September 23, 2025
4 min read
Key takeaways:
- Trajectories negatively impacted by early paternal passive smoking included a below average FEV1 and an early low-rapid decline FEV1/FVC.
- Offspring passive smoke exposure raised the odds for a poor trajectory.
Offspring faced an elevated likelihood for impaired lung function trajectories from childhood to middle age if their father had prepubertal passive smoke exposure, according to results published in Thorax.
“Exposure to passive (second-hand) smoke not only harms the children at that time but may also affect the lung health of their future children,” Dinh S. Bui, PhD, senior research fellow at the Centre for Epidemiology and Biostatistics at the University of Melbourne, and Shyamali C. Dharmage, MBBS, MSc, MD, PhD, head of the allergy and lung health unit at the University of Melbourne, told Healio in a statement. “This highlights the importance of keeping children away from second-hand smoke.”
Using data from the Tasmanian Longitudinal Health Study, Bui, Dharmage and colleagues evaluated 890 father-offspring pairs to determine the impact of paternal prepubertal (before age 15 years) passive smoke exposure on offspring lung function trajectories from age 7 to 53 years.
“COPD may originate at multiple stages across the lifespan, including the preconception,” Bui and Dharmage told Healio. “Our previous study has shown that paternal prepubertal passive smoke exposure was associated with an increased risk of asthma in their offspring by age 7 years.
“However, prior to the current study, it remained unclear whether this association persisted into offspring adulthood and contributed to impaired lung function trajectories at risk of COPD by middle age,” they said.
In the set of fathers, passive smoke exposure in childhood was reported by 68.7%. Among the offspring, 56.5% reported this exposure in childhood, according to the study.
When the offspring cohort was asked about active smoking, 49% reported a history of this type of smoking by age 53 years. Using spirometry, researchers found that 5.1% had COPD at this age.
In a model adjusted for parental Socio-Economic Indexes for Area-The Index of Relative Socio-economic Disadvantage scores, paternal lifetime history of asthma/wheeze and paternal age at baseline, the odds for the below average FEV1 trajectory among children with vs. without paternal prepubertal passive smoke exposure were significantly higher by 56% (adjusted multinomial OR [aMOR] = 1.56; 95% CI, 1.05-2.31).
Researchers also observed significantly heightened odds for early low-rapid decline FEV1/FVC trajectories in offspring with vs. without paternal prepubertal passive smoke exposure (aMOR = 2.3; 95% CI, 1.07-4.94).
In contrast, the link between COPD in offspring at 53 years and paternal prepubertal passive smoke exposure was not significant in the adjusted model, according to the study.
Notably, researchers found greater odds for the below average FEV1 trajectory among children with paternal prepubertal passive smoke exposure and passive smoke exposure in their childhood (aMOR = 2.36; 95% CI, 1.34-4.13) vs. children with paternal prepubertal passive smoke exposure and no passive smoke exposure in their childhood (aMOR = 0.9; 95% CI, 0.51-1.6).
Another factor that modified the odds for the below average FEV1 trajectory among offspring with paternal prepubertal passive smoke exposure was pneumonia/pleurisy, as the study reported that those without pneumonia/pleurisy during childhood had greater odds for this lung function trajectory (aMOR = 1.96; 95% CI, 1.26-3.04).
With regard for the odds for the early low-rapid decline FEV1/FVC trajectory among offspring with paternal prepubertal passive smoke exposure, researchers noted higher odds for this outcome in those without vs. with food allergy during childhood (aMOR = 3.85; 95% CI, 1.45-10.19).
Factors that did not significantly change the relationship between paternal prepubertal passive smoking exposure and offspring lung function trajectories included paternal active smoking, offspring sex at birth, offspring asthma/wheeze and/or bronchitis during childhood and offspring active smoking by age 53 years.
“We anticipated that inherited behavioral patterns, such as active paternal smoking and active offspring smoking, could mediate a substantial proportion of the associations between paternal prepubertal passive smoke exposure and impaired lung function trajectories in offspring,” Bui and Dharmage told Healio. “However, the contributions from active smoking were modest.
“This finding suggests that the remaining associations may reflect a direct effect of paternal passive smoke exposure on impaired lung function trajectories in offspring rather than being primarily explained by inherited behavioural patterns of active smoking,” they said.
Moving forward, Bui and Dharmage told Healio research could focus on epigenetic mechanisms.
“Further research into epigenetic mechanisms may provide insights into the association between parental prepubertal passive smoke exposure and impaired lung function overtime in their offspring,” Bui and Dharmage said.
For more information:
Dinh S. Bui, PhD, can be reached at dinh.bui@unimelb.edu.au.
Shyamali C. Dharmage, MBBS, MSc, MD, PhD, can be reached at s.dharmage@unimelb.edu.au.
Perspective
This study is significant and adds to the growing knowledge of the harmful effects of secondhand smoke exposure. It shows how secondhand smoke can impair lung function across generations. These findings match my 25 years of experience as a family physician, as patients of any age exposed to secondhand smoke exhibit reduced lung function.
Doctors can use these findings to enhance care by strongly advising prospective parents to avoid smoking because of the intergenerational risks highlighted by this research. Further validating studies are needed to confirm these conclusions.
I find it interesting that paternal prepubertal passive smoke exposure was linked to a higher risk of COPD in their children.
Felix Aguilar, MD, MPH
Disclosures: Aguilar reports no relevant financial disclosures.
Sources/Disclosures
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Disclosures:
Bui reports no relevant financial disclosures. Dharmage reports receiving investigator-initiated grants from AstraZeneca, GSK and Sanofi/Regeneron for unrelated research. Please see the study for all other authors’ relevant financial disclosures.
