Cardiorespiratory effects of indoor ozone exposure during sleep and the influencing factors: A prospective study among adults in China.

Ambient ozone (O3) is recognized as a significant air pollutant with implications for cardiorespiratory health, yet the effects of indoor O3 exposure have received less consideration. Furthermore, while sleep occupies one-third of life, research on the health consequences of O3 exposure during this crucial period is scarce. This study aimed to investigate associations of indoor O3 during sleep with cardiorespiratory function and potential predisposing factors. A prospective study among 81 adults was conducted in Beijing, China. Repeated measurements of cardiorespiratory indices reflecting lung function, airway inflammation, cardiac autonomic function, blood pressure, systemic inflammation, platelet and glucose were performed on each subject. Real-time concentrations of indoor O3 during sleep were monitored. Associations of O3 with cardiorespiratory indices were evaluated using linear mixed-effect model. Effect modification by baseline lifestyles (diet, physical activity, sleep-related factors) and psychological status (stress and depression) were investigated through interaction analysis. The average indoor O3 concentration during sleep was 20.3 µg/m3, which was well below current Chinese indoor air quality standard of 160 µg/m3. O3 was associated with most respiratory indicators of decreased airway function except airway inflammation; whereas the cardiovascular effects were only manifested in autonomic dysfunction and not in others. An interquartile range increases in O3 at 6-h average was associated with changes of -3.60 % (95 % CI: -6.19 %, -0.93 %) and -9.60 % (95 % CI: -14.53 %, -4.39 %) in FVC and FEF25-75, respectively. Further, stronger effects were noted among participants with specific dietary patterns, poorer sleep and higher level of depression. This study provides the first general population-based evidence that low-level exposure to indoor O3 during sleep has greater effects on the respiratory system than on the cardiovascular system. Our findings identify the respiratory system as an important target for indoor O3 exposure, and particularly highlight the need for greater awareness of indoor air quality, especially during sleep.

Long-term exposures to ambient particulate matter and ozone pollution with lower extremity deep vein thrombosis after surgical operations: a retrospective case-control study in Beijing, China.

BACKGROUND: Lower extremity deep vein thrombosis (LEDVT) after surgical operations is a common and fatal disease leading to unfavorable outcomes including death. Nevertheless, there has been insufficient evidence on the associations between ambient air pollution and LEDVT, particularly studies from developing regions. METHODS: Based on 302 LEDVT cases and 302 controls in a general hospital in Beijing, China, this unmatched retrospective case-control study investigated the associations of fine particulate matter (PM2.5), inhalable particulate matter (PM10), and ozone (O3) with odds of LEDVT. RESULTS: Per 10 µg/m3 increase in PM2.5, PM10, and O3 at 3-month, 6-month, and 2-year average was associated with increased LEDVT odds [odds ratios (ORs) for PM2.5: 1.10 (95%CI: 1.05, 1.14), 1.14 (95%CI: 1.09, 1.18), and 1.30 (95%CI: 1.06, 1.61); ORs for PM10: 1.06 (95%CI: 1.02, 1.10), 1.12 (95%CI: 1.08, 1.16), and 1.29 (95%CI: 1.03, 1.61); ORs for O3: 1.00 (95%CI: 0.96, 1.04), 1.16 (95%CI: 1.02, 1.31), and 2.08 (95%CI: 1.03, 4.18), respectively]. The stratified analyses, exposure-responses curves, and sensitivity analyses further highlighted the robustness of our findings. CONCLUSIONS: Long-term exposures to ambient PM2.5, PM10, and O3 may increase the risk of LEDVT in patients after surgical operations. The results may be implicated in the prevention and control of adverse clinical outcomes of surgical patients associated with ambient air pollution.

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.