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Ann Am Thorac Soc. 2017 Jun 14. doi: 10.1513/AnnalsATS.201701-091OC. [Epub ahead of print]

Obstructive Sleep Apnea and Subclinical Interstitial Lung Disease in MESA.

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Columbia University Medical Center, 21611, Department of Medicine, Division of Pulmonology, New York, New York, United States ;
Columbia University, Department of Medicine, New York, New York, United States ;
Brigham and Women's Hospital, 1861, Boston, Massachusetts, United States ;
University of Pennsylvania, Department of Medicine, Perelman School of Medicine, Philadelphia, Pennsylvania, United States ;
University of Washington Medical Center, 21617, Division of Pulmonary and Critical Care Medicine, Seattle, Washington, United States ;
University of Washington, 12Departments of Environmental & Occupational Health Sciences, Medicine, and Epidemiology, Seattle, Washington, United States ;
University of Washington, Department of Biostatistics, Seattle, Washington, United States ;
University of Iowa Carver College of Medicine, Radiology , Department of Radiology , 200 Hawkins Drive , Iowa City, Iowa, United States , 52242 ;
Columbia University, Epidemiology, New York, New York, United States ;
Harvard Medical School, Boston, Massachusetts, United States ; DJGOTTLIEB@PARTNERS.ORG.
Brigham and Women's Hospital and Harvard Medical School, Division of Sleep and Circadian Disorders , Boston, Massachusetts, United States.
Beth Israel Deaconess Medical Center, Department of Medicine, Boston, Massachusetts, United States ;
Columbia University, Divison of Pulmonary, Allergy, and Critical Care Medicine , 161 Fort Washington Ave , Room 3-321A , New York, New York, United States , 10032 ;



Obstructive sleep apnea (OSA) has been postulated to contribute to idiopathic pulmonary fibrosis by promoting alveolar epithelial injury via tractional forces and intermittent hypoxia.


To determine whether OSA is associated with subclinical interstitial lung disease (ILD) and with biomarkers of alveolar epithelial injury and remodeling.


We performed cross-sectional analyses of 1,690 community-dwelling adults who underwent 15-channel in-home polysomnography and thoracic computed tomography (CT) imaging in the Multi-Ethnic Study of Atherosclerosis. We measured the obstructive apnea-hypopnea index (oAHI) from polysomnography and high attenuation areas (HAA) and interstitial lung abnormalities (ILA) from CT. Serum matrix metalloproteinase-7 (MMP-7) and surfactant protein-A (SP-A) were measured by ELISA in 99 participants. We used generalized linear models to adjust for potential confounders.


The mean age was 68 years, and the mean forced vital capacity was 97% predicted. The median oAHI was 8.4 events/hr, and 32% had an oAHI >15. After adjusting for demographics, smoking, and center, an oAHI >15 was associated with a 4.0% HAA increment (95% CI 1.4-6.8%, p=0.003) and a 35% increased odds of ILA (95% CI 13-61%, p=0.001). However, there was evidence that these associations varied by body mass index (BMI) (p for interaction=0.08 and 0.04, respectively). Among those with a BMI <25 kg/m2, an oAHI>15 was associated with a 6.1% HAA increment (95% CI 0.5-12%, p=0.03) and a 2.3-fold increased odds of ILA (95% CI 1.3-4.1, p=0.005). Among those with a BMI >30 kg/m2, an oAHI >15 was associated with a 1.8 greater odds of ILA (95% CI 1.1-2.9, p=0.01) but was not associated with HAA. There were no meaningful associations detected among those with a BMI of 25-30 kg/m2. Greater oAHI was associated higher serum SP-A and MMP-7 levels, particularly among those with a body mass index <25 kg/m2.


Moderate to severe OSA is associated with subclinical ILD and with evidence of alveolar epithelial injury and extracellular matrix remodeling in community-dwelling adults, an association that is strongest among normal weight individuals. These findings support the hypothesis that OSA might contribute to early ILD.

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