The independent and combined effects of host and environmental factors on lung function in mid-adult life
Chronic Obstructive Pulmonary Disease is a global health issue, ranking as the equal third leading cause of death worldwide. Yet, the fundamental question of why only a fraction of smokers are susceptible to COPD remains largely unexplained. By using data from the Tasmanian Longitudinal Health Study (TAHS) cohort who were born in 1961 and first studied in 1968, my doctoral work has critically examined the potential for lifetime asthma, childhood infection, parental smoking and adult passive smoking to adversely influence lung function from childhood to middle age. While personal smoking is central to the development of COPD in Western countries, my analyses support the concept that childhood factors can also play a role. When exposures were combined, I found the early life insult from asthma and maternal smoking could effectively increase the lung’s susceptibility to the later harms of personal smoking.
These results strengthen the links between these less traditional respiratory ‘risk’ factors and spirometrically-defined COPD, as well as clarify the long-term lung function consequence of childhood pneumonia. These findings reinforce the benefits of smoking abstinence and childhood immunization programs as recommended by public health authorities, but with a greater emphasis on targeting those most at-risk.