A new study may change the way doctors view the lung-crippling condition known as chronic obstructive pulmonary disease, or COPD, and offer new evidence of the dangers of smoking for teenagers and young adults.
Researchers found that about half of COPD cases appear in people whose lungs have aged normally but have become crippled by breathing problems because they began adulthood with poor lung capacity.
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.
Looked at another way, among the 332 people who ended up with COPD, roughly half had started out in the low FEV-1 group while the rest had been in the normal FEV-1 group.
In addition, among the patients with COPD at the end of the study, the decline in FEV-1 turned out to have been steepest among people who had the higher, healthier FEV-1 values at the start.
Their average decline in FEV-1 was 53 ml per year. In the group with a starting FEV-1 of less than 80 percent who eventually developed COPD, their average decline was 27 ml per year, which is within normal limits.
Thus, "a substantial proportion of patients with COPD may not have had a rapid decline in FEV1, which for decades has been regarded as the hallmark of COPD," the researchers write.
"The theory that you can develop COPD by different pathways has been there for many years, but this is the first study quantifying how many get COPD from fast decline and how many don't," Lange noted.
The researchers cautioned that, on an individual basis, both mechanisms might play a role.
"It is possible that a single person over time can have periods of rapid decline in FEV-1 followed by periods when the decline is normal or almost normal," they said.
Panos said "there's a multitude of factors" that may be causing COPD victims to have low lung capacity to begin with "and they're all open to investigation. Is it infections? Is it bronchiolitis as an infant? The other possibility may be sidestream smoke from parents or others who are smoking. It could also include environmental pollutants, like car exhaust."
The research, he said, "is going to make us think, 'How did they get there?'"