Background Chronic lung disease is a leading contributor to the global disease burden; however, beyond tobacco smoke, we do not fully understand what risk factors contribute to lung function decline in low-income and middle-income countries.
Methods We collected sociodemographic and clinical data in a randomly selected, age-stratified, sex-stratified and site-stratified population-based sample of 3048 adults aged ≥35 years from four resource-poor settings in Peru. We assessed baseline and annual pre-bronchodilator and post-bronchodilator lung function over 3 years. We used linear mixed-effects models to assess biological, socioeconomic and environmental risk factors associated with accelerated lung function decline.
Results Mean±SD enrolment age was 55.4±12.5 years, 49.2% were male and mean follow-up time was 2.36 (SD 0.61) years. Mean annual pre-bronchodilator FEV1 decline was 30.3 mL/year (95% CI 28.6 to 32.0) and pre-bronchodilator FVC decline was 32.2 mL/year (30.0 to 34.4). Using multivariable linear mixed-effects regression, we found that urban living, high-altitude dwelling and having hypertension accounted for 25.9% (95% CI 15.7% to 36.1%), 21.3% (11.1% to 31.5%) and 15.7% (3.7% to 26.9%) of the overall mean annual decline in pre-bronchodilator FEV1/height2, respectively. Corresponding estimates for pre-bronchodilator FVC/height2 were 42.1% (95% CI% 29.8% to 54.4%), 36.0% (23.7% to 48.2%) and 15.8% (2.6% to 28.9%) of the overall mean annual decline, respectively.
Conclusion Urbanisation, living at high altitude and hypertension were associated with accelerated lung function decline in a population with low daily smoking prevalence.
- not applicable
- copd epidemiology
- tobacco and the lung
Statistics from Altmetric.com
Contributors CHM, MRG and WC were responsible for conducting analysis. JJM, AB-O, RHG and WC were responsible for study design and conduct. CHM, MRG, TS and WC were responsible for the first draft of the manuscript. CHM, MRG, TS, RHG, JJM, AB-O, RAW and WC participated in the interpretation of findings and development of conclusions. WC is ultimately responsible for the integrity of analyses and quality of data.
Funding This project was funded in whole with federal funds from the United States National Heart, Lung, and Blood Institute, National Institutes of Health, Department of Health and Human Services, under Contract No. HHSN268200900033C. Research reported in this publication was supported by the National Heart, Lung, and Blood Institute of the United States National Institutes of Health under Award Number T32HL007534. CHM was further supported by a Fogarty International Center training grant (5R25TW009340).
Competing interests None declared.
Patient consent Not required.
Ethics approval Johns Hopkins Bloomberg School of Public Health, Universidad Peruana Cayetano Heredia and A.B. PRISMA.
Provenance and peer review Not commissioned; internally peer reviewed.
Collaborators Cardiovascular Disease: Antonio Bernabé-Ortiz, Juan P. Casas, George Davey Smith, Shah Ebrahim, Robert H. Gilman, Luis Huicho, Germán Málaga, J. Jaime Miranda, Víctor M. Montori, Liam Smeeth; Chronic Pulmonary Disease: William Checkley, Gregory B. Diette, Robert H. Gilman, Luis Huicho, Fabiola León-Velarde, María Rivera, Robert A. Wise; Training and Capacity Building: William Checkley, Robert H. Gilman, J. Jaime Miranda, Katherine Sacksteder.
If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.