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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 (FEV 1 ) 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, FEV 1 , FVC and height at baseline, accounting for personal smoking., Findings: Decline in lung function was accelerated in participants with mothers that smoked during pregnancy (FEV 1 2.3 ml/year; 95% CI: 0.7, 3.8) (FVC 2.2 ml/year; 0.2, 4.2), with asthmatic mothers (FEV 1 2.6 ml/year; 0.9, 4.4) (FEV 1 /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 FEV 1 (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 FEV 1 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., Competing Interests: SCD and CJL have received an investigator-initiated grant from GSK and a partnership grant from AZ for unrelated work. All other authors declare no conflict of interest., (© 2023 The Authors.)

Background: Emerging evidence suggests that androgens and estrogens have a role in respiratory health, but it is largely unknown whether levels of these hormones can affect lung function in adults from the general population. This study investigated whether serum dehydroepiandrosterone sulfate (DHEA-S), a key precursor of both androgens and estrogens in peripheral tissues, was related to lung function in adult women participating in the European Community Respiratory Health Survey (ECRHS)., Methods: Lung function and serum DHEA-S concentrations were measured in n  = 2,045 and n  = 1,725 women in 1999-2002 and in 2010-2013, respectively. Cross-sectional associations of DHEA-S levels (expressed as age-adjusted z-score) with spirometric outcomes were investigated, adjusting for smoking habits, body mass index, menopausal status, and use of corticosteroids. Longitudinal associations of DHEA-S levels in 1999-2002 with incidence of restrictive pattern and airflow limitation in 2010-2013 were also assessed., Findings: Women with low DHEA-S (z-score<-1) had lower FEV1 (% of predicted, adjusted difference: -2.2; 95%CI: -3.5 to -0.9) and FVC (-1.7; 95%CI: -2.9 to -0.5) and were at a greater risk of having airflow limitation and restrictive pattern on spirometry than women with higher DHEA-S levels. In longitudinal analyses, low DHEA-S at baseline was associated with a greater incidence of airflow limitation after an 11-years follow-up (incidence rate ratio, 3.43; 95%CI: 1.91 to 6.14)., Interpretation: Low DHEA-S levels in women were associated with impaired lung function and a greater risk of developing airflow limitation later in adult life. Our findings provide new evidence supporting a role of DHEA-S in respiratory health., Funding: EU H2020, grant agreement no.633212., Competing Interests: Dr Demoly reports presentation honoraria from Stallergène Greer, ALK, Mylan, Astra Zeneca, Bausch&Lomb and personal fees as board advisor from Chiesi, Sanofi, Thermo Fisher Scientific, outside the submitted work. Dr Jogi reports personal grants from the Estonian Research Council [personal research grant no.562], and reports travel grants and presentation honoraria from GSK, Novartis, Boehringer, outside the submitted work. Dr Pin reports travel grants and presentation honoraria from GSK, Novartis, Astra Zeneca, Zambon Pharma, outside the submitted work. All the authors declare no competing interests., (© 2020 The Authors.)