Jiacheng Liu, Jennifer L Perret, Caroline J Lodge, Don Vicendese, Gayan Bowatte, Adrian J Lowe, Nur Sabrina Idrose, Peter Frith, Richard Wood-Baker, Gita D Mishra, John W Holloway, Cecilie Svanes, Michael J Abramson, Eugene Haydn Walters, Shyamali C Dharmage, Dinh S Bui
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The offspring were probands in the original cohort who underwent spirometry at six time points from ages 7 to 53 years. Lung function (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC) trajectories were previously derived using group-based trajectory modelling. Fathers reported their own passive smoke exposure before age 15 years. Multinomial logistic regressions assessed associations between paternal prepubertal passive smoke exposure and lung function trajectories in offspring. Potential mediations and interactions were assessed for active paternal smoking, offspring passive smoke exposure and respiratory illnesses during childhood, and subsequent active smoking. Results Paternal prepubertal passive smoke exposure was associated with the below average FEV1 (adjusted multinomial OR (aMOR) 1.56; 95% CI 1.05 to 2.31) and early low-rapid decline FEV1/FVC trajectories (aMOR 2.30; 95% CI 1.07 to 4.94) in offspring. The association with the below average FEV1 trajectory was augmented for offspring exposed to childhood passive smoke (aMOR 2.36; 95% CI 1.34 to 4.13; p-interaction=0.053). Observed associations partly mediated through smoking and respiratory illnesses in fathers and offspring (each contributing <15%). Conclusions Paternal prepubertal passive smoke exposure was associated with impaired lung function trajectories in offspring, which highlights the adverse impact of smoking on multiple generations. Data are available on reasonable request. Individual participant data can be provided on request to anyone with a suitable proposal. The proposal will be reviewed by the steering committee of the Tasmanian Longitudinal Health Study (TAHS). Requests can be directed to SCD, the principal investigator of the TAHS and the corresponding author of this paper. Individual deidentified data for all TAHS participants may be provided.","PeriodicalId":23284,"journal":{"name":"Thorax","volume":"162 1","pages":""},"PeriodicalIF":7.7000,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Paternal prepubertal passive smoke exposure is related to impaired lung function trajectories from childhood to middle age in their offspring\",\"authors\":\"Jiacheng Liu, Jennifer L Perret, Caroline J Lodge, Don Vicendese, Gayan Bowatte, Adrian J Lowe, Nur Sabrina Idrose, Peter Frith, Richard Wood-Baker, Gita D Mishra, John W Holloway, Cecilie Svanes, Michael J Abramson, Eugene Haydn Walters, Shyamali C Dharmage, Dinh S Bui\",\"doi\":\"10.1136/thorax-2024-222482\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Introduction Paternal prepubertal passive smoke exposure may increase the risk of childhood asthma. However, its association with impaired lung function trajectories at risk of chronic obstructive pulmonary disease in offspring was not investigated. We assessed the association between paternal prepubertal passive smoke exposure and lung function from childhood to middle age in their offspring. Methods Data were analysed from 890 father-offspring pairs from the Tasmanian Longitudinal Health Study. The offspring were probands in the original cohort who underwent spirometry at six time points from ages 7 to 53 years. Lung function (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC) trajectories were previously derived using group-based trajectory modelling. Fathers reported their own passive smoke exposure before age 15 years. Multinomial logistic regressions assessed associations between paternal prepubertal passive smoke exposure and lung function trajectories in offspring. Potential mediations and interactions were assessed for active paternal smoking, offspring passive smoke exposure and respiratory illnesses during childhood, and subsequent active smoking. Results Paternal prepubertal passive smoke exposure was associated with the below average FEV1 (adjusted multinomial OR (aMOR) 1.56; 95% CI 1.05 to 2.31) and early low-rapid decline FEV1/FVC trajectories (aMOR 2.30; 95% CI 1.07 to 4.94) in offspring. The association with the below average FEV1 trajectory was augmented for offspring exposed to childhood passive smoke (aMOR 2.36; 95% CI 1.34 to 4.13; p-interaction=0.053). Observed associations partly mediated through smoking and respiratory illnesses in fathers and offspring (each contributing <15%). Conclusions Paternal prepubertal passive smoke exposure was associated with impaired lung function trajectories in offspring, which highlights the adverse impact of smoking on multiple generations. Data are available on reasonable request. Individual participant data can be provided on request to anyone with a suitable proposal. The proposal will be reviewed by the steering committee of the Tasmanian Longitudinal Health Study (TAHS). Requests can be directed to SCD, the principal investigator of the TAHS and the corresponding author of this paper. 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引用次数: 0
摘要
父亲在青春期前被动吸烟可能会增加儿童哮喘的风险。然而,其与后代慢性阻塞性肺疾病风险中肺功能受损轨迹的关系尚未调查。我们评估了父亲青春期前被动吸烟暴露与其后代从童年到中年肺功能之间的关系。方法对来自塔斯马尼亚纵向健康研究的890对父子进行数据分析。后代为原队列的先证者,在7岁至53岁的6个时间点接受肺活量测定。肺功能(1秒内用力呼气量(FEV1)、用力肺活量(FVC)和FEV1/FVC)轨迹先前使用基于组的轨迹建模得到。父亲们报告了自己在15岁之前被动吸烟的情况。多项逻辑回归评估了父亲青春期前被动吸烟暴露与后代肺功能轨迹之间的关系。评估了父亲主动吸烟、子女被动吸烟和儿童时期呼吸系统疾病以及随后的主动吸烟的潜在中介和相互作用。结果父亲青春期前被动吸烟暴露与FEV1低于平均水平相关(调整多项OR (aMOR) 1.56;95% CI 1.05 - 2.31)和早期低快速下降的FEV1/FVC轨迹(aMOR 2.30; 95% CI 1.07 - 4.94)。暴露于儿童期被动吸烟的后代与低于平均FEV1轨迹的关联被增强(aMOR 2.36; 95% CI 1.34至4.13;p交互作用=0.053)。观察到父亲和后代吸烟和呼吸系统疾病部分介导的关联(各贡献<15%)。结论父亲青春期前被动吸烟暴露与后代肺功能轨迹受损相关,这表明吸烟对多代人的不利影响。如有合理要求,可提供资料。个人参加者资料可应要求提供给任何有合适建议的人士。该提案将由塔斯马尼亚纵向健康研究(TAHS)指导委员会审查。请求可以直接发送给SCD, TAHS的首席研究员和本文的通讯作者。可提供所有TAHS参与者的个人身份资料。
Paternal prepubertal passive smoke exposure is related to impaired lung function trajectories from childhood to middle age in their offspring
Introduction Paternal prepubertal passive smoke exposure may increase the risk of childhood asthma. However, its association with impaired lung function trajectories at risk of chronic obstructive pulmonary disease in offspring was not investigated. We assessed the association between paternal prepubertal passive smoke exposure and lung function from childhood to middle age in their offspring. Methods Data were analysed from 890 father-offspring pairs from the Tasmanian Longitudinal Health Study. The offspring were probands in the original cohort who underwent spirometry at six time points from ages 7 to 53 years. Lung function (forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC) trajectories were previously derived using group-based trajectory modelling. Fathers reported their own passive smoke exposure before age 15 years. Multinomial logistic regressions assessed associations between paternal prepubertal passive smoke exposure and lung function trajectories in offspring. Potential mediations and interactions were assessed for active paternal smoking, offspring passive smoke exposure and respiratory illnesses during childhood, and subsequent active smoking. Results Paternal prepubertal passive smoke exposure was associated with the below average FEV1 (adjusted multinomial OR (aMOR) 1.56; 95% CI 1.05 to 2.31) and early low-rapid decline FEV1/FVC trajectories (aMOR 2.30; 95% CI 1.07 to 4.94) in offspring. The association with the below average FEV1 trajectory was augmented for offspring exposed to childhood passive smoke (aMOR 2.36; 95% CI 1.34 to 4.13; p-interaction=0.053). Observed associations partly mediated through smoking and respiratory illnesses in fathers and offspring (each contributing <15%). Conclusions Paternal prepubertal passive smoke exposure was associated with impaired lung function trajectories in offspring, which highlights the adverse impact of smoking on multiple generations. Data are available on reasonable request. Individual participant data can be provided on request to anyone with a suitable proposal. The proposal will be reviewed by the steering committee of the Tasmanian Longitudinal Health Study (TAHS). Requests can be directed to SCD, the principal investigator of the TAHS and the corresponding author of this paper. Individual deidentified data for all TAHS participants may be provided.
期刊介绍:
Thorax stands as one of the premier respiratory medicine journals globally, featuring clinical and experimental research articles spanning respiratory medicine, pediatrics, immunology, pharmacology, pathology, and surgery. The journal's mission is to publish noteworthy advancements in scientific understanding that are poised to influence clinical practice significantly. This encompasses articles delving into basic and translational mechanisms applicable to clinical material, covering areas such as cell and molecular biology, genetics, epidemiology, and immunology.