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. 2021 May 27;57(5):2000838.
doi: 10.1183/13993003.00838-2020. Print 2021 May.

High eosinophil counts predict decline in FEV1: results from the CanCOLD study

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Free article

High eosinophil counts predict decline in FEV1: results from the CanCOLD study

Wan C Tan et al. Eur Respir J. .
Free article

Abstract

Introduction: The aim of this study was to examine the association between blood eosinophil levels and the decline in lung function in individuals aged >40 years from the general population.

Methods: The study evaluated the eosinophil counts from thawed blood in 1120 participants (mean age 65 years) from the prospective population-based Canadian Cohort of Obstructive Lung Disease (CanCOLD) study. Participants answered interviewer-administered respiratory questionnaires and performed pre-/post-bronchodilator spirometric tests at 18-month intervals; computed tomography (CT) imaging was performed at baseline. Statistical analyses to describe the relationship between eosinophil levels and decline in forced expiratory volume in 1 s (FEV1) were performed using random mixed-effects regression models with adjustments for demographics, smoking, baseline FEV1, ever-asthma and history of exacerbations in the previous 12 months. CT measurements were compared between eosinophil subgroups using ANOVA.

Results: Participants who had a peripheral eosinophil count of ≥300 cells·µL-1 (n=273) had a greater decline in FEV1 compared with those with eosinophil counts of <150 cells·µL-1 (n=430; p=0.003) (reference group) and 150-<300 cells·µL-1 (n=417; p=0.003). The absolute change in FEV1 was -32.99 mL·year-1 for participants with eosinophil counts <150 cells·µL-1; -38.78 mL·year-1 for those with 150-<300 cells·µL-1 and -67.30 mL·year-1 for participants with ≥300 cells·µL-1. In COPD, higher eosinophil count was associated with quantitative CT measurements reflecting both small and large airway abnormalities.

Conclusion: A blood eosinophil count of ≥300 cells·µL-1 is an independent risk factor for accelerated lung function decline in older adults and is related to undetected structural airway abnormalities.

Trial registration: ClinicalTrials.gov NCT00920348.

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Conflict of interest statement

Conflict of interest: W.C. Tan reports grants from Canadian Institute of Heath Research (CIHR/Rx&D Collaborative Research Program, operating grants 93326) with industry partners AstraZeneca Canada Ltd, Boehringer Ingelheim Canada Ltd, GlaxoSmithKline Canada Ltd, Merck, Novartis Pharma Canada Inc., Nycomed Canada Inc. and Pfizer Canada Ltd, during the conduct of the study. Conflict of interest: J. Bourbeau reports funding for the current study from GlaxoSmithKline; grants from CIHR, Canadian Respiratory Research Network (CRRN), Foundation of the MUHC and Aerocrine, personal fees for consultancy and lectures from Canadian Thoracic Society and Chest, grants and personal fees for advisory board work and lectures from AstraZeneca, Boehringer Ingelheim, Grifols, GlaxoSmithKline, Novartis and Trudell, outside the submitted work. Conflict of interest: G. Nadeau was an employee of and held shares in a pharmaceutical company at the time of the study. Conflict of interest: W. Wang has nothing to disclose. Conflict of interest: N. Barnes was an employee of and held shares in a pharmaceutical company at the time of the study. Conflict of interest: S.H. Landis held stocks and shares in GlaxoSmithKline, during the conduct of the study. Conflict of interest: M. Kirby is a consultant for VIDA Diagnostics Inc., outside the submitted work. Conflict of interest: J.C. Hogg has nothing to disclose. Conflict of interest: D.D. Sin reports grants from Merck, personal fees for advisory board work from Sanofi-Aventis and Regeneron, grants and personal fees for research from Boehringer Ingelheim, grants and personal fees for advisory board work and lectures from AstraZeneca, personal fees for advisory board work and lectures from Novartis, outside the submitted work.

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