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New research published in the respiratory journal Thorax adds further evidence to support the intergenerational harms of tobacco smoking.
The Australian study has found that a father’s exposure to second-hand smoke in his childhood might impair the lifelong lung function of his children too.
This association was further exacerbated when fathers went on to smoke around their children, highlighting the need to limit children’s passive exposure to tobacco.
“These findings suggest that smoking may adversely affect lung function not only in smokers but also in their children and grandchildren,” the authors write.
“Fathers exposed to tobacco smoke during prepuberty may still reduce risk for future generations by avoiding smoking around their children.”
The authors analysed data from the Tasmanian Longitudinal Health Study (TAHS), which followed more than 8,500 children born in 1961 who went on to attend school in the Australian state of Tasmania.
Parents completed baseline respiratory health surveys for themselves and their children, who also underwent spirometry test to assess lung function.
A spirometry test measures forced expiratory volume in 1 (FEV1) – the volume of air exhaled in the first second after a deep inhale – and forced vital capacity (FVC), a measurement of the total volume of air exhaled in one breath.
The offspring were followed up at ages 13, 18, 43, 50 and 53 years.
In 2010, parents were resurveyed to determine whether they had ever been exposed to second hand smoke during their own childhoods. The final analysis included a total of 890 father-offspring pairs.
Nearly 69% of fathers, and more than half of their children (56.5%), had been exposed to passive smoking during their childhoods.
About half of the children (49%) went on to have a history of active smoking by middle age, and just over 5% of them developed chronic obstructive pulmonary disease (COPD) by age 53.
Statistical analysis revealed that a father’s passive smoke exposure as a child was associated with 56% higher risk of his children having a below average FEV1, but not FVC, across their lifespan.
It was also associated with a doubling in the odds of an early low-rapid decline in the FEV1/FVC of his children.
They were also twice as likely to have below average FEV1 if they too had been exposed to passive smoking during their childhood.
“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 authors write.
Because the study is observational, the researchers cannot conclude fathers’ childhood exposure to second hand smoke directly caused the effects seen in their children. However, the findings do provide important clues to inform future research and “can inform public health messages about the harms of passive smoke exposure”.
“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,” the authors write.