Children whose fathers experienced passive smoke exposure in childhood were significantly more likely to show impaired lung function as adults, based on data from more than 800 father-child pairs.

Previous research has shown a possible link between fathers’ childhood exposure to passive smoking and their offspring’s risk for childhood asthma, but data on the impact of fathers’ passive smoking on offspring long-term lung health are lacking, wrote Jiacheng Liu, a PhD candidate at the University of Melbourne, Melbourne, Australia, and colleagues.

Active paternal smoking before puberty has been associated with impaired lung function in offspring during early adulthood in prior studies, said senior author Dinh S. Bui, BPharm, MPH, PhD, a senior research fellow at the University of Melbourne, in an interview. However, passive smoke exposure was far more prevalent than active smoking among children and adolescents, but the relationship between paternal prepubertal passive smoke exposure and impaired lung function trajectories across the lifespan of offspring had not been investigated, he said. “Clarifying this association is important, as it may provide evidence to better understand the potential risks of passive (second-hand) smoke exposure,” he added.

In a study published in Thorax, the researchers reviewed data from 890 father-offspring pairs who were enrolled in the Tasmanian Longitudinal Health Study. The offspring, the children of the study’s original birth cohort, underwent spirometry at 6 points between the ages of 7 and 53 years. Fathers self-reported passive smoke exposure prior to age 15 years.

Approximately two thirds of the fathers (68.7%) had been exposed to passive smoking during their childhoods, as had 56.5% of the children.

Overall, fathers’ passive prepubertal smoke exposure was significantly associated with below-average measures of forced expiratory volume in 1 second (FEV₁) in offspring in a multivariate analysis, with an adjusted multinomial odds ratio of 1.56. Fathers’ passive prepubertal smoke exposure also was associated with an early low-rapid decline of FEV₁ and forced vital capacity trajectories (adjusted multinomial odds ratio [OR], 2.30). The trajectory association was even greater for offspring who themselves experienced childhood passive smoke exposure (adjusted multinomial OR, 2.36).

By age 53 years, half (49%) of the children had a history of active smoking, and 5.1% of them had developed chronic obstructive pulmonary disease (COPD) by age 53 years, based on spirometry. Active smoking and respiratory illnesses in the fathers and offspring partly mediated the associations, but each contributed less than 15%, the researchers wrote.

The findings were limited by several factors including the potential for misclassifying light-to-moderate smokers as nonsmokers in terms of passive smoke exposure, and the challenge of isolating exposure windows for fathers who reported continuous passive smoke exposure from birth to 15 years, the researchers noted.

However, the results suggested an intergenerational impact of passive smoke exposure, they concluded.

Raising Awareness and Researching Mechanisms

“We speculated that inherited behavioral patterns, such as active smoking in fathers and subsequently in their offspring, would explain a considerable proportion of the associations between paternal prepubertal passive smoke exposure and impaired lung function trajectories in offspring,” Bui told Medscape Medical News. However, the contribution of active smoking was modest, he said. This finding indicates that the associations may not be primarily attributable to inherited smoking behaviors, such as offspring adopting smoking behavior from their fathers, Bui said. Instead, the findings “could reflect some direct effects of paternal prepubertal passive smoke exposure on impaired lung function trajectories in offspring,” he noted.

“Raising awareness among families about the importance of smoke-free environments for children is essential, as passive smoke exposure may not only harm the children directly but also have intergenerational associations for lung function impairment in the future generations,” Bui emphasized. “Incorporating this perspective into public health advocacy may support early prevention of lung function impairment,” he said.

“Future research on biological mechanisms, including epigenetic pathways, may provide further understanding of the intergenerational associations between paternal prepubertal passive smoke exposure and impaired lung function trajectories in offspring,” said Bui.

Informing COPD Risk Assessment

The current study is important because it goes beyond prior research on passive smoke exposure to assess the lung function trajectories from childhood to adulthood, including the development of COPD, said Arianne K. Baldomero, a pulmonologist and assistant professor of medicine at the University of Minnesota, Minneapolis, in an interview.

“It is surprising that passive smoke exposure experienced by fathers before puberty, meaning from a generation ago, can be associated with impairment of their children’s lifelong lung function, with detectable effects lasting into middle age,” said Baldomero, who was not involved in the study. “The finding that this risk increases further when the next generation is also exposed to passive smoke in childhood highlights the profound and lasting harm of tobacco and underscores that the consequences of early-life smoke exposure are broader and longer-lasting than previously appreciated,” she said.

The findings support the need for clinicians to routinely assess not only active smoking but also active and passive tobacco smoke exposure in children and families, Baldomero told Medscape Medical News. “Aggressive tobacco prevention and cessation interventions should be implemented, especially for children at risk,” she added.

Looking ahead, more research is needed to determine the longitudinal associations of vaping and e-cigarette use on lung health and also to evaluate the impact of paternal exposure to vaping or e-cigarettes on offspring’s lung health, Baldomero said.

The Tasmanian Longitudinal Health Study was supported by the National Health and Medical Research Council (NHMRC) of Australia and the NHMRC European collaborative grant scheme as part of ALEC, which was funded by the European Union’s Horizon 2020 research and innovation programme.

The current study was also supported by the University of Melbourne; the Clifford Craig Medical Research Trust of Tasmania; the Victorian, Queensland & Tasmanian Asthma Foundations; the Royal Hobart Hospital; the Helen MacPherson Smith Trust; and GlaxoSmithKline.

Liu was supported by the China Scholarship Council-University of Melbourne PhD Scholarship.

Bui and Baldomero declared having no financial conflicts.