Association of multiple air pollutants with oxygen saturation during sleep in COPD patients: Effect modification by smoking status and airway inflammatory phenotypes

Air pollution contributes substantially to the development of chronic obstructive pulmonary disease (COPD). To date, the effect of air pollution on oxygen saturation (SpO₂) during sleep and potential susceptibility factors remain unknown. In this longitudinal panel study, real-time SpO₂ was monitored in 132 COPD patients, with 270 nights (1615 h) of sleep SpO₂ recorded. Exhaled nitric oxide (NO), hydrogen sulfide (H₂S) and carbon monoxide (CO) were measured to assess airway inflammatory characteristics. Exposure levels of air pollutants were estimated by infiltration factor method. Generalized estimating equation was used to investigate the effect of air pollutants on sleep SpO₂. Ozone, even at low levels (<60 μg/m³), was significantly associated with decreased SpO₂ and extended time of oxygen desaturation (SpO₂ < 90%), especially in the warm season. The associations of other pollutants with SpO₂ were weak, but significant adverse effects of PM₁₀ and SO₂ were observed in the cold season. Notably, stronger effects of ozone were observed in current smokers. Consistently, smoking-related airway inflammation, characterized by higher levels of exhaled CO and H₂S but lower NO, significantly augmented the effect of ozone on SpO₂ during sleep. This study highlights the importance of ozone control in protecting sleep health in COPD patients.