starts in utero and continues during childhood through to adolescence, reaching its peak in early adulthood. This growth is followed by gradual decline due to physiological lung ageing. Lung-function development can be altered by several host and environmental factors during the life course. As a result, a range of lung-function trajectories exist in the population. Below average trajectories are associated with respiratory, cardiovascular, metabolic, and mental health comorbidities, as well as with premature death. This Review presents progressive research into lung-function trajectories and assists the implementation of this knowledge in clinical practice as an innovative approach to detect poor lung health early, monitor respiratory disease progression, and promote lung health. Specifically, we propose that, similar to paediatric height and weight charts used globally to monitor children's growth, lung-function charts could be used for both children and adults to monitor lung health status across the life course. To achieve this proposal, we introduce our free online Lung Function Tracker tool. Finally, we discuss challenges and opportunities for effective implementation of the trajectory concept at population level and outline an agenda for crucial research needed to support such implementation. [ABSTRACT FROM AUTHOR]

A study published in the journal Clinical & Experimental Allergy investigated the association between a Mediterranean-type diet in childhood and the development of asthma and lung function in adulthood. The study, conducted in Sweden, found no consistent association between adherence to a Mediterranean-type diet and asthma, allergic/non-allergic phenotypes, or lung function overall. However, among participants with asthma, higher adherence to the diet was associated with higher forced vital capacity (FVC) and lower forced expiratory volume in 1 second (FEV1)/FVC ratio. The study suggests that further research with larger sample sizes and the use of nutritional biomarker scores is needed. [Extracted from the article]

Systemic inflammation is one potential mechanism underlying negative impact of air pollution on lung function. Levels of inflammation-related proteins have the potential to characterize infants' susceptibility to air pollution induced lung function impairment. This study aimed to examine the interplay between air pollution exposure and inflammation-related proteins on lung function in 6-months-old infants. In the EMIL birth cohort from Stockholm (n = 82), dynamic spirometry, along with measurement of plasma levels of 92 systemic inflammation-related proteins (Olink Proseek Multiplex Inflammation panel) have been carried out in infants aged six months. Time-weighted average exposure to particles with an aerodynamic diameter of <10 μm (PM 10), <2.5 μm (PM 2.5), and nitrogen dioxide (NO 2) at residential addresses from birth and onwards was estimated via validated dispersion models. To characterize the abnormality of inflammation-related protein profile, for each protein in each infant, we calculated the relative deviance of the protein level from age- and sex-specific median in terms of its age- and sex-specific interquartile range (IQR), followed by computing the absolute value of the smallest relative deviance, "minimum absolute deviance". Using linear regression models, interaction of air pollution and the abnormal inflammatory profile on lung function was estimated on the additive scale. We found joint association of PM exposure and an abnormal inflammatory protein profile in relation to FEV 0.5 and FVC. For 0.1 unit increase in minimum absolute deviance, one IQR increase in PM 10 was associated with 85.9 ml (95% CI: −122.9, −48.9) additional decrease in FEV 0.5, and 72.3 ml (95% CI: −121.5, −23.2) additional decrease in FVC. Similar results were obtained with PM 2.5 exposure, while less apparent for NO 2. Early life air pollution exposure and abnormal inflammation-related protein profiles may interact synergistically towards lower lung function in infants. [ABSTRACT FROM AUTHOR]

Background: Adolescence is a significant period for the gender-dependent development of lung function. Prior studies have shown that DNA methylation (DNA-M) is associated with lung function and DNA-M at some cytosine-phosphate-guanine dinucleotide sites (CpGs) changes over time. This study examined whether changes of DNA-M at lung-function-related CpGs are associated with changes in lung function during adolescence for each gender, and if so, the biological significance of the detected CpGs.Methods: Genome-scale DNA-M was measured in peripheral blood samples at ages 10 (n = 330) and 18 years (n = 476) from the Isle of Wight (IOW) birth cohort in United Kingdom, using Illumina Infinium arrays (450 K and EPIC). Spirometry was conducted at both ages. A training and testing method was used to screen 402,714 CpGs for their potential associations with lung function. Linear regressions were applied to assess the association of changes in lung function with changes of DNA-M at those CpGs potentially related to lung function. Adolescence-related and personal and family-related confounders were included in the model. The analyses were stratified by gender. Multiple testing was adjusted by controlling false discovery rate of 0.05. Findings were further examined in two independent birth cohorts, the Avon Longitudinal Study of Children and Parents (ALSPAC) and the Children, Allergy, Milieu, Stockholm, Epidemiology (BAMSE) cohort. Pathway analyses were performed on genes to which the identified CpGs were mapped.Results: For females, 42 CpGs showed statistically significant associations with change in FEV1/FVC, but none for change in FEV1 or FVC. No CpGs were identified for males. In replication analyses, 16 and 21 of the 42 CpGs showed the same direction of associations among the females in the ALSPAC and BAMSE cohorts, respectively, with 11 CpGs overlapping across all the three cohorts. Through pathway analyses, significant biological processes were identified that have previously been related to lung function development.Conclusions: The detected 11 CpGs in all three cohorts have the potential to serve as the candidate epigenetic markers for changes in lung function during adolescence in females. [ABSTRACT FROM AUTHOR]

Exposure to polycyclic aromatic hydrocarbons (PAHs) has been linked to adverse pulmonary effects. However, the impact of low-level environmental PAH exposure on lung function in early adulthood remains uncertain. To evaluate the associations between urinary PAH metabolites and lung function parameters in young adults. Urinary metabolites of pyrene, phenanthrene, and fluorene were analysed in 1000 young adults from Sweden (age 22–25 years) using LC-MS/MS. Lung function and eosinophilic airway inflammation were measured by spirometry and exhaled nitric oxide fraction (FeNO), respectively. Linear regression analysis was used to evaluate associations between PAH metabolites and the outcomes. Median urinary concentrations of 1-OH-pyrene, ∑OH-phenanthrene, and ∑OH-fluorene were 0.066, 0.36, 0.22 μg/L, respectively. We found inverse associations of ∑OH-phenanthrene and ∑OH-fluorene with FEV1 and FVC, as well as between 1-OH-pyrene and FEV1/FVC ratio (adjusted P < 0.05; all participants). An increase of 1% in ∑OH-fluorene was associated with a decrease of 73 mL in FEV1 and 59 mL in FVC. In addition, ∑OH-phenanthrene concentrations were, in a dose-response manner, inversely associated with FEV1 (B from −109 to −48 compared with the lowest quartile of ∑OH-phenanthrene; p trend 0.004) and FVC (B from −159 to −102 compared with lowest quartile; p-trend <0.001). Similar dose-response associations were also observed between ∑OH-fluorene and FEV1 and FVC, as well as between 1-OH-pyrene and FEV1/FVC (p-trend <0.05). There was no association between PAH exposure and FeNO, nor was there an interaction with smoking, sex, or asthma. Low-level PAH exposure was, in a dose-response manner, associated with reduced lung function in young adults. Our findings have public health implications due to i) the widespread occurrence of PAHs in the environment and ii) the clinical relevance of lung function in predicting all-cause and cardiovascular disease mortality. [Display omitted] • Young adults in Sweden had low PAH exposure. • Urinary PAH metabolites were inversely associated with lung function. • The inverse associations were observed in smokers and nonsmokers. [ABSTRACT FROM AUTHOR]

Background: Few studies have investigated the influence of body mass index (BMI) trajectories on lung function covering the entire growth period., Methods: We conducted a prospective study using data from the Swedish BAMSE birth cohort. Latent class mixture modelling was employed to examine the diversity in BMI z-scores from birth to 24 years of age. Participants with four or more BMI z-scores were included (n=3204, 78.4%). Pre-bronchodilator spirometry was tested at 8, 16 and 24 years, while post-bronchodilator spirometry, multiple-breath nitrogen washout (for lung clearance index) and urinary metabolomics data were assessed at 24 years., Results: Six distinct BMI development groups were identified. Compared to the stable normal BMI group, the accelerated increasing BMI group exhibited reduced pre- and post-bronchodilator forced expiratory volume in 1 s (FEV 1 )/forced vital capacity (FVC) ratio z-scores (pre: β= -0.26, 95% CI -0.44- -0.08; post: β= -0.22, 95% CI -0.39- -0.05), along with elevated lung clearance index (0.30, 95% CI 0.22-0.42) at 24 years. The persistent high BMI group demonstrated lower FEV 1 (-0.24, 95% CI -0.42- -0.05) and FVC (-0.27, 95% CI -0.45- -0.01) z-score growth between 16 and 24 years, and elevated lung clearance index (0.20, 95% CI 0.03-0.39) at 24 years. However, those impairments were not observed in the accelerated resolving BMI group. Conversely, the persistent low BMI group displayed persistently decreased FEV 1 and FVC from 8 to 24 years, as well as decreased lung function growth. Additionally, histidine-related metabolites were associated with pre- and post-bronchodilator FEV 1 (hypergeometric false discovery rate=0.008 and <0.001, respectively)., Conclusions: Early interventions aiming for normal BMI during childhood may contribute to improved lung health later in life., Competing Interests: Conflicts of interest: N. Hernandez-Pacheco reports grants from European Academy of Allergy and Clinical Immunology (EAACI) and European Respiratory Society (ERS), and payment for lectures from OMNI PREX S.L., outside the submitted work. The remaining authors have no potential conflicts of interest to disclose., (Copyright ©The authors 2025.)

Background: Asthma is associated with impaired lung function; however, it is uncertain if a lower childhood lung function is associated with asthma onset and persistence during adolescence. The aims of the present study were to investigate the association between childhood lung function and onset and persistence of asthma during adolescence., Methods: In the population-based BAMSE (Sweden), PIAMA (Netherlands) and MAAS (UK) birth cohorts, we analysed the association of forced expiratory volume in 1 s (FEV 1 ), forced vital capacity (FVC), FEV 1 /FVC and forced expiratory volume at 75% of FVC at age 8 years with asthma onset and persistence in adolescence (age 12-16 years) using cohort-specific logistic regression analysis followed by meta-analysis., Results: In the BAMSE, PIAMA and MAAS cohorts, asthma incidence in adolescence was 6.1% (112/1824), 3.4% (36/1050) and 5.0% (39/779), respectively. Persistent asthma from childhood to adolescence was observed in 8.2%, 6.4% and 7.7% of all subjects within the respective cohorts. A higher FEV 1 % predicted and FEV 1 /FVC at age 8 years was associated with a lower odds for adolescent-onset asthma: OR 0.98 (95% CI 0.97-1.00) and 0.97 (0.94-0.99). These associations remained significant also when restricting the analyses to subjects with no wheezing or asthma treatment in childhood. A higher FEV 1 /FVC at age 8 years was associated with a lower odds for asthma persistence in adolescence (0.96 (0.93-0.99)). Sex by lung function interaction analysis was not significant., Conclusions: A higher lung function at school age was associated with a lower risk of adolescent-onset asthma, predominantly in males. This indicates that a lower lung function in childhood may precede and or potentially contribute to asthma incidence and persistence., Competing Interests: Conflict of interest: H.J.L. Koefoed, A. Ullah, S.K. Merid, L. Lowe, R. Vermeulen, M.M. Kere, U. Gehring, A. Bergström, J. Hallberg and J.M. Vonk have no conflicts of interest to report. G.H. Koppelman reports grant support from Netherlands Lung Foundation, TEVA the Netherlands, GSK, Vertex, Ubbo Emmius Foundation, European Union (H2020) and Zon-MW outside the submitted work; and lecture and/or advisory fees from GSK, AstraZeneca, Sanofi, Boehringer Ingelheim and Pure-IMS (money to institution). E. Melén reports lecture and/or advisory board fees from ALK, Airsonett, AstraZeneca, Chiesi, Novartis and Sanofi outside the submitted work. C.S. Murray reports grants from GSK, lecture fees from Sanofi, Novartis and GSK, and support for attending meetings and/or travel from Sanofi. I. Kull reports lecture fees from AstraZeneca outside the submitted work. A. Custovic reports personal fees from Novartis, Sanofi, Stallergenes Greer, AstraZeneca, GSK ad La Roche-Posay, outside the submitted work. A. Simpson reports grants from the Medical Research Council, J.P. Moulton Charitable Foundation and Asthma UK (grants to institution)., (Copyright ©The authors 2024.)

Background: Both depression and respiratory disease are common today in young populations. However, little is known about the relationship between them., Aims: This study aims to explore the association between depression in childhood to early adulthood and respiratory health outcomes in early adulthood, and the potential underlying mechanisms., Method: A prospective study was conducted based on the Swedish BAMSE (Barn, Allergi, Miljö, Stockholm, Epidemiologi [Children, Allergy, Milieu, Stockholm, Epidemiology]) birth cohort ( n = 4089). We identified clinically diagnosed depression through the dispensation of antidepressants, using national register data confirmed by self-reported diagnosis. At the 24-year follow-up, respiratory health was assessed via questionnaires and clinical evaluation. Metabolic and inflammatory profiles were analysed to explore potential mechanisms., Results: Among the 2994 participants who provided study data, 403 (13.5%) had depression at any time point from around age 10 to 25 years. Depression was associated with higher risks of any chronic bronchitis symptoms (odds ratio = 1.58, 95% CI 1.21-2.06) and respiratory symptoms (odds ratio = 1.41, 95% CI 1.11-1.80) in early adulthood, independent of body mass index (BMI) and smoking status. Compared to individuals without depression, those with depression had a higher fat mass index (FMI (β = 0.48, 95% CI 0.22-0.74)) and increased blood levels of fibroblast growth factor 21 and Interleukin-6 in early adulthood. These markers together with FMI were found to partly mediate the association between depression and respiratory symptoms (total mediation proportion: 19.8 and 15.4%, respectively, P < 0.01)., Conclusions: Depression in childhood to early adulthood was associated with an increased risk of respiratory ill-health in early adulthood, independently of smoking. Metabolic and inflammatory dysregulations may underlie this link.

Background: Chronic obstructive pulmonary disease (COPD) is caused by interactions between many factors across the life course, including genetics. A proportion of COPD may be due to reduced lung growth in childhood. We hypothesized that a polygenic risk score (PRS) for COPD is associated with lower lung function already in childhood and up to adulthood., Methods: A weighted PRS was calculated based on the 82 association signals ( p  ≤ 5 × 10 -8 ) revealed by the largest GWAS of airflow limitation (defined as COPD) to date. This PRS was tested in association with lung function measures (FEV 1 , FVC, and FEV 1 /FVC) in subjects aged 4-50 years from 16 independent cohorts participating in the Chronic Airway Diseases Early Stratification (CADSET) Clinical Research Collaboration. Age-stratified meta-analyses were conducted combining the results from each cohort (n = 45,406). These findings were validated in subjects >50 years old., Findings: We found significant associations between the PRS for airflow limitation and: (1) lower pre-bronchodilator FEV 1 /FVC from school age (7-10 years; β: -0.13 z-scores per one PRS z-score increase [-0.15, -0.11], q -value = 7.04 × 10 -53 ) to adulthood (41-50 years; β: -0.16 [-0.19, -0.13], q -value = 1.31 × 10 -24 ); and (2) lower FEV 1 (from school age: 7-10 years; β: -0.07 [-0.09, -0.05], q -value = 1.65 × 10 -9 , to adulthood: 41-50 years; β: -0.17 [-0.20, -0.13], q -value = 4.48 x 10 -20 ). No effect modification by smoking, sex, or a diagnosis of asthma was observed., Interpretation: We provide evidence that a higher genetic risk for COPD is linked to lower lung function from childhood onwards., Funding: This study was supported by CADSET, a Clinical Research Collaboration of the European Respiratory Society., Competing Interests: NH-P was supported with a Medium-Term Research Fellowship by the European Academy of Allergy and Clinical Immunology (EAACI) and a Long-Term Research Fellowship by the European Respiratory Society (ERS) (LTRF202101-00861), and lecture honoraria from OMNIPREX, S.L (outside of the submitted work). LLa was supported by the Fund for Scientific Research Flanders (Grant 3G037618), lecture honoraria from IPSA vzw, a non-profit organization facilitating lifelong learning for health care providers, and Chiesi; and consulting fees from AstraZeneca, all paid to the institution. LLa also declares unpaid membership of faculty board and faculty committees of the European Respiratory Society and Belgian Respiratory Society. LB received support from the K.G. Jebsen Center for Genetic Epidemiology funded by Stiftelsen Kristian Gerhard Jebsen; Faculty of Medicine and Health Sciences, NTNU; The Liaison Committee for Education, Research and Innovation in Central Norway; and the Joint Research Committee between St Olavs Hospital and the Faculty of Medicine and Health Sciences, NTNU. YS was supported by a grant from the China Scholarship Council. AL declares consulting fees regarding presentation of spirometry from Diagnostica Ltb and lecture honoraria from AstraZeneca, Boehringer Ingelheim, and GlaxoSmithKline. AC reports research grants funded by MRC, EPSRC, and Wellcome Trust; consulting fees from Worg Pharmaceuticals; lecture honoraria from GlaxoSmithKline, AstraZeneca, Stallergens-Greer, and Sanofi; and unpaid membership of a board of officers of the World Allergy Organization. GK was supported by grants from ZON-MW, Lung Foundation of the Netherlands, UBBO EMMIUS Foundation, GSK, Vertex, European Union (H2020 program), TEVA the Netherlands; consulting fees from AstraZeneca and PURE IMS; lecture fees from AstraZeneca, Boehringer Ingelheim and Sanofi; and participation as a chair at the exquAIro foundation (AI education for medicine and pharma). RF received funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (grant agreement No. 101044387), Instituto de Salud Carlos III (PI18/00018, PI21/00735), SEPAR and Serra Hunter Program. AA reports research grants, consulting fees, and lecture honoraria by GlaxoSmithKline, AstraZeneca, Menarini, Chiesi, and Sanofi; and unpaid roles as Chair Board of Directors of GOLD and Co-chair of CADSET. MS received funding from ERC under the European Union's Horizon 2020 research and innovation program (grant agreement No. 949906). EM is supported by grants from the EU (ERC, TRIBAL No 757919). EM also declares advisory board and lecture fees from ALK, AstraZeneca, and Chiesi outside the submitted work. The rest of the authors declare no conflicts of interest that might be perceived to influence the interpretation of this article., (© 2024 The Author(s).)

Background: Airway obstruction is defined by spirometry as a low forced expiratory volume in 1 s (FEV 1 ) to forced vital capacity (FVC) ratio. This impaired ratio may originate from a low FEV 1 (classic) or a normal FEV 1 in combination with a large FVC (dysanaptic). The clinical implications of dysanaptic obstruction during childhood and adolescence in the general population remain unclear., Aims: To investigate the association between airway obstruction with a low or normal FEV 1 in childhood and adolescence, and asthma, wheezing and bronchial hyperresponsiveness (BHR)., Methods: In the BAMSE (Barn/Child, Allergy, Milieu, Stockholm, Epidemiology; Sweden) and PIAMA (Prevention and Incidence of Asthma and Mite Allergy; the Netherlands) birth cohorts, obstruction (FEV 1 :FVC ratio less than the lower limit of normal, LLN) at ages 8, 12 (PIAMA only) or 16 years was classified as classic (FEV 1 1 ≥LLN) obstruction. Cross-sectional and longitudinal associations between these two types of obstruction and respiratory health outcomes were estimated by cohort-adjusted logistic regression on pooled data., Results: The prevalence of classic obstruction at ages 8, 12 and 16 in the two cohorts was 1.5%, 1.1% and 1.5%, respectively. Dysanaptic obstruction was slightly more prevalent: 3.9%, 2.5% and 4.6%, respectively. Obstruction, regardless of FEV 1 , was consistently associated with higher odds of asthma (dysanaptic obstruction: OR 2.29, 95% CI 1.40 to 3.74), wheezing, asthma medication use and BHR compared with the normal lung function group. Approximately one-third of the subjects with dysanaptic obstruction in childhood remained dysanaptic during adolescence., Clinical Implications: Children and adolescents with airway obstruction had, regardless of their FEV 1 level, a higher prevalence of asthma and wheezing. Follow-up and treatment at these ages should be guided by the presence of airway obstruction., Competing Interests: Competing interests: GHK reports grant support from the Netherlands Lung Foundation, TEVA the Netherlands, GSK, Vertex, Ubbo Emmius Foundation, European Union (H2020) and ZonMW outside the submitted work. GHK reports lecture and/or advisory fees from GSK, AstraZeneca and PureIMS (money to institution). EM reports lecture and/or advisory board fees from ALK, Airsonett, AstraZeneca, Chiesi, Novartis and Sanofi outside the submitted work. GW reports lecture fees from Sanofi outside the submitted work., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Many survivors of preterm birth will have abnormal lung development, reduced peak lung function and, potentially, an increased rate of physiological lung function decline, each of which places them at increased risk of chronic obstructive pulmonary disease across the lifespan. Current rates of preterm birth indicate that by the year 2040, around 50 years since the introduction of surfactant therapy, more than 700 million individuals will have been born prematurely-a number that will continue to increase by about 15 million annually. In this Personal View, we describe current understanding of the impact of preterm birth on lung function through the life course, with the aim of putting this emerging health crisis on the radar for the respiratory community. We detail the potential underlying mechanisms of prematurity-associated lung disease and review current approaches to prevention and management. Furthermore, we propose a novel way of considering lung disease after preterm birth, using a multidimensional model to determine individual phenotypes of lung disease-a first step towards optimising management approaches for prematurity-associated lung disease., Competing Interests: Declaration of interests SJS and JH have received funding from the European Respiratory Society and the Government of Western Australia for the Prematurity's Effects on the Lungs in Children and Adults Network (PELICAN) clinical research collaboration. All authors, except KG, are members of PELICAN. CDB, DJE, JTDG, MV, TH, KG, EL, SS, JRH, PU-B, LWD, and SK declare no competing interests., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Background: Moderate-to-late preterm birth (32 to <37 weeks of gestation) has been associated with impaired lung function in adolescence, but data in adulthood and physiological phenotyping beyond spirometry are scarce. We aimed to investigate lung function development from adolescence into young adulthood and to provide physiological phenotyping in individuals born moderate-to-late preterm., Methods: Lung function data from individuals born moderate-to-late preterm (n=110) and term (37 to <42 weeks of gestation, n=1895) in the Swedish birth cohort BAMSE were used for analysis and included dynamic spirometry, fractional exhaled nitric oxide and multiple breath nitrogen wash-out. Data from 16- and 24-year follow-ups were analysed using regression models stratified on sex and adjusted for smoking. Data-driven latent class analysis was used to phenotype moderate-to-late preterm individuals at 24 years, and groups were related to background factors., Results: Males born moderate-to-late preterm had lower forced expiratory volume in 1 s (FEV 1 ) at 24 years of age (-0.28 z-score, p=0.045), compared to males born term. In females, no difference was seen at 24 years, partly explained by a significant catch up in FEV 1 between 16 and 24 years (0.18 z-score, p=0.01). Lung function phenotypes described as "asthma-like", "dysanapsis-like" and "preterm reference" were identified within the preterm group. Maternal overweight in early pregnancy was associated with "asthma-like" group membership (OR 3.59, p=0.02)., Conclusion: Our results show impaired FEV 1 at peak lung function in males born moderate-to-late preterm, while females born moderate-to-late preterm had significant catch up between the ages of 16 and 24 years. Several phenotypes of lung function impairment exist in individuals born moderate-to-late preterm., Competing Interests: Conflict of interest: G. Wang reports receiving lecture fees from Sanofi outside the submitted work. Conflict of interest: E. Melén reports payment for lectures and/or advisory board fees from ALK, AstraZeneca, Chiesi, Novartis and Sanofi, outside the submitted work. Conflict of interest: The remaining authors have nothing to disclose., (Copyright ©The authors 2024.)

Background: Epidemiological studies suggest beneficial associations between dietary fibre intake, lung function and chronic respiratory symptoms in adults. Our aim was to investigate the association between dietary fibre intake in childhood and respiratory health up to adulthood., Methods: The individual fibre intake of 1956 participants from the Swedish population-based birth cohort BAMSE was estimated from 98- and 107-item food frequency questionnaires at ages 8 and 16 years, respectively. At 8, 16 and 24 years, lung function was measured by spirometry. Respiratory symptoms (cough, mucus production, breathing difficulties/wheeze) were assessed by questionnaires, and airway inflammation by exhaled nitric oxide fraction ( F ENO ) (≥25 ppb) at 24 years. Longitudinal associations with lung function were analysed by mixed-effects linear regression; associations with respiratory symptoms and airway inflammation were analysed by logistic regression, adjusting for potential confounders., Results: There were no associations between fibre intake at 8 years, as total and from different sources, spirometry measurements and respiratory symptoms at 24 years. Higher fruit fibre intake tended to be inversely associated with airway inflammation at 24 years (OR 0.70, 95% CI 0.48-1.00), which became non-significant after exclusion of participants with food-related allergic symptoms (OR 0.74, 95% CI 0.49-1.10). No associations between fibre intake at 8 and 16 years as an updated lagged exposure and spirometry measurements up to 24 years were observed., Conclusion: In this longitudinal study, we observed no consistent association between dietary fibre intake in childhood and lung function or respiratory symptoms up to adulthood. Further research on dietary fibre in relation to respiratory health across the life course is needed., Competing Interests: Conflict of interest: The authors have no conflicts of interest to disclose., (Copyright ©The authors 2023.)

Background: The beneficial effect of improving air quality on lung function development remains understudied. We assessed associations of changes in ambient air pollution levels with lung function growth from childhood until young adulthood in a Swedish cohort study., Methods: In the prospective birth cohort BAMSE (Children, Allergy, Environment, Stockholm, Epidemiology (in Swedish)), spirometry was conducted at the 8-year (2002-2004), 16-year (2011-2013) and 24-year (2016-2019) follow-ups. Participants with spirometry data at 8 years and at least one other measurement in subsequent follow-ups were included (1509 participants with 3837 spirometry measurements). Ambient air pollution levels (particulate matter with diameter ≤2.5 μm (PM 2.5 ), particulate matter with diameter ≤10 μm (PM 10 ), black carbon (BC) and nitrogen oxides (NO x )) at residential addresses were estimated using dispersion modelling. Linear mixed effect models were used to estimate associations between air pollution exposure change and lung function development., Results: Overall, air pollution levels decreased progressively during the study period. For example, the median (interquartile range (IQR)) level of PM 2.5 decreased from 8.24 (0.92) μg·m -3 during 2002-2004 to 5.21 (0.67) μg·m -3 during 2016-2019. At the individual level, for each IQR reduction of PM 2.5 the lung function growth rate increased by 4.63 (95% CI 1.64-7.61) mL per year (p<0.001) for forced expiratory volume in 1 s and 9.38 (95% CI 4.76-14.00) mL per year (p<0.001) for forced vital capacity. Similar associations were also observed for reductions of BC and NO x . Associations persisted after adjustment for potential confounders and were not modified by asthma, allergic sensitisation, overweight, early-life air pollution exposure or dietary antioxidant intake., Conclusions: Long-term reduction of air pollution is associated with positive lung function development from childhood to young adulthood., Competing Interests: Conflict of interest: The authors have no potential conflicts of interest to disclose., (Copyright ©The authors 2023.)

Rationale: Recent evidence highlights the importance of optimal lung development during childhood for health throughout life. Objectives: To explore the plasticity of individual lung function states during childhood. Methods: Prebronchodilator FEV 1 z -scores determined at age 8, 16, and 24 years in the Swedish population-based birth cohort BAMSE (Swedish abbreviation for Child [Barn], Allergy, Milieu, Stockholm, Epidemiological study) ( N  = 3,069) were used. An unbiased, data-driven dependent mixture model was applied to explore lung function states and individual state chains. Lung function catch-up was defined as participants moving from low or very low states to normal or high or very high states, and growth failure as moving from normal or high or very high states to low or very low states. At 24 years, we compared respiratory symptoms, small airway function (multiple-breath washout), and circulating inflammatory protein levels, by using proteomics, across states. Models were replicated in the independent Dutch population-based PIAMA (Prevention and Incidence of Asthma and Mite Allergy) cohort. Measurements and Main Results: Five lung function states were identified in BAMSE. Lung function catch-up and growth failure were observed in 74 (14.5%) BAMSE participants with low or very low states and 36 (2.4%) participants with normal or high or very high states, respectively. The occurrence of catch-up and growth failure was replicated in PIAMA. Early-life risk factors were cumulatively associated with the very low state, as well as with catch-up (inverse association) and growth failure. The very low state as well as growth failure were associated with respiratory symptoms, airflow limitation, and small airway dysfunction at adulthood. Proteomics identified IL-6 and CXCL10 (C-X-C motif chemokine 10) as potential biomarkers of impaired lung function development. Conclusions: Individual lung function states during childhood are plastic, including catch-up and growth failure.

Background: PUFAs may influence the risk of asthma; however, long-term prospective studies including objective biomarkers of PUFA intake are lacking., Objectives: The objective was to investigate the role of dietary intake and plasma concentrations of n-3 and n-6 (ω-3 and ω-6) PUFAs in childhood and adolescence for the development of asthma and lung function up to young adulthood., Methods: The study included participants from the Swedish prospective birth cohort BAMSE. Dietary intake of PUFAs was calculated from FFQs (n = 1992) and plasma proportions of PUFAs were measured in phospholipids (n = 831). We analyzed the n-3 PUFA α-linolenic acid (ALA; 18:3n-3); the sum of very-long-chain (VLC) n-3 PUFAs: EPA (20:5n-3), DHA (22:6n-3), and docosapentaenoic acid (22:5n-3); and the n-6 PUFAs linoleic acid (LA; 18:2n-6) and arachidonic acid (AA; 20:4n-6). Asthma was assessed by questionnaires at 8, 16, and 24 y and lung function was measured by spirometry at 24 y., Results: A high (≥median) self-reported dietary intake of LA at 8 y and AA at 16 y was associated with increased risk of prevalent asthma at 24 y (OR: 1.41; 95% CI: 1.10, 1.82 and OR: 1.32; 95% CI: 1.02, 1.70, respectively). In contrast, plasma proportions of ALA, ∑VLC n-3 PUFAs, and AA at 8 y, as well as LA at 16 y, were inversely associated with prevalent asthma at 24 y (e.g., OR: 0.55; 95% CI: 0.38, 0.81 for ∑VLC n-3 PUFAs). No consistent associations were observed with lung function., Conclusions: High dietary intake of certain n-6 PUFAs in childhood or adolescence may be associated with increased risk of asthma up to young adulthood, whereas dietary biomarkers of certain n-3 and n-6 PUFAs in plasma may be associated with decreased risk. Thus, the role of diet compared with altered metabolism of PUFAs needs further investigation to improve dietary preventive strategies for asthma., (© The Author(s) 2021. Published by Oxford University Press on behalf of the American Society for Nutrition.)

Background: Spirometric restriction, defined as a reduced forced vital capacity (FVC) with a preserved FEV 1 /FVC ratio, is associated with increased respiratory and non-respiratory comorbidities and all-cause mortality in adulthood. Little is known about the early origins of this condition. We sought to identify early-life risk factors for spirometric restriction in adult life., Methods: In this longitudinal, multicohort, population-based study, we used data from the Tucson Children's Respiratory Study (TCRS), which recruited 1246 healthy infants at birth between April 1980, and October 1984, in Tucson, AZ, USA. Questionnaires were answered by the primary caregiver at enrolment, immediately after the child's birth, and multiple follow-up questionnaires were completed through childhood and adulthood. At the age of 22, 26, 32, and 36 years, lung function was measured with spirometry. At each survey, three mutually exclusive spirometric patterns were defined: (1) normal (FEV 1 /FVC ≥10th percentile and FVC ≥10th percentile); (2) restrictive (FEV 1 /FVC ≥10th percentile and FVC <10th percentile); and (3) obstructive (FEV 1 /FVC <10th percentile, independent of FVC). Data on demographic features and parental health factors were collected from questionnaires; pregnancy and perinatal data (including nutritional problems) and birth measurements were obtained from medical records; and weight, height, and body-mass index (BMI) during childhood (age 6-16 years) were measured by study nurses. The associations between early-life risk factors and spirometric patterns were assessed by multivariate multinomial logistic regression analysis, adjusted for survey year, sex, and race-ethnicity. Significant risk factors were further tested for replication in the Swedish Child (Barn), Allergy, Milieu, Stockholm, Epidemiological (BAMSE; n=1817; spirometry surveys were done at age 24 years) survey and the UK Manchester Asthma and Allergy Study (MAAS; n=411; spirometry surveys were done at age 18 years) birth cohorts, and fixed-effect meta-analyses of relative risk ratios (RRRs) from multinomial logistic regression models were done to generate a pooled estimate of the effect across the three cohorts. Measurements of body composition (MAAS; n=365) and total lung capacity (TCRS; n=173 and MAAS; n=407) were also available for a subset of participants., Findings: Of 1246 healthy infants included in TCRS, for the present study we included data for 652 participants who had at least one set of spirometry data, contributing up to 1668 observations. In the TCRS cohort, results from the multivariate models showed that maternal nutritional problems during pregnancy (RRR 2·48 [95% CI 1·30-4·76]; p=0·0062), being born small for gestational age (birthweight <10th percentile; 3·26 [1·34-7·93]; p=0·0093), and being underweight in childhood (BMI-for-age <5th percentile; 3·54 [1·35-9·26]; p=0·010) were independent predictors of spirometric restriction in adult life. Associations between being small for gestational age (p=0·0028) and underweight in childhood (p<0·0001) with adult spirometric restriction were supported by the results of meta-analysis of data from all three cohorts. In the MAAS cohort, having a low lean BMI (ie, <10th percentile) at age 11 years predicted adult (age 18 years) spirometric restriction (RRR 3·66 [1·48-9·02]; p=0·0048). These associations of spirometric restriction with small for gestational age, childhood underweight, and low lean BMI in childhood were verified in participants with spirometric restriction who had diminished total lung capacity, indicating that these factors specifically increase the risk of lung restriction., Interpretation: Poor growth and nutritional deficits in utero and throughout childhood precede and predict the development of spirometric restriction in adult life. Strategies to improve prenatal and childhood growth trajectories could help to prevent spirometric restriction and its associated morbidity and mortality burden., Funding: National Institutes of Health., Competing Interests: Declaration of interests WJM has received grant funding for this work from the National Institutes of Health; funding from the National Institutes of Health and the Cystic Fibrosis Foundation outside of the submitted work; and personal fees from the Cystic Fibrosis Foundation, the American Thoracic Society, and the American College of Chest Physicians outside of the submitted work. AC has received personal fees from Novartis, Thermo Fisher Scientific, Philips, Sanofi, Stallergenes Greer, and AstraZeneca outside of the submitted work. AS and CSM are supported by the NIHR Manchester Biomedical Research Centre. All other authors declare no competing interests., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

We aimed to determine prevalence and early-life risk factors for reversible and irreversible airflow limitation in young adults from the general population. Among young adults in their 20s, the prevalence was 5.3% for reversible airflow limitation and 2.0% for irreversible airflow limitation. While parental asthma was the only risk factor for development of reversible airflow limitation, the risk factors for development of irreversible airflow limitation were current asthma, childhood respiratory tract infections and asthma, and exposure to air pollution., Competing Interests: Competing interests: EM reports personal fees from Sanofi, Chiesi and AstraZeneca, outside the submitted work., (© Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY. Published by BMJ.)

Background: Chronic bronchitis is associated with substantial morbidity among elderly adults, but little is known about its prevalence and risk factors in young adults. Our aim was to assess the prevalence and early-life risk factors for chronic bronchitis in young adults., Methods: Questionnaire data and clinical measures from the 24-year follow-up of the Swedish BAMSE (Child (Barn), Allergy, Milieu, Stockholm, Epidemiological) cohort were used. We assessed chronic bronchitis (CB) as the combination of cough and mucus production in the morning during winter. Environmental and clinical data from birth and onwards were used for analyses of risk factors., Results: At the 24-year follow-up, 75% (n=3064) participants completed the questionnaire and 2030 performed spirometry. The overall prevalence of CB was 5.5% (n=158) with similar estimates in males and females. 49% of CB cases experienced more than three self-reported respiratory infections in the past year compared to 18% in non-CB subjects (p<0.001), and 37% of cases were current smokers ( versus 19% of non-CB cases). Statistically significant lower post-bronchodilator forced expiratory volume in 1 s/forced vital capacity were observed in CB compared to non-CB subjects (mean z-score -0.06 versus 0.13, p=0.027). Daily smoking (adjusted (a)OR 3.85, p<0.001), air pollution exposure (black carbon at ages 1-4 years aOR 1.71 per 1 μg·m -3 increase, p=0.009) and exclusive breastfeeding for ≤4 months (aOR 0.66, p=0.044) were associated with CB., Conclusion: Chronic bronchitis in young adults is associated with recurrent respiratory infections. Besides smoking, our results support the role of early-life exposures, such as air pollution and exclusive breastfeeding, for respiratory health later in life., Competing Interests: Conflict of interest: G. Wang has nothing to disclose. Conflict of interest: J. Hallberg has nothing to disclose. Conflict of interest: P. Um Bergström has nothing to disclose. Conflict of interest: C. Janson has nothing to disclose. Conflict of interest: G. Pershagen has nothing to disclose. Conflict of interest: O. Gruzieva has nothing to disclose. Conflict of interest: M. van Hage reports personal fees for lectures from Thermo Fisher Scientific and ALK, outside the submitted work. Conflict of interest: A. Georgelis has nothing to disclose. Conflict of interest: A. Bergström has nothing to disclose. Conflict of interest: I. Kull has nothing to disclose. Conflict of interest: A. Lindén has nothing to disclose. Conflict of interest: E. Melén has nothing to disclose., (Copyright ©ERS 2021.)

Dietary antioxidant intake has been hypothesised to influence lung function. The association between total antioxidant capacity (TAC) of the diet at age 8 years and lung function development up to 16 years in 2307 participants from the Swedish population-based birth cohort BAMSE (Children, Allergy, Milieu, Stockholm, Epidemiology) was investigated.Information on TAC was obtained from a food frequency questionnaire at 8 years. Lung function was measured by spirometry at 8 and 16 years, impulse oscillometry (IOS) and exhaled nitric oxide fraction ( F eNO ) at 16 years. Low lung function was defined as forced expiratory volume in 1 s (FEV 1 ) z-score below the 25th percentile. Longitudinal associations between TAC and lung function were analysed by mixed effect models adjusted for potential confounders. Stratification by asthma at 8 years was performed to examine effect modification.The median TAC intake was 10 067 μmol Trolox equivalents (TE)·g -1 , with males having a lower mean compared to females (9963 versus 10 819 μmol TE·g -1 ). In analyses of lung function change between 8 and 16 years, there were no statistically significant associations between TAC in tertiles and spirometry results for the total study population. Among children with asthma at 8 years (prevalence 7%), higher TAC was associated with higher mean FEV 1 (0.46 sd, 95% CI 0.11-0.80) and decreased odds of low lung function at 16 years (OR 0.28, 95% CI 0.12-0.65). There were no associations between TAC and forced vital capacity or IOS/ F eNO results.High dietary antioxidant intake in school age may be associated with improved lung function development from school age to adolescence among children with asthma., Competing Interests: Conflict of interest: E. Sdona has nothing to disclose. Conflict of interest: J. Hallberg reports personal fees from AstraZeneca, outside the submitted work. Conflict of interest: N. Andersson has nothing to disclose. Conflict of interest: S. Ekström has nothing to disclose. Conflict of interest: S. Rautiainen has nothing to disclose. Conflict of interest: N. Håkansson has nothing to disclose. Conflict of interest: A. Wolk has nothing to disclose. Conflict of interest: I. Kull has nothing to disclose. Conflict of interest: E. Melén has nothing to disclose. Conflict of interest: A. Bergström has nothing to disclose., (Copyright ©ERS 2020.)

Rationale: Little is known about how perinatal and childhood factors influence lung function change between childhood and adolescence., Objectives: To investigate possible early life predictors of change in FEV 1 between age 8 and 16 years. In addition, to investigate possible predictors of having persistently low lung function (FEV 1 <25th percentiles both at age 8 and 16) up to adolescence., Methods: The BAMSE birth cohort study collected data throughout childhood on environmental factors, individual characteristics, and spirometric measures at 8 and 16 years (n = 1425). Associations between early life predictors (n = 31) and FEV 1 increase between 8 and 16 years were assessed with linear regression. Predictors of having persistently low lung function were examined., Results: Few factors were consistently associated with altered lung function growth, although low birth weight, asthma heredity (paternal), secondhand smoke in infancy, and season of birth had a significant impact (p-value ≤0.01). The majority of subjects stayed however within the same category of lung function between ages 8 and 16 years (in total 821/1425 = 58%). Predictors associated with having persistently low lung function were gestational age, secondhand smoke (at 2 and 8 years of age), and factors related to lower respiratory tract infections in infancy., Conclusions: In summary, rather few exposures in childhood were identified to have a significant impact on lung function growth between childhood and adolescence. Our data support previous study findings indicating that lung function development is influenced by factors before birth and in infancy, including second hand tobacco smoke., (Copyright © 2018. Published by Elsevier Ltd.)

Smoking is the main risk factor for COPD (chronic obstructive pulmonary disease) but genetic factors are of importance, since only a subset of smokers develops the disease. Sex differences have been suggested both in disease prevalence and response to environmental exposures. Furthermore, it has been shown that acquisition of 'addiction' to smoking is partly genetically mediated. Disease cases and smoking habits were identified in 44919 twins aged >40 years from the Swedish Twin Registry. Disease was defined as self-reported chronic bronchitis or emphysema, or recurrent cough with phlegm. The results showed that chronic bronchitis seems to be more prevalent among females, and that the heritability estimate for chronic bronchitis was a moderate 40% and only 14% of the genetic influences were shared by smoking. In addition, 392 twins have been invited to a clinical investigation to evaluate: (i) to what extent genetic factors contribute to individual differences (variation) in FEV(1) (forced expiratory volume in 1 s), vital capacity and DL(CO) (diffusion capacity), taking sex into consideration, and (ii) whether smoking behaviour and respiratory symptoms influence these estimates.