Lung capacity typically maxes out around age 20 to 30. Smoking can stunt that development, the study team points out in the New England Journal of Medicine.
"If you then observe them for 20 or 30 years, you find that their risk for having COPD will be 3 or 4 times greater than if they had normal lung function as young adults," lead author Dr. Peter Lange of Copenhagen University in Denmark told Reuters Health.
Because the study shows that early lung development is so important, "every effort should be done to achieve normal growth of lung function, including nonsmoking during teenage years, treatment of asthma in childhood and reducing exposure to agents like passive smoking," Lange said.
"It’s really a provocative study that addresses a fundamental question - how do individual patients develop this obstructive lung disease? And it suggests there's more than one way to get there," said Dr. Ralph Panos, chief of medicine at the Cincinnati VA Medical Center, who was not involved in the research.
Until now, doctors had thought that COPD was primarily caused by an unexplained but rapid decline in lung capacity.
"COPD was originally considered to be accelerated aging" of the lungs, Panos told Reuters Health.
The Lange team found that the steep decrease in lung capacity, as measured by a test of forced expiratory volume (FEV-1) – how much air a person can exhale rapidly - only accounted for about half the cases.
Knowing that COPD has a combination of causes may also help researchers develop better tests to gauge treatments for the disease.
COPD is the fourth most common cause of death among adults. For decades, it has been linked to smoking and other exposures to inhaled particles.
But when population studies found that long-term declines in lung capacity were not as steep as anticipated, researchers began wondering if normal age-related decline was responsible for the COPD in some people because their lung capacity was low to begin with.
To find the answer, the researchers tapped data from three population studies and sorted people based on whether their starting FEV-1s were above and below 80 percent of expected lung capacity.
After 22 years of observation, 26 percent of the people who started out with a low FEV-1 ended up with COPD compared to just 7 percent of those with an initial FEV-1 of 80 percent or higher.