Study links childhood passive smoking in fathers to higher COPD risk in offspring

A father's exposure to passive smoking as a child may impair the lifelong lung function of his children, putting them at risk of COPD-a risk that is heightened further if they are childhood passive smokers themselves-finds research published online in the respiratory journal Thorax.

The findings highlight the intergenerational harms of smoking, say the researchers, who urge fathers to intercept this harmful legacy by avoiding smoking around their children.

Chronic obstructive pulmonary disease, more usually known by its acronym of COPD, includes chronic bronchitis and emphysema. Now the third leading cause of death around the world, COPD kills around 3 million people every year, say the researchers.

Several factors throughout the lifespan 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, they explain.

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 7, it's not clear if compromised lung function may extend into middle age and beyond, they add. 

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).

Their 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 2 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 re-surveyed about whether either of their own parents had smoked when they were under the age of 5 and/or up to when they were 15.

Among the 5097 respondents with complete data, 2096 were fathers. 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. 

Similarly, 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.

And 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 observed associations were only partly mediated through smoking and respiratory illnesses in fathers and their children (each contributing less than 15%).

This is an observational study, and as such, no firm conclusions can be drawn about cause and effect. And the researchers acknowledge that TAHS lacks data on paternal lung function and genetics, preventing assessment of familial aggregation as a potential mechanism. 

And their children's childhood passive smoke exposure was defined as at least one parent smoking 6 days a week, which might have misclassified moderate/light smokers as non-smokers, they add.

But 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, say the researchers by way of an explanation for their findings. 

"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," they write. 

"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." 

They conclude: "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."