Increasing evidence suggests that chronic obstructive pulmonary disease (COPD) develops earlier in life than previously thought, with progression occurring over years or decades. Numerous risk factors that may indicate the potential for progression in patients with COPD are being investigated, reinforcing the importance of the careful consideration of a patient’s history.

The identification of risk factors for COPD progression has recently been a topic of intense research, and the new information has been eye opening. When I was in medical school, we were taught that most people reach adulthood with relatively good lung function—and if they did not, they would know why. Someone who smoked or worked in a setting where they regularly inhaled irritants could end up with COPD. Now we know that lung function is highly variable and has multiple potential trajectories from birth through adulthood.

For some people, COPD likely starts developing in the womb. Prenatal factors can affect lung size at birth, and there are many potential contributors to COPD development throughout the life span, including exposure to secondhand smoke, childhood respiratory infections, vaccination status, and air pollution. We now realize that air pollution in particular has a bigger impact on lung function than we previously appreciated. It not only causes flare-ups of existing disease but also can be causative. Moreover, bronchitis and longstanding asthma may also lead to permanent airflow obstruction, although we do not fully understand the links.

The bottom line is that there are multiple pathways to COPD development. It is a culmination of genetics, biology, environment, and social factors throughout a person’s life that may prevent them from ever reaching “normal” lung function as an adult. As a society, we need to reduce the burden of COPD. It is the fourth leading cause of death in the world, making it a public health problem, not just an individual health problem.

Once a patient has established COPD, how do we identify their risk for progression? One primary area of research is the potential role of the computed tomography analysis of anatomic lesions. We are learning that the airways can scar down, narrow, and start to drop out. It appears that once a patient starts developing emphysema, emphysema itself begets more emphysema, likely due to local inflammation. There may also be mechanical elements involved, such as lung tissue losing its structural integrity at a microscopic level, and we are working to identify the causes of those changes.

We know that smoking cessation can help slow COPD progression. Using pharmacotherapy to prevent exacerbations is also important. Additionally, there are interesting data suggesting that viral infections among young susceptible individuals can lead to increased rates of lung function decline. The role of viruses in COPD exacerbations is becoming increasingly appreciated, and this is going to be another active area of research moving forward. Taking precautions against viral infection, including appropriate vaccination and/or antiviral therapy, is likely valuable in preventing COPD progression.

Interestingly, the curve for disease progression seems to be fastest in mild COPD among young and middle-aged adults, when many patients still might not have received a diagnosis, so we often miss an opportunity to intervene. How can we better screen for COPD and diagnose it earlier? I think that identifying risk factors for an earlier spirometry referral can help. If we can intervene earlier in the disease course, our patients will do much better.