Do we need to think differently about COPD?

The internal structure of the lungs by Dave Farnham (CC BY 4.0)

Ann Morgan, a PhD student at the National Heart and Lung Institute, gives us her thoughts on why smoking isn’t the only culprit behind the rise in COPD. 

The traditional view of COPD (chronic obstructive pulmonary disease) is that it is a self-inflicted disease caused by smoking. However, it is increasingly likely that this description is something of an oversimplification. While still very much associated with smoking, clinicians and researchers alike are getting to grips with the reality that COPD is a more complex and heterogeneous disease than previously thought. We are also becoming more aware of the fact that it is a disease which rarely occurs in isolation. The vast majority of people who present with COPD have at least one other co-existing disease or condition, and around 50% have four or more accompanying chronic diseases or ‘comorbidities’.

A disease still on the rise

This changing perception of COPD comes not before time. Unlike the situation for some other leading causes of death, we have not seen the same downturn in COPD mortality and morbidity rates over the last decade or so. Better screening programmes and primary prevention strategies have contributed much to reduced mortality rates from ischaemic heart disease in both North America and Europe, but in the meantime, the proportion of deaths due to COPD has risen. More significantly, COPD is projected to move from fourth to third place in the World Health Organization’s (WHO) top-ten list of causes of global mortality, overtaking deaths due to lower respiratory tract infections in the process.

Smoking, not the only guilty party

So is COPD really all about smoking or are there other preventable risk factors that we should be targeting in order to reduce the rising burden of COPD morbidity and mortality? Two pieces of epidemiological evidence, in particular, suggest that there may well be.  The first is the observation that – entirely contrary to expectations – the global distribution of COPD mortality and patterns of smoking prevalence do not in fact overlap but are instead almost mirror images of one another. According to WHO’s Global Burden Disease data, COPD mortality is higher in Ethiopia than it is in Russia.

Tempting though it is to point the finger of accusation at the use of biomass fuels, a recent analysis of data collected as part of the Burden of Obstructive Lung Disease (BOLD) study suggests that this might not necessarily be the explanation either. This analysis, to which several National Heart and Lung Institute staff contributed, was unable to find evidence of an association between the use of solid fuels for cooking or heating and airflow obstruction.

What does seem to correlate strongly with COPD mortality, and also with airflow obstruction is poverty. In countries with a low overall consumption of tobacco, there appears to be an inverse association between wealth and airflow obstruction. The poorer the individual the greater their airflow obstruction, or respiratory distress. While it’s not easy to establish precisely what drives the link between poverty and poor lung health, it’s not unreasonable to speculate that nutritional factors may be playing a role.

The road to COPD

The other piece of work that has done much to change our thinking about COPD, perhaps more than any other, is a study reported by Lange and co-workers in 2015. This work challenges the traditional perception of COPD in that it suggests that not everyone develops COPD in the same way. There are different pathways. The traditional route involves a rapid loss of lung function in late middle age, down from a maximally attained level which is normally achieved at around the age of 25–30 years. For years this was assumed to be the road to COPD, and smoking was almost exclusively to blame. However, Lange showed that at least half his study cohort members with moderate COPD never experienced a rapid decline in lung function (measured by how much air they can exhale in a set time), but instead because they started out with a low maximally attained lung function, even a moderate rate of lung function decline meant they also ended up with obstructive lung disease in later life. This is an important finding and shifts at least some of the focus away from smoking towards those factors that contribute to a poor lung development in childhood, such as exposure to air pollution, low birth weight and physical inactivity, all of which correlate with low socioeconomic status.

These epidemiological observations, coupled with a new understanding of the biological mechanisms and pathways that underpin the development of COPD and its multiplicity of comorbidities, means that today COPD is increasingly being perceived as the lung component of a multi-organ response to a lifetime of exposures to environmental stressors and other risk factors, including unhealthy lifestyle choices. And while this new-found thinking doesn’t mean that we can let up on efforts to promote the benefits of smoking cessation, it does imply that there are other ways to prevent COPD. These all involve paying more attention to the lung health of children and adolescents – because the rot may have set in long before they even think of picking up a cigarette.

Ann Morgan is a PhD student with the Respiratory Epidemiology group at the National Heart and Lung Institute.

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