Thorax · 2026
Paternal prepubertal passive smoke exposure is related to impaired lung function trajectories from childhood to middle age in their offspring.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Liu Jiacheng, Perret Jennifer L, Lodge Caroline J, Vicendese Don, Bowatte Gayan, Lowe Adrian J, Idrose Nur Sabrina, Frith Peter, Wood-Baker Richard, Mishra Gita D, Holloway John W, Svanes Cecilie, Abramson Michael J, Walters Eugene Haydn, Dharmage Shyamali C, Bui Dinh S
Аннотация
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.
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.