Background Cigarette smoking is the strongest risk factor for COPD. Smoking burden is frequently measured in pack-years, but the relative contribution of cigarettes smoked per day versus duration towards the development of structural lung disease, airflow obstruction and functional outcomes is not known.
Methods We analysed cross-sectional data from a large multicentre cohort (COPDGene) of current and former smokers. Primary outcome was airflow obstruction (FEV1/FVC); secondary outcomes included five additional measures of disease: FEV1, CT emphysema, CT gas trapping, functional capacity (6 min walk distance, 6MWD) and respiratory morbidity (St George’s Respiratory Questionnaire, SGRQ). Generalised linear models were estimated to compare the relative contribution of each smoking variable with the outcomes, after adjustment for age, race, sex, body mass index, CT scanner, centre, age of smoking onset and current smoking status. We also estimated adjusted means of each outcome by categories of pack-years and combined groups of categorised smoking duration and cigarettes/day, and estimated linear trends of adjusted means for each outcome by categorised cigarettes/day, smoking duration and pack-years.
Results 10 187 subjects were included. For FEV1/FVC, standardised beta coefficient for smoking duration was greater than for cigarettes/day and pack-years (P<0.001). After categorisation, there was a linear increase in adjusted means FEV1/FVC with increase in pack-years (regression coefficient β=−0.023±SE0.003; P=0.003) and duration over all ranges of smoking cigarettes/day (β=−0.041±0.004; P<0.001) but a relatively flat slope for cigarettes/day across all ranges of smoking duration (β=−0.009±0.0.009; P=0.34). Strength of association of duration was similarly greater than pack-years for emphysema, gas trapping, FEV1, 6MWD and SGRQ.
Conclusion Smoking duration alone provides stronger risk estimates of COPD than the composite index of pack-years.
Trial registration number Post-results; NCT00608764.
- COPD epidemiology
- tobacco and the lung
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Contributors SPB had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design: SPB, YK and WCB. Acquisition, analysis or interpretation of data: all authors. Drafting of the manuscript: SPB. Critical revision of the manuscript for important intellectual content: all authors. Statistical analysis: YK and SPB. Study supervision: all authors.
Funding The project was supported by Awards R01 HL089897 and R01 HL089856 from the National Heart, Lung and Blood Institute. The COPDGene project is also supported by the COPD Foundation through contributions made to an Industry Advisory Board which comprised AstraZeneca, Boehringer Ingelheim, Novartis, Pfizer, Siemens, Sunovion and GlaxoSmithKline. SPB is supported by NIH K23 Grant K23HL133438.
Competing interests None declared.
Ethics approval The institutional review boards of all 21 participating centres approved the COPDGene study.
Provenance and peer review Not commissioned; externally peer reviewed.
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