Lung function decline in former smokers and low-intensity current smokers: a secondary data analysis of the NHLBI Pooled Cohorts Study

Elizabeth C. Oelsner, Pallavi P. Balte, Surya P. Bhatt, Patricia A. Cassano, David Couper, Aaron R. Folsom, Neal D. Freedman, David R. Jacobs, Ravi Kalhan, Amanda R. Mathew, Richard A. Kronmal, Laura R. Loehr, Stephanie J. London, Anne B. Newman, George T. O'Connor, Joseph E. Schwartz, Lewis J. Smith, Wendy B. White, Sachin Yende

Research output: Contribution to journalArticlepeer-review

21 Scopus citations

Abstract

Background: Former smokers now outnumber current smokers in many developed countries, and current smokers are smoking fewer cigarettes per day. Some data suggest that lung function decline normalises with smoking cessation; however, mechanistic studies suggest that lung function decline could continue. We hypothesised that former smokers and low-intensity current smokers have accelerated lung function decline compared with never-smokers, including among those without prevalent lung disease. Methods: We used data on six US population-based cohorts included in the NHLBI Pooled Cohort Study. We restricted the sample to participants with valid spirometry at two or more exams. Two cohorts recruited younger adults (≥17 years), two recruited middle-aged and older adults (≥45 years), and two recruited only elderly adults (≥65 years) with examinations done between 1983 and 2014. FEV1 decline in sustained former smokers and current smokers was compared to that of never-smokers by use of mixed models adjusted for sociodemographic and anthropometric factors. Differential FEV1 decline was also evaluated according to duration of smoking cessation and cumulative (number of pack-years) and current (number of cigarettes per day) cigarette consumption. Findings: 25 352 participants (ages 17–93 years) completed 70 228 valid spirometry exams. Over a median follow-up of 7 years (IQR 3–20), FEV1 decline at the median age (57 years) was 31·01 mL per year (95% CI 30·66–31·37) in sustained never-smokers, 34·97 mL per year (34·36–35·57) in former smokers, and 39·92 mL per year (38·92–40·92) in current smokers. With adjustment, former smokers showed an accelerated FEV1 decline of 1·82 mL per year (95% CI 1·24–2·40) compared to never-smokers, which was approximately 20% of the effect estimate for current smokers (9·21 mL per year; 95% CI 8·35–10·08). Compared to never-smokers, accelerated FEV1 decline was observed in former smokers for decades after smoking cessation and in current smokers with low cumulative cigarette consumption (<10 pack-years). With respect to current cigarette consumption, the effect estimate for FEV1 decline in current smokers consuming less than five cigarettes per day (7·65 mL per year; 95% CI 6·21–9·09) was 68% of that in current smokers consuming 30 or more cigarettes per day (11·24 mL per year; 9·86–12·62), and around five times greater than in former smokers (1·57 mL per year; 1·00–2·14). Among participants without prevalent lung disease, associations were attenuated but were consistent with the main results. Interpretation: Former smokers and low-intensity current smokers have accelerated lung function decline compared with never-smokers. These results suggest that all levels of smoking exposure are likely to be associated with lasting and progressive lung damage. Funding: National Institutes of Health, National Heart Lung and Blood Institute, and US Environmental Protection Agency.

Original languageEnglish (US)
Pages (from-to)34-44
Number of pages11
JournalThe Lancet Respiratory Medicine
Volume8
Issue number1
DOIs
StatePublished - Jan 2020

Bibliographical note

Funding Information:
All sources of funding are listed below. The NHLBI Pooled Cohorts Study was funded by grants NIH/NHLBI R21-HL121457, R21-HL-129924, and K23-HL-130627. The authors thank the staff and participants of the Atherosclerosis Risk In Communities (ARIC) study for their important contributions. The ARIC study has been funded in whole or in part with federal funds from the National Heart, Lung, and Blood Institute (NHLBI), NIH, and Department of Health and Human Services (contract numbers HHSN268201700001I, HHSN268201700003I, HHSN268201700005I, HHSN268201700004I, and HHSN2682017000021). The Jackson Heart Study has been funded by NHLBI and National Institute for Minority Health and Health Disparities (contracts HHSN268201300049C and HHSN268201300050C to Jackson State University, HHSN268201300048C to Tougaloo College, and HHSN268201300046C and HHSN268201300047C to the University of Mississippi Medical Center). The Coronary Artery Risk Development in Young Adults (CARDIA) Study was done and supported by the NHLBI in collaboration with the University of Alabama at Birmingham (HHSN268201300025C and HHSN268201300026C), Northwestern University (HHSN268201300027C), University of Minnesota (HHSN268201300028C), Kaiser Foundation Research Institute (HHSN268201300029C), and Johns Hopkins University School of Medicine (HHSN268200900041C). CARDIA is also partially supported by the Intramural Research Program of the National Institute on Aging (NIA) and an intra-agency agreement between NIA and NHLBI (AG0005), as well as an NHLBI grant (R01 HL122477; to RK). This manuscript has been reviewed by CARDIA for scientific content. The Cardiovascular Health Study (CHS) was supported by contracts HHSN268201200036C, HHSN268200800007C, N01HC55222, N01HC85079, N01HC85080, N01HC85081, N01HC85082, N01HC85083, and N01HC85086, and grants U01HL080295 and U01HL130114 from the NHLBI, with additional contributions from the National Institute of Neurological Disorders and Stroke (NINDS). Additional support was provided by R01AG023629 from the NIA. A full list of principal CHS investigators and institutions can be found at CHS-NHLBI.org. This work also was supported by the NHLBI's Framingham Heart Study (contract numbers N01-HC-25195; HHSN268201500001I). The Health Aging and Body Composition (Health ABC) Study was supported by NIA contracts N01-AG-6-2101, N01-AG-6-2103, N01-AG-6-2106, NIA grant R01-AG028050, and a National Institute of Nursing Research (NINR) grant R01-NR012459. The Multi-Ethnic Study of Atherosclerosis (MESA) was funded by NIH/NHLBI R01-HL-077612, R01-HL-093081, RC1-HL-100543, N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, and N01-HC-95169. This publication was also developed under a STAR research assistance agreement, number RD831697 (MESA Air), awarded by the US Environmental Protection Agency. This work has not been formally reviewed by the US Environmental Protection Agency (EPA). The views expressed in this Article are solely those of the authors and the EPA does not endorse any products or commercial services mentioned in this publication.

Publisher Copyright:
© 2020 Elsevier Ltd

PubMed: MeSH publication types

  • Journal Article
  • Research Support, N.I.H., Extramural
  • Research Support, N.I.H., Intramural
  • Research Support, U.S. Gov't, Non-P.H.S.

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