The research, published in The Lancet Respiratory Medicine journal, draws on data from the Tasmanian Longitudinal Health Study which has tracked the lung function of nearly 2500 participants from childhood to age 53.
It found that while smoking remains the biggest risk factor for chronic obstructive pulmonary disease (COPD) that childhood illnesses (such as asthma, bronchitis, pneumonia, allergic rhinitis, eczema) and exposures to parental smoking are also linked to the disease. Three-quarters of the Tasmanian cohort with COPD – the group of lung diseases that includes emphysema, chronic bronchitis and chronic asthma – had their origins in poor lung function pathways beginning in childhood, that were aggravated by smoking and having asthma in adulthood.
The study’s authors say that their findings back how important it was to reduce parental smoking, encourage immunisation and avoid smoking to promote health lung function and minimise COPD risk – especially for people who had low childhood lung function or whose parents smoked. They added that ensuring all people with asthma have appropriate treatment may be vital to preserve lung function.
A second study in the journal – tracking 2632 participants from birth to 24 years – also suggests that there could be a window of opportunity during childhood to reduce the risk of poor lung function in later life as 3/4s of babies aged one to six months with poor lung function went on to improve their lung function throughout their childhood.
“These findings highlight the importance of preventing both early life adverse exposures that could lead to poorer lung growth, and adult risk factors contributing to accelerated lung decline,” said study author Professor Shyamali Dharmage, School of Population and Global Health at tge The University of Melbourne.
“COPD is expected to be the third largest cause of death globally by 2030, and it is important that we identify its key causes so that this burden can be reduced.”
“Reduction of maternal smoke exposure and personal smoking and promotion of immunisation are identified as public health targets to prevent poor lung function pathways. Doctors and patients with asthma should be made aware of the potential long-term implications of non-optimal asthma control throughout life, and this should be investigated in future research.”
The authors note some limitations, including that most patients are diagnosed with COPD in their sixties and the last measurement in the Tasmanian study was at the age of 53, when COPD is just starting to emerge. It believed tracking lung function pathways later into life may give a clearer picture of COPD risk.
In the Tasmanian Longitudinal Health Study (Australia) 2438 participants had their lung function measured at the ages of 7, 13, 18, 45, 50 and 53 years old, and participants’ exposure to various risk factors was also recorded.
The authors identified six distinct pathways describing how lung function changes with age. Three of these pathways were associated with COPD – the group with below average lung function in early life and a quick decline in lung function in later life; those with persistently low lung function; and those with below average lung function. Combined, these three pathways were linked to an estimated three-quarters of all cases of COPD occurring at the age of 53 (75.2% overall). For moderate-to-severe COPD, all cases only arose from these three trajectories.
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