Passive smoking as a child may impact your own children's health

A father’s exposure to passive smoking as a child may impair the lifelong lung function of his children, putting them at risk of chronic obstructive pulmonary disease (COPD) — a risk that is heightened further if they are childhood passive smokers themselves.

That’s according to a new study that has been published in the journal Thorax and was led by University of Melbourne researchers, who urge fathers to intercept this harmful legacy by avoiding smoking around their children.

COPD, which includes chronic bronchitis and emphysema, is the third leading cause of death around the world, killing around 3 million people every year. The researchers explained that several factors throughout one’s life may increase the risk of poor lung function and subsequent COPD, and attention is now beginning to focus on the potential role of intergenerational factors.

While previously published research showed that passive smoking during a father’s childhood may be linked to a heightened risk of asthma in his children by the time they are seven, it was not clear if compromised lung function extended into middle age and beyond. To explore this further, the researchers drew on 8022 child participants in the Tasmanian Longitudinal Health Study (TAHS), all of whom had tests to assess their lung function (spirometry).

The children’s parents completed an initial comprehensive survey on their and their children’s respiratory health. Further check-ups ensued when those children were 13, 18, 43, 50 and 53. These included spirometry to assess two measures of lung function (FEV₁ and FVC), as well as questionnaires on demographics and respiratory symptoms/disease.

Of the 7243 parents who were alive and could be traced in 2010, 5111 were resurveyed about whether either of their own parents had smoked when they were under the age of five and/or up to when they were 15. The final analysis included 890 father–child pairs with data on the father’s passive smoke exposure before puberty and lung function data for their children up to the age of 53.

More than two-thirds of the fathers (nearly 69%) and more than half of their children (56.5%) had been exposed to passive smoking during their childhoods. Around half of the children (49%) had a history of active smoking by middle age, and just over 5% of them had developed COPD by this time point, as assessed by spirometry.

After adjusting for potentially influential factors, including the father’s lifetime history of asthma/wheeze and his age, his passive smoke exposure as a child was associated with 56% higher odds of below average FEV₁, but not FVC, across the lifespan of his children. Fathers’ childhood passive smoke exposure was also associated with a doubling in the odds of an early low-rapid decline in FEV₁/FVC in their children; this was statistically significant even after adjusting for potentially influential factors.

Paternal exposure to passive smoking as a child was also associated with a doubling in the risk of COPD by the age of 53 in his children, although this was no longer statistically significant after adjusting for potentially influential factors. But children whose fathers had been exposed to passive smoking as a child were twice as likely to have below-average FEV₁ if they, too, had been exposed to passive smoking during their childhood.

The researchers acknowledged the limitations of their research, including the fact that it was an observational study, so no firm conclusions can be drawn about cause and effect; that TAHS lacks data on paternal lung function and genetics, preventing assessment of familial aggregation as a potential mechanism; and that childhood passive smoke exposure was defined as at least one parent smoking six days a week, which might have misclassified moderate/light smokers as non-smokers. Nevertheless, they claimed that the period before puberty is especially critical for boys, when exposure to harmful substances may change gene expression and modify repair mechanisms, which may then become heritable.

“Our findings are novel as this is the first study to investigate and provide evidence for an adverse association of paternal prepubertal passive smoke exposure, rather than just active smoking, on impaired lung function of offspring by middle age,” the researchers wrote.

“This is of importance from a public health perspective, as passive smoke exposure affects about 63% of adolescents, which is significantly higher than the approximately 7% affected by active smoking.

“These findings suggest that smoking may adversely affect lung function not only in smokers but also in their children and grandchildren … Fathers exposed to tobacco smoke during prepuberty may still reduce risk for future generations by avoiding smoking around their children.”

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