Lung Function Decline and Airflow Limitation Risk in Preserved Ratio Impaired Spirometry Subtypes by Smoking Status
Cuiqiong Dai1, Fan Wu2, Jia Tian3
1State Key Laboratory of Respiratory Disease & National Clinical Research Center for Respiratory Disease & Guangzhou Institute of Respiratory Health & National Center for Respiratory Medicine & Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou Medical University, Guangzhou, Guangdong, China.
Background:
Preserved ratio impaired spirometry (PRISm) is regarded as a COPD precursor, but whether this varies by smoking status remains unclear.
Research Question:
Are annual lung function decline and the risk of developing airflow limitation different among PRISm subtypes by smoking status?
Study Design And Methods:
A total of 2,850 participants from a 15-year population-based prospective cohort were included in this analysis. Participants were categorized into 3 groups: patients with normal spirometry who do not smoke (normal control), patients with PRISm who do not smoke (NS-PRISm), and patients with PRISm who have ever smoked (ES-PRISm). We compared annual lung function decline and the risk of developing airflow limitation among the 3 groups.
Results:
Participants in the normal control group exhibited the fastest decline in annual lung function, followed by the ES-PRISm group, with the NS-PRISm group showing the slowest decline. Participants in the ES-PRISm group had significantly faster annual lung function decline than the NS-PRISm group. Participants in the ES-PRISm group had a significantly increased risk of developing airflow limitation than the NS-PRISm group (95 of 256 [37.1%] vs 69 of 470 [14.7%]; adjusted hazard ratio [HR], 1.90; 95% CI, 1.31-2.77; P = .001) and normal control group (95 of 256 [37.1%] vs 193 of 2,124 [9.1%]; adjusted HR, 2.69; 95% CI, 1.96-3.69; P < .001). Participants in the NS-PRISm group also exhibited a higher risk of developing airflow limitation than those in the normal control group (69 of 470 [14.7%] vs 193 of 2,124 [9.1%]; adjusted HR, 1.41; 95% CI, 1.07-1.87; P = .016). When the ES-PRISm group was further divided into participants with PRISm who currently smoke and those who formerly smoked, both of these PRISm subtypes showed a faster annual lung function decline and a similarly higher risk of airflow limitation than the NS-PRISm group.
Interpretation:
These findings suggest that both NS-PRISm and ES-PRISm may be potential precursors to COPD and indicate that PRISm should not be restricted to evaluating individuals with a history of smoking alone.
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