Study links adult lung conditions to childhood illnesses and parental smoking
Three-quarters of cases of chronic obstructive pulmonary disease (COPD) can be traced back to exposures during childhood, a study has found.
COPD is the name for a group of lung conditions which cause breathing difficulties including emphysema and chronic bronchitis, which mainly affect middle-aged or older adults who smoke.
While smoking remains the biggest risk factor for COPD, the Australian study showed that childhood illnesses - such as asthma, bronchitis, pneumonia and eczema - and exposures to parental smoking were also linked to the disease.
A second study published in the Lancet Respiratory Medicine journal also suggested there could be a window of opportunity during childhood to reduce the risk of poor lung function in later life.
Both studies identified pathways of how lung function changed over life, which were associated with different risk factors and disease risk in later life.
The study authors believe these insights are important for lung disease prediction, prevention and treatment.
The first piece of research, led by the University of Melbourne, saw 2,438 participants from the Tasmanian Longitudinal Health Study tracked from childhood to the age of 53, making it the largest and longest-running study of its kind.
Lung function was measured at the ages of seven, 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 changed with age, three of which were associated with COPD.
These three groups were described as having below average lung function in early life and a quick decline in lung function in later life, having persistently low lung function, and having below average lung function.
The three pathways were also 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 arose from these three trajectories.
These three pathways were also linked to childhood asthma, bronchitis, pneumonia, allergic rhinitis, eczema, parents having asthma or smoking, and the participants themselves smoking or having asthma.
The study authors suggested the childhood risk factors were important indicators of COPD risk, which were aggravated by smoking and having asthma in adulthood.
This amplified the damage already caused by childhood risk factors, and may have resulted in a more rapid decline in lung function.
As a result, the authors said it would be important to reduce parental smoking, encourage immunisation, and avoid smoking to promote healthy lung function pathways and minimise COPD risk, especially for people who had low childhood lung function or whose parents smoked.
Ensuring all people with asthma had appropriate treatment may also be vital to preserving lung function.
Study author Professor Shyamali Dharmage, of the University of Melbourne, said: "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.
"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."
In the second study, 2,632 participants were tracked from birth to 24-years-old, with their lung function measured.
It found that around three-quarters of infants aged one to six months with poor lung function improved throughout their childhood, indicating a window of opportunity to increase lung function and potentially reduce risk of COPD in later life.
The study authors said this suggested interventions to maximise lung growth in early childhood might modify the risk of COPD in older age.