Martha E Billings1, Diane Gold2,3, Adam Szpiro4, Carrie P Aaron5, Neal Jorgensen4, Amanda Gassett6,7, Peter J Leary1, Joel D Kaufman6,7, Susan R Redline2. 1. 1 UW Medicine Sleep Center, Division of Pulmonary, Critical Care & Sleep Medicine, Department of Medicine. 2. 2 Department of Medicine, Brigham and Women's Hospital, Harvard School of Medicine, Boston, Massachusetts. 3. 3 Department of Environmental Health, School of Public Health, Harvard University, Boston, Massachusetts; and. 4. 4 Department of Statistics. 5. 5 Department of Medicine, Columbia University, New York, New York. 6. 6 Department of Environmental and Occupational Health Sciences, and. 7. 7 Department of Epidemiology, School of Public Health, University of Washington, Seattle, Washington.
Abstract
RATIONALE: Air pollution may influence sleep through airway inflammation or autonomic nervous system pathway alterations. Epidemiological studies may provide evidence of relationships between chronic air pollution exposure and sleep apnea. OBJECTIVES: To determine whether ambient-derived pollution exposure is associated with obstructive sleep apnea and objective sleep disruption. METHODS: We analyzed data from a sample of participants in MESA (Multi-Ethnic Study of Atherosclerosis) who participated in both the Sleep and Air studies. Mean annual and 5-year exposure levels to nitrogen dioxide (NO2) and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) were estimated at participants' homes using spatiotemporal models based on cohort-specific monitoring. Participants completed in-home full polysomnography and 7 days of wrist actigraphy. We used multivariate models, adjusted for demographics, comorbidities, socioeconomic factors, and site, to assess whether air pollution was associated with sleep apnea (apnea-hypopnea index ≥ 15) and actigraphy-measured sleep efficiency. RESULTS: The participants (n = 1,974) were an average age of 68 (±9) years, 46% male, 36% white, 24% Hispanic, 28% black, and 12% Asian; 48% had sleep apnea and 25% had a sleep efficiency of ≤88%. A 10 ppb annual increase in NO2 exposure was associated with 39% greater adjusted odds of sleep apnea (95% confidence interval [CI], 1.03-1.87). A 5 μg/m3 greater annual PM2.5 exposure was also associated with 60% greater odds of sleep apnea (95% CI, 0.98-2.62). Sleep efficiency was not associated with air pollution levels in fully adjusted models. CONCLUSIONS: Individuals with higher annual NO2 and PM2.5 exposure levels had a greater odds of sleep apnea. These data suggest that in addition to individual risk factors, environmental factors also contribute to the variation of sleep disorders across groups, possibly contributing to health disparities.
RATIONALE: Air pollution may influence sleep through airway inflammation or autonomic nervous system pathway alterations. Epidemiological studies may provide evidence of relationships between chronic air pollution exposure and sleep apnea. OBJECTIVES: To determine whether ambient-derived pollution exposure is associated with obstructive sleep apnea and objective sleep disruption. METHODS: We analyzed data from a sample of participants in MESA (Multi-Ethnic Study of Atherosclerosis) who participated in both the Sleep and Air studies. Mean annual and 5-year exposure levels to nitrogen dioxide (NO2) and particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) were estimated at participants' homes using spatiotemporal models based on cohort-specific monitoring. Participants completed in-home full polysomnography and 7 days of wrist actigraphy. We used multivariate models, adjusted for demographics, comorbidities, socioeconomic factors, and site, to assess whether air pollution was associated with sleep apnea (apnea-hypopnea index ≥ 15) and actigraphy-measured sleep efficiency. RESULTS: The participants (n = 1,974) were an average age of 68 (±9) years, 46% male, 36% white, 24% Hispanic, 28% black, and 12% Asian; 48% had sleep apnea and 25% had a sleep efficiency of ≤88%. A 10 ppb annual increase in NO2 exposure was associated with 39% greater adjusted odds of sleep apnea (95% confidence interval [CI], 1.03-1.87). A 5 μg/m3 greater annual PM2.5 exposure was also associated with 60% greater odds of sleep apnea (95% CI, 0.98-2.62). Sleep efficiency was not associated with air pollution levels in fully adjusted models. CONCLUSIONS: Individuals with higher annual NO2 and PM2.5 exposure levels had a greater odds of sleep apnea. These data suggest that in addition to individual risk factors, environmental factors also contribute to the variation of sleep disorders across groups, possibly contributing to health disparities.
Entities:
Keywords:
environmental pollutants; health status disparities; obstructive sleep apnea
Authors: Martha E Billings; Robyn T Cohen; Carol M Baldwin; Dayna A Johnson; Brian N Palen; Sairam Parthasarathy; Sanjay R Patel; Maureen Russell; Ignacio E Tapia; Ariel A Williamson; Sunil Sharma Journal: Chest Date: 2020-09-30 Impact factor: 10.262