IMPORTANCE Exposure to ozone has been associated with cardiovascular mortality, but the underlying biological mechanisms are not yet understood.OBJECTIVE To examine the association between ozone exposure and cardiopulmonary pathophysiologic mechanisms. DESIGN, SETTING, AND PARTICIPANTSA longitudinal study involving 89 healthy adult participants living on a work campus in Changsha City, China, was conducted from December 1, 2014, to January 31, 2015. This unique quasiexperimental setting allowed for better characterization of air pollutant exposure effects because the participants spent most of their time in controlled indoor environments. Concentrations of indoor and outdoor ozone, along with the copollutants particulate matter, nitrogen dioxide, and sulfur dioxide, were monitored throughout the study period and then combined with time-activity information and filtration conditions of each residence and office to estimate 24-hour and 2-week combined indoor and outdoor mean exposure concentrations. Associations between each exposure measure and outcome measure were analyzed using single-pollutant and 2-pollutant linear mixed models controlling for ambient temperature, secondhand smoke exposure, and personal-level time-varying covariates.MAIN OUTCOMES AND MEASURES Biomarkers indicative of inflammation and oxidative stress, arterial stiffness, blood pressure, thrombotic factors, and spirometry were measured at 4 sessions. RESULTSOf the 89 participants, 25 (28%) were women and the mean (SD) age was 31.5 (7.6) years. The 24-hour ozone exposure concentrations ranged from 1.4 to 19.4 parts per billion (ppb), corresponding to outdoor concentrations ranging from 4.3 to 47.9 ppb. Within this range, in models controlling for a second copollutant and other potential confounders, a 10-ppb increase in 24-hour ozone was associated with mean increases of 36.3% (95% CI, 29.9%-43.0%) in the level of platelet activation marker soluble P-selectin, 2.8% (95% CI, 0.6%-5.1%) in diastolic blood pressure, 18.1% (95% CI, 4.5%-33.5%) in pulmonary inflammation markers fractional exhaled nitric oxide, and 31.0% (95% CI, 0.2%-71.1%) in exhaled breath condensate nitrite and nitrate as well as a −9.5% (95% CI, −17.7% to −1.4%) decrease in arterial stiffness marker augmentation index. A 10-ppb increase in 2-week ozone was associated with increases of 61.1% (95% CI, 37.8%-88.2%) in soluble P-selectin level and 126.2% (95% CI, 12.1%-356.2%) in exhaled breath condensate nitrite and nitrate level. Other measured biomarkers, including spirometry, showed no significant associations with either 24-hour ozone or 2-week ozone exposures.CONCLUSIONS AND RELEVANCE Short-term ozone exposure at levels not associated with lung function changes was associated with platelet activation and blood pressure increases, suggesting a possible mechanism by which ozone may affect cardiovascular health.
This study evaluates the COVID-19 impacts on traffic-related air pollution, including ultrafine particles (UFPs), PM 2.5 , black carbon (BC), NO, NO 2 , NO x , and CO in a Northwestern US city. Hourly traffic, air pollutants, and meteorological data on/near a major freeway in the downtown of Seattle, Washington, were collected for five weeks before and ten weeks after the Washington Stay Home Order (SHO) was enacted, respectively (February 17–May 31, 2020). The pollutants between pre- and post-SHO periods were compared, and their differences were statistically tested. Besides, first-order multivariate autoregressive (MAR(1)) models were developed to reveal the impacts specific to the change of traffic due to the COVID-19 responses while controlling for meteorological conditions. Results indicate that compared with those in the post-SHO period, the median traffic volume and road occupancy decreased by 37% and 52%, respectively. As for pollutants, the median BC and PM 2.5 levels significantly decreased by 25% and 33%, relatively, while NO, NO 2 , NO x , and CO decreased by 33%, 29%, 30%, and 17%, respectively. In contrast, neither size-resolved UFPs nor total UFPs showed significant changes between the two periods, although larger particles (≥115.5 nm) decreased by 4–29%. Additionally, significant differences were found in meteorological conditions between the two periods. Based on the MAR(1) models, controlling for meteorological conditions, the COVID-19 responses were associated with significant decreases in median levels of traffic-related pollutants including 11.5–154.0 nm particles (ranging from −3% [95% confidence interval (CI): −1%, −4%] to −12% [95% CI: −10%, −14%]), total UFPs (−7% [95% CI: −5%, −8%]), BC (−6% [95% CI: −5%, −7%]), PM 2.5 (−2% [95% CI: −1%, −3%]), NO, NO 2 , NO x (ranging from −3% [95% CI: −2%, −4%] to −10% [95% CI: −18%, −12%]), and CO (−4% [95% CI, −3%, −5%]). These findings illustrate that the conclusion of the COVID-19 impacts on urban traffic-related air pollutant levels could be completely different in scenarios whether meteorology was adjusted for or not. Fully adjusting for meteorology, this study shows that the COVID-19 responses were associated with much more reductions in traffic-related UFPs than PM 2.5 in the Seattle region, in contrast to the reverse trend from the direct empirical data comparison.
High-efficiency particulate air (HEPA) filtration in combination with an electrostatic precipitator (ESP) can be a cost-effective approach to reducing indoor particulate exposure, but ESPs produce ozone. The health effect of combined ESP-HEPA filtration has not been examined. We conducted an intervention study in 89 volunteers. At baseline, the air-handling units of offices and residences for all subjects were comprised of coarse, ESP, and HEPA filtration. During the 5-week long intervention, the subjects were split into 2 groups, 1 with just the ESP removed and the other with both the ESP and HEPA removed. Each subject was measured for cardiopulmonary risk indicators once at baseline, twice during the intervention, and once 2 weeks after baseline conditions were restored. Measured indoor and outdoor PM and ozone concentrations, coupled with time-activity data, were used to calculate exposures. Removal of HEPA filters increased 24-hour mean PM exposure by 38 (95% CI: 31, 45) μg/m . Removal of ESPs decreased 24-hour mean ozone exposure by 2.2 (2.0, 2.5) ppb. No biomarkers were significantly associated with HEPA filter removal. In contrast, ESP removal was associated with a -16.1% (-21.5%, -10.4%) change in plasma-soluble P-selectin and a -3.0% (-5.1%, -0.8%) change in systolic blood pressure, suggesting reduced cardiovascular risks.
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