In the best of all worlds, we would convince smokers that they need to quit and assist them in that process. Even though smoking is associated with diverse risk in multiple anatomic compartments, it is lung disease that the public most commonly associates with smoking. Yet, we have to acknowledge that only a minority (20-25%) of smokers incur problems like chronic obstructive pulmonary disease (COPD). Is there a way to identify which smokers are most likely destined to develop COPD, thereby garnering an additional motivational tool — especially since so many smokers see consequences as either “it won’t happen to me” or “it’s a long, long way off”?

Petersen et al studied ever smokers (n = 809) who were free of spirometric abnormalities at baseline with periodic spirometry (q 18 months) for a mean of 6 years. Concordant with current guidelines, the metric utilized to quantify lung function was post-bronchodilator FEV1. One premise of the investigation was that study subjects who exhibited the most rapid rate of decline in FEV1 would also be most likely to develop COPD. Study subjects were categorized by rate of decline as rapid decline (≥ 30 mL/year), normal (0-29.9 mL/year), and no decline (unchanged from baseline). At the conclusion of the mean follow-up of 6 years, about one-third of the subjects fell into each of these categories.

As hypothesized by the authors, subjects who experienced rapid decline were approximately twice as likely to develop COPD. Another interesting insight from this trial was an evaluation of the association of various medications with outcomes. Seven different medication classes were addressed that were being used by these patients: angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers, beta-blockers, CCBs, statins, insulin, and oral hypoglycemic agents. ACE inhibitors were associated with a 45% lesser incidence of rapid decline, but no other statistically significant associations with other medications were demonstrated. The authors posit that salutary effects of ACE inhibitors upon development of COPD are related to anti-inflammatory activity of this class.

These data suggest that we may be able to identify smokers destined to develop COPD by rate of decline in FEV1.