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.

No abstract

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.

This study estimates adult mortalities attributed to PM2.5 across urban China in 2015 and the corresponding mortalities that might be avoided by meeting the yearly averaged indoor PM2.5 threshold in the newly established Assessment Standard for Healthy Building (ASHB) and seven other potential thresholds. We use outdoor PM2.5 concentrations from ∼1500 monitoring sites in 339 Chinese cities, coupled with a detailed exposure model, to estimate outdoor and indoor exposures to PM2.5 originating outdoors. We proceed to calculate premature mortality attributable to PM2.5 exposure using an integrated exposure-response model. Results indicate that indoor exposures accounted for 66%–87% of total exposure to PM2.5 of outdoor origin and 81% (95% confidence interval (CI), 71%–87%), i.e., 316 000 (95% CI, 176 000–435 000), of the 389 000 (95% CI, 245 000–501 000) mortalities attributable to “outdoor PM2.5” for the urban population ≥25 years of age in China in 2015. Potentially 14 000 (95% CI, 8000–20 000) deaths might be avoided if indoor PM2.5 of outdoor origin met the ASHB guideline of 35 μg/m3 for annual mean indoor PM2.5, and 162 000 (95% CI, 79 000–237 000) deaths might be avoided by meeting a 10 μg/m3 threshold. The analysis in this work should be helpful in formulating indoor air quality policies.

Major wildfires starting in the summer of 2020 along the west coast of the United States made PM 2.5 concentrations in this region rank among the highest in the world. Washington was impacted both by active wildfires in the state and aged wood smoke transported from fires in Oregon and California. This study aims to estimate the magnitude and disproportionate spatial impacts of increased PM 2.5 concentrations attributable to these wildfires on population health. Daily PM 2.5 concentrations for each county before and during the 2020 Washington wildfire episode (September 7–19) were obtained from regulatory air monitors. Utilizing previously established concentration‐response function (CRF) of PM 2.5 (CRF of total PM 2.5 ) and odds ratio (OR) of wildfire smoke days (OR of wildfire smoke days) for mortality, we estimated excess mortality attributable to the increased PM 2.5 concentrations in Washington. On average, daily PM 2.5 concentrations increased 97.1 μg/m 3 during the wildfire smoke episode. With CRF of total PM 2.5 , the 13‐day exposure to wildfire smoke was estimated to lead to 92.2 (95% CI: 0.0, 178.7) more all‐cause mortality cases; with OR of wildfire smoke days, 38.4 (95% CI: 0.0, 93.3) increased all‐cause mortality cases and 15.1 (95% CI: 0.0, 27.9) increased respiratory mortality cases were attributable to the wildfire smoke episode. The potential impact of avoiding elevated PM 2.5 exposures during wildfire events significantly reduced the mortality burden. Because wildfire smoke episodes are likely to impact the Pacific Northwest in future years, continued preparedness and mitigations to reduce exposures to wildfire smoke are necessary to avoid excess health burden.

No abstract

The Mobile ObserVations of Ultrafine Particles study was a two-year project to analyze potential air quality impacts of ultrafine particles (UFPs) from aircraft traffic for communities near an international airport. The study assessed UFP concentrations within 10 miles of the airport in the directions of aircraft flight. Over the course of four seasons, this study conducted a mobile sampling scheme to collect time-resolved measures of UFP, CO 2 , and black carbon (BC) concentrations, as well as UFP size distributions. Primary findings were that UFPs were associated with both roadway traffic and aircraft sources, with the highest UFP counts found on the major roadway (I-5). Total concentrations of UFPs alone (10–1000 nm) did not distinguish roadway and aircraft features. However, key differences existed in the particle size distribution and the black carbon concentration for roadway and aircraft features. These differences can help distinguish between the spatial impact of roadway traffic and aircraft UFP emissions using a combination of mobile monitoring and standard statistical methods.