Careful assessment of the research on the etiology and natural course of chronic obstructive pulmonary disease (COPD) leaves us with a glimpse of a glass that is halffull or half empty. On one hand, there are countless original reports containing irrefutable evidence that smoking is the primary and major cause of COPD. With regard to COPD, smoking fulfils virtually all 10 of the causality criteria postulated 50 years ago by Sir Austin Bradford Hill, with the exception of reversibility, because smoking cessation in advanced COPD does not reverse the inflammation that is already present. Moreover, many original reports describe the quantity, quality and chronology of known risk factors, modifiable or not, including: genes, exposure to particles and dust, indoor and outdoor air pollution, respiratory infections, socioeconomic status, nutrition and comorbidities. On the other hand, and contrary to other common chronic conditions such as cardiovascular disease or cancer, there are no population studies with a primary respiratory origin describing the natural course of COPD, which is usually defined as the accelerated decline in respiratory function occurring in COPD patients. Current consensus is that COPD is a preventable and treatable disease, but once it is diagnosed there is a steady progression and worsening of patients' health, with increased symptoms, poorer quality of life, a phenomenon of adaptation and more frequent and severe exacerbations, all of which eventually lead to premature death. To date, no patient with severe COPD has ever been "cured" of the disease. However, preventing disease progression by improving the slope of FEV₁ decline to nearly that of patients who have never smoked has been successfully documented with smoking cessation. Compared to prevention of disease progression in non-respiratory conditions, research into the success (or lack of it) of current treatment for COPD, including the use of pharmaceuticals, is taking its first baby steps.
The World Health Organization recently issued a warning regarding the fact that more people smoke today than at any other time in human history. Every 10 seconds, 1 person dies from a smoking-related disease. If current smoking patterns continue unabated, by 2020 some 10 million deaths will occur each year from this cause. Half of all people who smoke today, or about 650 million individuals, will eventually die from tobacco use. Therefore, tobacco has firmly established itself as public health enemy number 1 for the foreseeable future: it is the most prolific killer of human life. Research evidence from previous years shows an even bleaker picture of the health risk of active and passive smoking in COPD than we had previously realized.
Perhaps we have started building the house from the roof, and this overwhelming evidence has drawn the lion's share of attention toward more research on the effects of smoking in COPD. This has likely diverted efforts and funding away from the study of factors besides cigarette smoking in COPD in favor of studying the effects of smoking on non-respiratory disorders. Unsurprisingly, in 2006 the British Thoracic Society recommended 7 priorities for respiratory research. Number 1 on the list was to study the natural course of early development of the respiratory tract and immune system and the techniques needed to understand normal air growth, development and decline in health and disease. As a token gesture, the Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines included in its latest issue a mention of biofuel smoke as a definitive causal risk factor for COPD in women (and men) who have never been regular cigarette smokers.
This new issue in the series Hot Topics in Respiratory Medicine nicely summarizes in 3 concise chapters a number of related and relevant topics such as smoking and smoking cessation in COPD, biofuel smoke exposure as an alternate etiology to tobacco-induced COPD, and the natural course of COPD.